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  • 1.
    Biglarnia, Ali-Reza
    et al.
    Skåne University Hospital;Lund University.
    Huber-Lang, Markus
    Univ Hosp Ulm, Germany.
    Mohlin, Camilla
    Linnéuniversitetet, Fakulteten för Hälso- och livsvetenskap (FHL), Institutionen för kemi och biomedicin (KOB).
    Nilsson Ekdahl, Kristina
    Linnéuniversitetet, Fakulteten för Hälso- och livsvetenskap (FHL), Institutionen för kemi och biomedicin (KOB). Uppsala University.
    Nilsson, Bo
    Uppsala University.
    The multifaceted role of complement in kidney transplantation2018Ingår i: Nature Reviews Nephrology, ISSN 1759-5061, E-ISSN 1759-507X, Vol. 14, nr 12, s. 767-781Artikel, forskningsöversikt (Refereegranskat)
    Abstract [en]

    Increasing evidence indicates an integral role for the complement system in the deleterious inflammatory reactions that occur during critical phases of the transplantation process, such as brain or cardiac death of the donor, surgical trauma, organ preservation and ischaemia-reperfusion injury, as well as in humoral and cellular immune responses to the allograft. Ischaemia is the most common cause of complement activation in kidney transplantation and in combination with reperfusion is a major cause of inflammation and graft damage. Complement also has a prominent role in antibody-mediated rejection (ABMR) owing to ABO and HL A incompatibility, which leads to devastating damage to the transplanted kidney. Emerging drugs and treatment modalities that inhibit complement activation at various stages in the complement cascade are being developed to ameliorate the damage caused by complement activation in transplantation. These promising new therapies have various potential applications at different stages in the process of transplantation, including inhibiting the destructive effects of ischaemia and/or reperfusion injury, treating ABMR, inducing accommodation and modulating the adaptive immune response.

  • 2. Demirel, Isak
    et al.
    Vumma, Ravi
    Mohlin, Camilla
    Linnéuniversitetet, Fakultetsnämnden för naturvetenskap och teknik, Institutionen för naturvetenskap, NV.
    Svensson, Lovisa
    Linnéuniversitetet, Fakultetsnämnden för naturvetenskap och teknik, Institutionen för naturvetenskap, NV.
    Säve, Susanne
    Linnéuniversitetet, Fakultetsnämnden för naturvetenskap och teknik, Institutionen för naturvetenskap, NV.
    Persson, Katarina
    Linnéuniversitetet, Fakultetsnämnden för naturvetenskap och teknik, Institutionen för naturvetenskap, NV.
    Nitric Oxide Activates IL-6 Production and Expression in Human Renal Epithelial Cells2012Ingår i: American Journal of Nephrology, ISSN 0250-8095, E-ISSN 1421-9670, Vol. 36, nr 6, s. 524-530Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Background/Aims: Increased nitric oxide (NO) production or inducible form of NO synthase activity have been documented in patients suffering from urinary tract infection (UTI), but the role of NO in this infection is unclear. We investigated whether NO can affect the host response in human renal epithelial cells by modulating IL-6 production and mRNA expression. Methods: The human renal epithelial cell line A498 was infected with a uropathogenic Escherichia coli (UPEC) strain and/or the NO donor DETA/NO. The IL-6 production and mRNA expression were evaluated by ELISA and real-time RT-PCR. IL-6 mRNA stability was evaluated by analyzing mRNA degradation by real-time RT-PCR. Results: DETA/NO caused a significant (p < 0.05) increase in IL-6 production. Inhibitors of p38 MAPK and ERK1/2 signaling, but not JNK, were shown to significantly suppress DETA/NO-induced IL-6 production. UPEC-induced IL-6 production was further increased (by 73 +/- 23%, p < 0.05) in the presence of DETA/NO. The IL-6 mRNA expression increased 2.1 +/- 0.17-fold in response to DETA/NO, while the UPEC-evoked increase was pronounced (20 +/- 4.5-fold). A synergistic effect of DETA/NO on UPEC-induced IL-6 expression was found (33 +/- 7.2-fold increase). The IL-6 mRNA stability studies showed that DETA/NO partially attenuated UPEC-induced degradation of IL-6 mRNA. Conclusions: NO was found to stimulate IL-6 in renal epithelial cells through p38 MAPK and ERK1/2 signaling pathways and also to increase IL-6 mRNA stability in UPEC-infected cells. This study proposes a new role for NO in the host response during UTI by modulating the transcription and production of the cytokine IL-6. Copyright (C) 2012 S. Karger AG, Basel

  • 3.
    Englund-Johansson, Ulrika
    et al.
    Department of Ophthalmology, Clinical Sciences, Lund, University of Lund, Sweden..
    Mohlin, Camilla
    Linnéuniversitetet, Fakultetsnämnden för naturvetenskap och teknik, Institutionen för naturvetenskap, NV.
    Liljekvist-Soltic, Ingela
    Department of Ophthalmology, Clinical Sciences, Lund, University .
    Ekström, Per
    Department of Ophthalmology, Clinical Sciences, Lund, University .
    Johansson, Kjell
    Linnéuniversitetet, Fakultetsnämnden för naturvetenskap och teknik, Institutionen för naturvetenskap, NV.
    Human neural progenitor cells promote photoreceptor survival in retinal explants2010Ingår i: Experimental Eye Research, ISSN 0014-4835, E-ISSN 1096-0007, Vol. 90, nr 2, s. 292-299Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Different types of progenitor and stem cells have been shown to provide neuroprotection in animal models of photoreceptor degeneration. The present study was conducted to investigate whether human neural progenitor cells (HNPCs) have neuroprotective properties on retinal explants models with calpain- and caspase-3-dependent photoreceptor cell death. In the first experiments, HNPCs in a feeder layer were co-cultured for 6 days either with postnatal rd1 mouse or normal rat retinas. Retinal histological sections were used to determine outer nuclear layer (ONL) thickness, and to detect the number of photoreceptors with labeling for calpain activity, cleaved caspase-3 and TUNEL. The ONL thickness of co-cultured rat and rd1 retinas was found to be almost 10% and 40% thicker, respectively, compared to controls. Cell counts of calpain activity, cleaved caspase-3 and TUNEL labeled photoreceptors in both models revealed a 30-50% decrease when co-cultured with HNPCs. The results represent significant increases of photoreceptor survival in the co-cultured retinas. In the second experiments, for an identification of putative survival factors, or a combination of them, a growth factor profile was performed on conditioned medium. The relative levels of various growth factors were analyzed by densitometric measurements of growth factor array membranes. Following growth factors were identified as most potential survival factors; granulocyte colony stimulating factor (G-CSF), granulocyte-macrophage colony stimulating factor (GMCSF), insulin-like growth factor II (IGF-II), neurotrophic factor 3 (NT-3), placental growth factor (PIGF), transforming growth factors (TGF-beta1 and TGF-beta2) and vascular endothelial growth factor (VEGF-D). HNPCs protect both against calpain- and caspase-3-dependent photoreceptor cell death in the rd1 mouse and against caspase-3-dependent photoreceptor cell death in normal rat retinas in vitro. The protective effect is possibly achieved by a variety of growth factors secreted from the HNPCs.

