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  • 201.
    Sandholm, Kerstin
    et al.
    Linnéuniversitetet, Fakulteten för Hälso- och livsvetenskap (FHL), Institutionen för kemi och biomedicin (KOB).
    Carlsson, Hanna
    Linköping University, Sweden;Region Kalmar county, Sweden.
    Persson, Barbro
    Uppsala University, Sweden.
    Skattum, Lillemor
    Lund University, Sweden.
    Tjernberg, Ivar
    Linköping University, Sweden;Region Kalmar county, Sweden.
    Nilsson, Bo
    Uppsala University, Sweden.
    Nilsson Ekdahl, Kristina
    Linnéuniversitetet, Fakulteten för Hälso- och livsvetenskap (FHL), Institutionen för kemi och biomedicin (KOB). Uppsala University, Sweden.
    Discrepancies in plasma levels of complement components measured by a newly introduced commercially available magnetic bead technique compared to presently available clinical reference intervals2019Ingår i: Scandinavian Journal of Immunology, ISSN 0300-9475, E-ISSN 1365-3083, artikel-id e12831Artikel i tidskrift (Refereegranskat)
  • 202.
    Sandholm, Kerstin
    et al.
    Linnéuniversitetet, Fakultetsnämnden för naturvetenskap och teknik, Institutionen för naturvetenskap, NV.
    Henningsson, Anna J.
    Bergstrom, Sven
    Ernerudh, Jan
    Nilsson Ekdahl, Kristina
    Linnéuniversitetet, Fakultetsnämnden för naturvetenskap och teknik, Institutionen för naturvetenskap, NV.
    Complement activation and phagocytosis in vitro of two strains of Borrelia burgdorferi S.L2012Ingår i: Immunobiology, ISSN 0171-2985, E-ISSN 1878-3279, Vol. 217, nr 11, s. 1153-1153Artikel i tidskrift (Övrigt vetenskapligt)
  • 203.
    Sandholm, Kerstin
    et al.
    Linnéuniversitetet, Fakulteten för Hälso- och livsvetenskap (FHL), Institutionen för kemi och biomedicin (KOB).
    Henningsson, Anna J.
    Linköping University.
    Säve, Susanne
    Linnéuniversitetet, Fakulteten för Hälso- och livsvetenskap (FHL), Institutionen för kemi och biomedicin (KOB).
    Bergström, Sven
    Umeå University.
    Forsberg, Pia
    Linköping University.
    Jonsson, Nina
    Linnéuniversitetet, Fakulteten för Hälso- och livsvetenskap (FHL), Institutionen för kemi och biomedicin (KOB).
    Ernerudh, Jan
    Linköping University.
    Nilsson Ekdahl, Kristina
    Linnéuniversitetet, Fakulteten för Hälso- och livsvetenskap (FHL), Institutionen för kemi och biomedicin (KOB).
    Early Cytokine Release in Response to Live Borrelia burgdorferi Sensu Lato Spirochetes Is Largely Complement Independent2014Ingår i: PLoS ONE, ISSN 1932-6203, E-ISSN 1932-6203, Vol. 9, nr 9, s. e108013-Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Aim: Here we investigated