  • 4.
    Eriksson, Oskar
    et al.
    Uppsala University, Sweden.
    Mohlin, Camilla
    Linnéuniversitetet, Fakulteten för Hälso- och livsvetenskap (FHL), Institutionen för kemi och biomedicin (KOB).
    Nilsson, Bo
    Uppsala University, Sweden.
    Nilsson Ekdahl, Kristina
    Linnéuniversitetet, Fakulteten för Hälso- och livsvetenskap (FHL), Institutionen för kemi och biomedicin (KOB). Uppsala University, Sweden.
    The Human Platelet as an Innate Immune Cell: Interactions Between Activated Platelets and the Complement System2019Ingår i: Frontiers in Immunology, ISSN 1664-3224, E-ISSN 1664-3224, Vol. 10, s. 1-16, artikel-id 1590Artikel, forskningsöversikt (Refereegranskat)
    Abstract [en]

    Platelets play an essential role in maintaining homeostasis in the circulatory system after an injury by forming a platelet thrombus, but they also occupy a central node in the intravascular innate immune system. This concept is supported by their extensive interactions with immune cells and the cascade systems of the blood. In this review we discuss the close relationship between platelets and the complement system and the role of these interactions during thromboinflammation. Platelets are protected from complement-mediated damage by soluble and membrane-expressed complement regulators, but they bind several complement components on their surfaces and trigger complement activation in the fluid phase. Furthermore, localized complement activation may enhance the procoagulant responses of platelets through the generation of procoagulant microparticles by insertion of sublytic amounts of C5b9 into the platelet membrane. We also highlight the role of post-translational protein modifications in regulating the complement system and the critical role of platelets in driving these reactions. In particular, modification of disulfide bonds by thiol isomerases and protein phosphorylation by extracellular kinases have emerged as important mechanisms to fine-tune complement activity in the platelet microenvironment. Lastly, we describe disorders with perturbed complement activation where part of the clinical presentation includes uncontrolled platelet activation that results in thrombocytopenia, and illustrate how complement-targeting drugs are alleviating the prothrombotic phenotype in these patients. Based on these clinical observations, we discuss the role of limited complement activation in enhancing platelet activation and consider how these drugs may provide opportunities for further dissecting the complex interactions between complement and platelets.

  • 5.
    Gullberg, Maria
    et al.
    Linnéuniversitetet, Fakultetsnämnden för naturvetenskap och teknik, Institutionen för naturvetenskap, NV.
    Tolf, Conny
    Linnéuniversitetet, Fakultetsnämnden för naturvetenskap och teknik, Institutionen för naturvetenskap, NV.
    Jonsson, Nina
    Linnéuniversitetet, Fakultetsnämnden för naturvetenskap och teknik, Institutionen för naturvetenskap, NV.
    Polacek, Charlotta
    Precechtelova, Jana
    Badurova, Miriam
    Sojka, Martin
    Mohlin, Camilla
    Linnéuniversitetet, Fakultetsnämnden för naturvetenskap och teknik, Institutionen för naturvetenskap, NV.
    Israelsson, Stina
    Linnéuniversitetet, Fakultetsnämnden för naturvetenskap och teknik, Institutionen för naturvetenskap, NV.
    Johansson, Kjell
    Linnéuniversitetet, Fakultetsnämnden för naturvetenskap och teknik, Institutionen för naturvetenskap, NV.
    Bopegamage, Shubhada
    Hafenstein, Susan
    Lindberg, A. Michael
    Linnéuniversitetet, Fakultetsnämnden för naturvetenskap och teknik, Institutionen för naturvetenskap, NV.
    A single coxsackievirus B2 capsid residue controls cytolysis and apoptosis in rhabdomyosarcoma cells.2010Ingår i: Journal of Virology, ISSN 0022-538X, E-ISSN 1098-5514, Vol. 84, nr 12, s. 5868-5879Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Coxsackievirus B2 (CVB2), one of six human pathogens of the group B coxsackieviruses within the enterovirus genus of Picornaviridae, causes a wide spectrum of human diseases ranging from mild upper respiratory illnesses to myocarditis and meningitis. The CVB2 prototype strain Ohio-1 (CVB2O) was originally isolated from a patient with summer grippe in the 1950s. Later on, CVB2O was adapted to cytolytic replication in rhabdomyosarcoma (RD) cells. Here, we present analyses of the correlation between the adaptive mutations of this RD variant and the cytolytic infection in RD cells. Using reverse genetics, we identified a single amino acid change within the exposed region of the VP1 protein (glutamine to lysine at position 164) as the determinant for the acquired cytolytic trait. Moreover, this cytolytic virus induced apoptosis, including caspase activation and DNA degradation, in RD cells. These findings contribute to our understanding of the host cell adaptation process of CVB2O and provide a valuable tool for further studies of virus-host interactions.

  • 6.
    Mohlin, Camilla
    Linnéuniversitetet, Fakulteten för Hälso- och livsvetenskap (FHL), Institutionen för kemi och biomedicin (KOB).
    Evaluation of Congo red fluorescence in degenerating cultured porcine retina.2016Konferensbidrag (Refereegranskat)
  • 7.
    Mohlin, Camilla
    Linnéuniversitetet, Fakulteten för Hälso- och livsvetenskap (FHL), Institutionen för medicin och optometri (MEO).
    Neural progenitor cell-derived neurotrophic support for the degenerating retina: an in vitro study2013Doktorsavhandling, sammanläggning (Övrigt vetenskapligt)
  • 8.
    Mohlin, Camilla
    et al.
    Linnéuniversitetet, Fakulteten för Hälso- och livsvetenskap (FHL), Institutionen för kemi och biomedicin (KOB).
    Delbro, Dick
    Örebro University.
    Kvanta, Anders
    Karolinska Institutet.
    Johansson, Kjell
    Kristianstad University.
    Evaluation of Congo Red Staining in Degenerating Porcine Photoreceptors In Vitro: Protective Effects by Structural and Trophic Support2018Ingår i: Journal of Histochemistry and Cytochemistry, ISSN 0022-1554, E-ISSN 1551-5044, Vol. 66, nr 9Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Congo red (CR) is a histological stain used for the detection of extracellular amyloids mediating various neurodegenerative diseases. Given that damaged photoreceptors appear to degenerate similarly to other nerve cells, CR staining was evaluated in experimentally injured porcine retina. CR staining appeared mostly as discrete cytosolic deposits with no obvious plaque formation during the investigated time period. Increases of CR labeling coincided temporally with the known accumulation of mislocalized opsins and increases of cell death. Coculture, either with human retinal pigment epithelium (ARPE) or human neural progenitor (ReN) cells, was accompanied by a significant reduction of CR labeling. Of particular interest was the reduction of CR labeling in cone photoreceptors, which are important for the perception of color and fine details and afflicted in age-related macular degeneration (AMD). Electron microscopy revealed inclusions in the inner segment, cell body, and occasionally synaptic terminals of photoreceptor cells in cultured specimens. Closer examinations indicated the presence of different types of inclusions resembling protein aggregates as well as inclusion bodies. The current results indicate that injury-related response resulted in accumulation of CR deposits in photoreceptor cells, and that trophic and/or structural support attenuated this response.

  • 9.
    Mohlin, Camilla
    et al.
    Linnéuniversitetet, Fakultetsnämnden för naturvetenskap och teknik, Institutionen för naturvetenskap, NV.
    Johansson, Kjell
    Linnéuniversitetet, Fakultetsnämnden för naturvetenskap och teknik, Institutionen för naturvetenskap, NV.
    Death of photoreceptors in organotypic retinal explant cultures: implication of rhodopsin accumulation and endoplasmic reticulum stress.2011Ingår i: Journal of Neuroscience Methods, ISSN 0165-0270, E-ISSN 1872-678X, ISSN 0165-0270, Vol. 197, nr 1, s. 56-64Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Here we suggest that endoplasmic reticulum (ER)-stress may be induced following aberrant rhodopsin accumulation in photoreceptors in explanted rat retinas. Rhodopsin accumulation was accompanied by increased phosphorylation of pancreatic ER-kinase and eukaryotic initiator factor 2α as well as increased levels of C/EBP homologous protein, glucose-regulated protein 78 and eventually increased cleaved caspase-12 and cleaved caspase-3. Glucose-regulated protein 78, pancreatic ER-kinase, caspase-12 and cleaved caspase-3 were present in photoreceptors, indicating that ER-stress and apoptosis are induced in this cell population. These results suggest that ER-stress and subsequent apoptosis is induced in healthy photoreceptors, presumably by aberrant accumulation of rhodopsin and the phosphorylation of eukaryotic initiator factor 2α. The explant culture system may allow investigations of neuroprotective strategies.

  • 10.
    Mohlin, Camilla
    et al.
    Linnéuniversitetet, Fakulteten för Hälso- och livsvetenskap (FHL), Institutionen för kemi och biomedicin (KOB).
    Johansson, Kjell
    Örebro University.
    Nilsson Ekdahl, Kristina
    Linnéuniversitetet, Fakulteten för Hälso- och livsvetenskap (FHL), Institutionen för kemi och biomedicin (KOB). Uppsala University.
    Complement factor involvement during experimental AMD2015Ingår i: Molecular Immunology, ISSN 0161-5890, E-ISSN 1872-9142, Vol. 67, nr 1, s. 163-163Artikel i tidskrift (Övrigt vetenskapligt)
  • 11.
    Mohlin, Camilla
    et al.
    Linnéuniversitetet, Fakultetsnämnden för naturvetenskap och teknik, Institutionen för naturvetenskap, NV.
    Liljekvist-Soltic, Ingela
    Linnéuniversitetet, Fakultetsnämnden för naturvetenskap och teknik, Institutionen för naturvetenskap, NV.
    Johansson, Kjell
    Linnéuniversitetet, Fakultetsnämnden för naturvetenskap och teknik, Institutionen för naturvetenskap, NV.
    Further assessment of neuropathology in retinal explants and neuroprotection by human neural progenitor cells.2011Ingår i: Journal of Neural Engineering, ISSN 1741-2560, E-ISSN 1741-2552, Vol. 8, nr 6, s. Article ID: 066012-Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Explanted rat retinas show progressive photoreceptor degeneration that appears to be caspase-12-dependent. Decrease in photoreceptor density eventually affects the inner retina, particularly in the bipolar cell population. Explantation and the induced photoreceptor degeneration are accompanied by activation of Müller and microglia cells. The goal of this study was to determine whether the presence of a feeder layer of human neural progenitor cells (hNPCs) could suppress the degenerative and reactive changes in the explants. Immunohistochemical analyses showed considerable sprouting of rod photoreceptor axon terminals into the inner retina and reduced densities of cone and rod bipolar cells. Both sprouting and bipolar cell degenerations were significantly lower in retinas cultured with feeder layer cells compared to cultured controls. A tendency toward reduced microglia activation in the retinal layers was also noted in the presence of feeder layer cells. These results indicate that hNPCs or factors produced by them can limit the loss of photoreceptors and secondary injuries in the inner retina. The latter may be a consequence of disrupted synaptic arrangement.

  • 12.
    Mohlin, Camilla
    et al.
    Linnéuniversitetet, Fakultetsnämnden för naturvetenskap och teknik, Institutionen för naturvetenskap, NV.
    Liljekvist-Soltic, Ingela
    Linnéuniversitetet, Fakultetsnämnden för naturvetenskap och teknik, Institutionen för naturvetenskap, NV.
    Olofsson, Jenny
    Linnéuniversitetet, Fakultetsnämnden för naturvetenskap och teknik, Institutionen för naturvetenskap, NV.
    Johansson, Kjell
    Linnéuniversitetet, Fakultetsnämnden för naturvetenskap och teknik, Institutionen för naturvetenskap, NV.
    Neuropathology of cultured retinas: degenerative events and rescue paradigms2011Ingår i: Advances in Eye Research. Volume 2 / [ed] William L. Thomsen, Nova Science Publishers, Inc., 2011, nr 2, s. 177-190Kapitel i bok, del av antologi (Refereegranskat)
  • 13.
    Mohlin, Camilla
    et al.
    Linnéuniversitetet, Fakulteten för Hälso- och livsvetenskap (FHL), Institutionen för kemi och biomedicin (KOB).
    Mollik, Tanzina
    Johansson, Kjell
    Human neural progenitor cells are not sufficient to support degenerating photoreceptors in cultured porcine retina.2014Konferensbidrag (Refereegranskat)
  • 14.
    Mohlin, Camilla
    et al.
    Linnéuniversitetet, Fakulteten för Hälso- och livsvetenskap (FHL), Institutionen för kemi och biomedicin (KOB).
    Petrus-Reurer, S.
    Karolinska Institutet;Karolinska Univ Hosp.
    Lanner, F.
    Karolinska Institutet;Karolinska Univ Hosp.
    Sandholm, Kerstin
    Linnéuniversitetet, Fakulteten för Hälso- och livsvetenskap (FHL), Institutionen för kemi och biomedicin (KOB).
    Kvanta, A.
    Karolinska Institutet.
    Nilsson, B.
    Uppsala University.
    Nilsson Ekdahl, Kristina
    Linnéuniversitetet, Fakulteten för Hälso- och livsvetenskap (FHL), Institutionen för kemi och biomedicin (KOB). Uppsala University.
    Complement system proteins in human embryonic stem cell-derived retinal pigment epithelial cells co-cultured with or without porcine retina2017Ingår i: Molecular Immunology, ISSN 0161-5890, E-ISSN 1872-9142, Vol. 89, s. 162-163Artikel i tidskrift (Övrigt vetenskapligt)
  • 15.
    Mohlin, Camilla
    et al.
    Linnéuniversitetet, Fakulteten för Hälso- och livsvetenskap (FHL), Institutionen för kemi och biomedicin (KOB).
    Petrus-Reurer, Sandra
    Karolinska Institutet;Karolinska University Hospital.
    Lanner, Fredrik
    Karolinska Institutet;Karolinska University Hospital.
    Sandholm, Kerstin
    Linnéuniversitetet, Fakulteten för Hälso- och livsvetenskap (FHL), Institutionen för kemi och biomedicin (KOB).
    Nilsson, Per H.
    Linnéuniversitetet, Fakulteten för Hälso- och livsvetenskap (FHL), Institutionen för kemi och biomedicin (KOB). Univ Oslo, Norway.
    Nilsson, Bo
    Uppsala University.
    Nilsson Ekdahl, Kristina
    Linnéuniversitetet, Fakulteten för Hälso- och livsvetenskap (FHL), Institutionen för kemi och biomedicin (KOB). Uppsala University.
    Is the polarized secretion of complement factor H of importance in age-related macular degeneration?2018Ingår i: Investigative Ophthalmology and Visual Science, ISSN 0146-0404, E-ISSN 1552-5783, Vol. 59, nr 9Artikel i tidskrift (Övrigt vetenskapligt)
  • 16.
    Mohlin, Camilla
    et al.
    Linnéuniversitetet, Fakulteten för Hälso- och livsvetenskap (FHL), Institutionen för kemi och biomedicin (KOB).
    Sandholm, Kerstin
    Linnéuniversitetet, Fakulteten för Hälso- och livsvetenskap (FHL), Institutionen för kemi och biomedicin (KOB).
    Kvanta, Anders
    Karolinska institutet.
    Nilsson Ekdahl, Kristina
    Linnéuniversitetet, Fakulteten för Hälso- och livsvetenskap (FHL), Institutionen för kemi och biomedicin (KOB). Uppsala university.
    Johansson, Kjell
    Örebro university.
    A model to study complement involvement in experimental retinal degeneration.2018Ingår i: Upsala Journal of Medical Sciences, ISSN 0300-9734, E-ISSN 2000-1967, Vol. 123, nr 1, s. 28-42Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    BACKGROUND: The complement system (CS) plays a role in the pathogenesis of a number of ocular diseases, including diabetic retinopathy (DR), glaucoma, uveitis, and age-related macular degeneration (AMD). Given that many of the complex eye-related degenerative diseases have limited treatment opportunities, we aimed to mimic the in vivo retinal degenerative process by developing a relevant co-culture system.

    METHOD AND MATERIALS: The adult porcine retina was co-cultured with the spontaneously arising human retinal pigment epithelial cells-19 (ARPE-19).

    RESULTS: Inflammatory activity was found after culture and included migrating microglial cells, gliosis, cell death, and CS activation (demonstrated by a minor increase in the secreted anaphylotoxin C3a in co-culture). CS components, including C1q, C3, C4, soluble C5b-9, and the C5a receptor, were expressed in the retina and/or ARPE cells after culture. C1q, C3, and CS regulators such as C4 binding protein (C4BP), factor H (CFH), and factor I (CFI) were secreted after culture.

    DISCUSSION: Thus, our research indicates that this co-culturing system may be useful for investigations of the CS and its involvement in experimental neurodegenerative diseases.

  • 17.
    Mohlin, Camilla
    et al.
    Linnéuniversitetet, Fakulteten för Hälso- och livsvetenskap (FHL), Institutionen för kemi och biomedicin (KOB).
    Sandholm, Kerstin
    Linnéuniversitetet, Fakulteten för Hälso- och livsvetenskap (FHL), Institutionen för kemi och biomedicin (KOB).
    Nilsson Ekdahl, Kristina
    Linnéuniversitetet, Fakulteten för Hälso- och livsvetenskap (FHL), Institutionen för kemi och biomedicin (KOB). Uppsala University, Sweden.
    Nilsson, Bo
    Uppsala University, Sweden.
    The link between morphology and complement in ocular disease2017Ingår i: Molecular Immunology, ISSN 0161-5890, E-ISSN 1872-9142, Vol. 89, s. 84-99Artikel, forskningsöversikt (Refereegranskat)
    Abstract [en]

    The complement system is a vital component of the immune-priveliged human eye that is always active at a low-grade level, preventing harmful intraocular injuries caused by accumulation of turnover products and controlling pathogens to preserve eye homeostasis and vision. The complement system is a double-edged sword that is essential for protection but may also become harmful and contribute to eye pathology. Here, we review the evidence for the involvement of complement system dysregulation in age-related macular degeneration, glaucoma, uveitis, and neuromyelitis optica, highlighting the relationship between morphogical changes and complement system protein expression and regulation in these diseases. The potential benefits of complement inhibition in age-related macular degeneration, glaucoma, uveitis, and neuromyelitis optica are abundant, as are those of further research to improve our understanding of complement-mediated injury in these diseases.

  • 18.
    Mohlin, Camilla
    et al.
    Högskolan i Kalmar, Naturvetenskapliga institutionen.
    Säve, Susanne
    Högskolan i Kalmar, Naturvetenskapliga institutionen.
    Nilsson, Mikael
    Högskolan i Kalmar, Naturvetenskapliga institutionen.
    Persson, Katarina
    Högskolan i Kalmar, Naturvetenskapliga institutionen.
    Studies of the Extracellular ATP-Adenosine Pathway in Human Urinary Tract Epithelial Cells2009Ingår i: Pharmacology, ISSN 0031-7012, E-ISSN 1423-0313, Vol. 84, nr 4, s. 196-202Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Aims: Extracellular ATP may be metabolized to AMP and adenosine by the ectonucleotidases CD39 and CD73 and, in this study, we characterized the pathways for adenosine formation in human urinary tract epithelial cells. Methods: Bladder (RT4) and kidney (A498) epithelial cells were grown in cell culture and the expression of CD39 and CD73 was investigated by reverse transcription-polymerase chain reaction (RT-PCR) and immunohistochemistry. High-performance liquid chromatography was used to determine adenosine formation in cell medium. Results: RT-PCR and immunohistochemistry revealed a high CD73 and a low CD39 expression in human urinary tract epithelial cells, whereas neutrophils had a higher CD39 than CD73 expression. Adenosine was produced when the cells were exposed to 5'-AMP (substrate for CD73), but not when exposed to 5'-ATP (substrate for CD39). A pronounced inhibition of 5'-AMP-induced adenosine formation by the CD73 inhibitor AMP-CP confirmed the involvement of CD73. Adenosine production from 5'-ATP was slightly increased (p < 0.05) when epithelial cells were cocultured with neutrophils. Conclusions: The data demonstrate that adenosine formation from extracellular ATP is negligible in urinary tract epithelial cells due to low CD39 expression in this cell type. However, the epithelial cells express CD73 and are able to convert extracellular AMP to adenosine.

  • 19.
    Mohlin, Camilla
    et al.
    Linnéuniversitetet, Fakulteten för Hälso- och livsvetenskap (FHL), Institutionen för medicin och optometri (MEO).
    Taylor, Linnea
    Univ Lund Hosp.
    Ghosh, Fredrik
    Univ Lund Hosp.
    Johansson, Kjell
    Linnéuniversitetet, Fakulteten för Hälso- och livsvetenskap (FHL), Institutionen för medicin och optometri (MEO). Örebro universitet.
    Autophagy and ER-stress contribute to photoreceptor degeneration in cultured adult porcine retina2014Ingår i: Brain Research, ISSN 0006-8993, E-ISSN 1872-6240, Vol. 1585, s. 167-183Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    The aim of this study was to investigate rod and cone photoreceptor degeneration in organotypic cultures of adult porcine retina. Our hypothesis was that the photoreceptors accumulate opsins, which, together with exposure to cyclic dim light illumination, induce autophagy and endoplasmic reticulum stress (ER-stress) to overcome damaging protein overload. For this purpose, retinas were cultured for 48 h and 72 h during which they were illuminated with dim light for 8 h/day; specimens were analyzed by means of immunohistochemistry, Western blot, real-time polymerase chain reaction (PCR) and transmission electron microscopy. ER-stress and photoreceptor degeneration was observed in conventionally cultured retinas. The additional stress in the form of dim light illumination for 8 h/day resulted in increased levels of the ER-stress markers GRP78/BiP and CHOP, as well as increased level of active caspase-12. Increased autophagic processes in cone and rod photoreceptors were detected by LC3B-II increases and occurrence of autophagosomes at the ultrastructural level. Illumination also resulted in altered protein expression for autophagy inducers such as p62 and Beclin-1. Moreover, there was a decrease in phosphorylated mammalian target of rapamycin (mTOR), which further indicate an increase of autophagy. Rod and cone photoreceptors in retinas from a diurnal animal that were exposed to dim light illumination in vitro displayed autophagy and ER-stress processes. As no alteration of rhodopsin mRNA was observed, autophagy and ER-stress are suggested to decrease rhodopsin protein at the posttranscriptional level. (C) 2014 Elsevier B.V. All rights reserved.

  • 20.
    Mohlin, Camilla
    et al.
    Linnéuniversitetet, Fakulteten för Hälso- och livsvetenskap (FHL), Institutionen för medicin och optometri (MEO).
    Taylor, Linnéa
    Lunds universitet.
    Ghosh, Fredrik
    Lunds universitet.
    Johansson, Kjell
    Linnéuniversitetet, Fakulteten för Hälso- och livsvetenskap (FHL), Institutionen för medicin och optometri (MEO).
    Autophagy en ER-stress contribute to photoreceptor degenenration in cultured adult porcine retinaManuskript (preprint) (Övrigt vetenskapligt)
  • 21.
    Mollick, Tanzina
    et al.
    Örebro University.
    Mohlin, Camilla
    Linnéuniversitetet, Fakulteten för Hälso- och livsvetenskap (FHL), Institutionen för kemi och biomedicin (KOB).
    Johansson, Kjell
    Örebro University.
    Human neural progenitor cells decrease photoreceptor degeneration, normalize opsin distribution and support synapse structure in cultured porcine retina2016Ingår i: Brain Research, ISSN 0006-8993, E-ISSN 1872-6240, Vol. 1646, s. 522-534Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Retinal neurodegenerative disorders like retinitis pigmentosa, age-related macular degeneration, diabetic retinopathy and retinal detachment decrease retinal functionality leading to visual impairment. The pathological events are characterized by photoreceptor degeneration, synaptic disassembly, remodeling of postsynaptic neurons and activation of glial cells. Despite intense research, no effective treatment has been found for these disorders. The current study explores the potential of human neural progenitor cell (hNPC) derived factors to slow the degenerative processes in adult porcine retinal explants. Retinas were cultured for 3 days with or without hNPCs as a feeder layer and investigated by terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL), immunohistochemical, western blot and quantitative real time-polymerase chain reaction (qRT-PCR) techniques. TUNEL showed that hNPCs had the capacity to limit photoreceptor cell death. Among cone photoreceptors, hNPC coculture resulted in better maintenance of cone outer segments and reduced opsin mislocalization. Additionally, maintained synaptic structural integrity and preservation of second order calbindin positive horizontal cells was also observed. However, Müller cell gliosis only seemed to be alleviated in terms of reduced Müller cell density. Our observations indicate that at 3 days of coculture, hNPC derived factors had the capacity to protect photoreceptors, maintain synaptic integrity and support horizontal cell survival. Human neural progenitor cell applied treatment modalities may be an effective strategy to help maintain retinal functionality in neurodegenerative pathologies. Whether hNPCs can independently hinder Müller cell gliosis by utilizing higher concentrations or by combination with other pharmacological agents still needs to be determined.

  • 22.
    Nilsson Ekdahl, Kristina
    et al.
    Linnéuniversitetet, Fakulteten för Hälso- och livsvetenskap (FHL), Institutionen för kemi och biomedicin (KOB). Uppsala University.
    Davoodpour, Padideh
    Uppsala University.
    Ekstrand-Hammarström, Barbro
    Swedish Defence Research Agency, Umeå.
    Fromell, Karin
    Uppsala University.
    Hamad, Osama A
    Uppsala University.
    Hong, Jaan
    Uppsala University.
    Bucht, Anders
    Swedish Defence Research Agency, Umeå;Umeå University.
    Mohlin, Camilla
    Linnéuniversitetet, Fakulteten för Hälso- och livsvetenskap (FHL), Institutionen för kemi och biomedicin (KOB).
    Seisenbaeva, Gulaim A
    Swedish University of Agricultural Sciences (SLU).
    Kessler, Vadim G
    Swedish University of Agricultural Sciences (SLU).
    Nilsson, Bo
    Uppsala University.
    Contact (kallikrein/kinin) system activation in whole human blood induced by low concentrations of α-Fe2O3 nanoparticles2018Ingår i: Nanomedicine: Nanotechnology, Biology and Medicine, ISSN 1549-9634, E-ISSN 1549-9642, Vol. 14, nr 3, s. 735-744Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Iron-oxide nanoparticles (NPs) generated by environmental events are likely to represent health problems. α-Fe2O3 NPs were synthesized, characterized and tested in a model for toxicity utilizing human whole blood without added anticoagulant. MALDI-TOF of the corona was performed and activation markers for plasma cascade systems (complement, contact and coagulation systems), platelet consumption and release of growth factors, MPO, and chemokine/cytokines from blood cells were analyzed. The coronas formed on the pristine α-Fe2O3 NPs contained contact system proteins and they induced massive activation of the contact (kinin/kallikrein) system, as well as thrombin generation, platelet activation, and release of two pro-angiogeneic growth factors: platelet-derived growth factor and vascular endothelial growth factor, whereas complement activation was unaffected. The α-Fe2O3 NPs exhibited a noticeable toxicity, with kinin/kallikreinactivation, which may be associated with hypotension and long-term angiogenesis in vivo, with implications for cancer, arteriosclerosis and pulmonary disease.

  • 23.
    Nilsson Ekdahl, Kristina
    et al.
    Linnéuniversitetet, Fakulteten för Hälso- och livsvetenskap (FHL), Institutionen för kemi och biomedicin (KOB). Uppsala university, Sweden.
    Fromell, Karin
    Uppsala university, Sweden.
    Mohlin, Camilla
    Linnéuniversitetet, Fakulteten för Hälso- och livsvetenskap (FHL), Institutionen för kemi och biomedicin (KOB).
    Teramura, Yuji
    Uppsala university, Sweden;Univ Tokyo, Japan.
    Nilsson, Bo
    Uppsala university, Sweden.
    A human whole-blood model to study the activation of innate immunity system triggered by nanoparticles as a demonstrator for toxicity2019Ingår i: Science and Technology of Advanced Materials, ISSN 1468-6996, E-ISSN 1878-5514, Vol. 20, nr 1, s. 688-698Artikel, forskningsöversikt (Refereegranskat)
    Abstract [en]

    In this review article, we focus on activation of the soluble components of the innate immune system triggered by nonbiological compounds and stress variances in activation due to the difference in size between nanoparticles (NPs) and larger particles or bulk material of the same chemical and physical composition. We then discuss the impact of the so-called protein corona which is formed on the surface of NPs when they come in contact with blood or other body fluids. For example, NPs which bind inert proteins, proteins which are prone to activate the contact system (e.g., factor XII), which may lead to clotting and fibrin formation or the complement system (e.g., IgG or C3), which may result in inflammation and vascular damage. Furthermore, we describe a whole blood model which we have developed to monitor activation and interaction between different components of innate immunity: blood protein cascade systems, platelets, leukocytes, cytokine generation, which are induced by NPs. Finally, we describe our own studies on innate immunity system activation induced by three fundamentally different species of NPs (two types of engineered NPs and diesel NPs) as demonstrator of the utility of an initial determination of the composition of the protein corona formed on NPs exposed to ethylenediaminetetraacetic acid (EDTA) plasma and subsequent analysis in our whole blood model. [GRAPHICS] .

  • 24.
    Nilsson Ekdahl, Kristina
    et al.
    Linnéuniversitetet, Fakulteten för Hälso- och livsvetenskap (FHL), Institutionen för kemi och biomedicin (KOB). Uppsala University.
    Persson, Barbro
    Uppsala University.
    Mohlin, Camilla
    Linnéuniversitetet, Fakulteten för Hälso- och livsvetenskap (FHL), Institutionen för kemi och biomedicin (KOB).
    Sandholm, Kerstin
    Linnéuniversitetet, Fakulteten för Hälso- och livsvetenskap (FHL), Institutionen för kemi och biomedicin (KOB).
    Skattum, Lillemor
    Lund University.
    Nilsson, Bo
    Uppsala University.
    Interpretation of Serological Complement Biomarkers in Disease2018Ingår i: Frontiers in Immunology, ISSN 1664-3224, E-ISSN 1664-3224, Vol. 9, artikel-id 2237Artikel, forskningsöversikt (Refereegranskat)
    Abstract [en]

    Complement systemaberrations have been identified as pathophysiological mechanisms in a number of diseases and pathological conditions either directly or indirectly. Examples of such conditions include infections, inflammation, autoimmune disease, as well as allogeneic and xenogenic transplantation. Both prospective and retrospective studies have demonstrated significant complement-related differences between patient groups and controls. However, due to the low degree of specificity and sensitivity of some of the assays used, it is not always possible to make predictions regarding the complement status of individual patients. Today, there are three main indications for determination of a patient's complement status: (1) complement deficiencies (acquired or inherited); (2) disorders with aberrant complement activation; and (3) C1 inhibitor deficiencies (acquired or inherited). An additional indication is to monitor patients on complement-regulating drugs, an indication which may be expected to increase in the near future since there is now a number of such drugs either under development, already in clinical trials or in clinical use. Available techniques to study complement include quantification of: (1) individual components; (2) activation products, (3) function, and (4) autoantibodies to complement proteins. In this review, we summarize the appropriate indications, techniques, and interpretations of basic serological complement analyses, exemplified by a number of clinical disorders.

  • 25.
    Svensson, Lovisa
    et al.
    Högskolan i Kalmar, Naturvetenskapliga institutionen.
    Mohlin, Camilla
    Högskolan i Kalmar, Naturvetenskapliga institutionen.
    Persson, Katarina
    Högskolan i Kalmar, Naturvetenskapliga institutionen.
    Upregulation of Heme Oxygenase-1 as a Host Mechanism for Protection Against Nitric Oxide–induced Damage in Human Renal Epithelial Cells2009Ingår i: Urology, ISSN 0090-4295, E-ISSN 1527-9995, Vol. 73, nr 5, s. 749-753Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    ObjectivesTo examine whether urinary tract infection–associated stimuli could regulate heme oxygenase-1 (HO-1) expression and to asses the significance of HO-1 in protecting urinary tract epithelial cells against nitric oxide (NO)-induced damage.

    MethodsHeme oxygenase-1 expression was investigated in the human renal epithelial cell line A498 in response to the uropathogenic Escherichia coli (UPEC) strain IA2, the NO-donor DETA/NONOate (DETA/NO), and proinflammatory cytokines (interleukin-1β, tumor necrosis factor-α, and interferon-γ) using reverse transcriptase polymerase chain reaction and Western blot analysis. Cell viability was examined by the trypan blue exclusion test and light microscopy.

    ResultsThe HO-1 inducer hemin and DETA/NO increased HO-1 expression in A498 cells, and glutathione depletion further increased HO-1 expression in response to DETA/NO and hemin. Stimulation with a UPEC strain or cytokines did not upregulate HO-1 expression. The cytokines induced inducible NO synthase expression and caused an increase in nitrite production. Hemin significantly decreased cytokine-induced NO production (P <0.001). DETA/NO decreased the cell viability by approximately 75%, but hemin was able to attenuate DETA/NO-induced cell damage.

    ConclusionsThe expression of HO-1 increased in human renal epithelial cells in response to NO, and the expression was further enhanced in glutathione-depleted cells. The bacteria per se or proinflammatory cytokines were not able to upregulate HO-1. Heme oxygenase-1 protects the cells against NO by feedback inhibition of NO production and by decreasing cell damage.

  • 26.
    Säve, Susanne
    et al.
    Högskolan i Kalmar, Naturvetenskapliga institutionen.
    Mjösberg, Jenny
    Högskolan i Kalmar, Naturvetenskapliga institutionen.
    Poljakovic, Mirjana
    Mohlin, Camilla
    Högskolan i Kalmar, Naturvetenskapliga institutionen.
    Persson, Katarina
    Högskolan i Kalmar, Naturvetenskapliga institutionen.
    Adenosine receptor expression in Escherichia coli-infected and cytokine-stimulated human urinary tract epithelial cells2009Ingår i: BJU International, ISSN 1464-4096, E-ISSN 1464-410X, Vol. 104, nr 11, s. 1758-1765Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    OBJECTIVETo assess the expression and regulation of adenosine receptors in unstimulated, uropathogenic Escherichia coli (UPEC)-infected and cytokine-stimulated human urinary tract epithelial cells, and to examine the regulation of interleukin (IL)-6 secretion in response to A(2A) receptor activation.

    MATERIALS AND METHODSHuman urinary tract epithelial cells (A498, T24 and RT4) were grown in cell culture and stimulated with a mixture of pro-inflammatory cytokines (CM) or UPEC. The expression of adenosine receptors was evaluated using semiquantitative reverse transcription-polymerase chain reaction (RT-PCR), Western blot analysis and immunocytochemistry. IL-6 secretion was measured with an enzyme-linked immunosorbent assay.

    RESULTSRT-PCR analysis showed the presence of transcripts for the A(1), A(2A) and A(2B) receptor subtypes but not for the A(3) receptor in A498 kidney epithelial cells. The expression of A(2A) receptor mRNA increased in A498 epithelial cells exposed to CM and UPEC, while A(1) and A(2B) receptor transcripts decreased or remained unchanged. Up-regulation of A(2A) receptors was confirmed at the protein level using Western blot analysis and immunocytochemistry. There was also an increase in A(2A) receptor mRNA in human bladder epithelial cells (T24 and RT4) and in mouse bladder uroepithelium in response to cytokines and UPEC. IL-6 secretion in UPEC-infected A498 cells was decreased by 38% when exposed to the A(2A) receptor agonist CGS 21680.

    CONCLUSIONOur data showed a subtype-selective plasticity among adenosine receptors in urinary tract epithelial cells in response to UPEC-infection and cytokines. There was a consistent up-regulation of A(2A) receptors in kidney and bladder epithelial cells. Functionally, A(2A) receptor activation reduced UPEC-induced IL-6 secretion. These findings suggest that adenosine might be a previously unrecognized regulator of the mucosal response in urinary tract infection.

  • 27.
    Säve, Susanne
    et al.
    Linnéuniversitetet, Fakultetsnämnden för naturvetenskap och teknik, Institutionen för naturvetenskap, NV.
    Mohlin, Camilla
    Linnéuniversitetet, Fakultetsnämnden för naturvetenskap och teknik, Institutionen för naturvetenskap, NV.
    Vumma, Ravi
    Persson, Katarina
    Linnéuniversitetet, Fakultetsnämnden för naturvetenskap och teknik, Institutionen för naturvetenskap, NV.
    Activation of adenosine A2A receptors inhibit neutrophil transuroepithelial migrationManuskript (preprint) (Övrigt vetenskapligt)
  • 28.
    Säve, Susanne
    et al.
    Linnéuniversitetet, Fakultetsnämnden för naturvetenskap och teknik, Institutionen för naturvetenskap, NV.
    Mohlin, Camilla
    Linnéuniversitetet, Fakultetsnämnden för naturvetenskap och teknik, Institutionen för naturvetenskap, NV.
    Vumma, Ravi
    Univ Örebro.
    Persson, Katarina
    Linnéuniversitetet, Fakultetsnämnden för naturvetenskap och teknik, Institutionen för naturvetenskap, NV.
    Activation of Adenosine A(2A) Receptors Inhibits Neutrophil Transuroepithelial Migration2011Ingår i: Infection and Immunity, ISSN 0019-9567, E-ISSN 1098-5522, Vol. 79, nr 8, s. 3431-3437Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Adenosine has been identified as a significant inhibitor of inflammation by acting on adenosine A(2A) receptors. In this study, we examined the role of adenosine and A(2A) receptors in the transmigration of human neutrophils across an in vitro model of the transitional bladder urothelium. Human uroepithelial cells (UROtsa) were grown on transwell inserts; uropathogenic Escherichia coli (UPEC) and neutrophils were added to the transwell system; and the number of migrating neutrophils was evaluated. Reverse transcription-PCR (RT-PCR), immunohistochemistry, and flow cytometry were used to investigate the expression of adenosine receptors, the epithelial adhesion molecule ICAM-1, and the neutrophil integrin CD11b. Levels of proinflammatory interleukin-8 (IL-8) and phosphorylated I kappa B alpha were measured by enzyme-linked immunosorbent assays (ELISA) and Luminex assays, respectively. The neutrophils expressed all four adenosine receptor subtypes (A(1), A(2A), A(2B), and A(3) receptors), but A(3) receptors were not expressed by UROtsa cells. UPEC stimulated neutrophil transuroepithelial migration, which was significantly decreased in response to the specific A(2A) receptor agonist CGS 21680. The inhibitory effect of CGS 21680 on neutrophil migration was reversed by the A(2A) receptor antagonist SCH 58261. The production of chemotactic IL-8 and the expression of the adhesion molecule ICAM-1 or CD11b were not significantly affected by CGS 21680. However, a significant decrease in the level of phosporylated I kappa B alpha was revealed in response to CGS 21680. In conclusion, UPEC infection in vitro evoked neutrophil migration through a multilayered human uroepithelium. The UPEC-evoked neutrophil transmigration decreased in response to A(2A) receptor activation, possibly through inhibition of NF-kappa B signaling pathways.

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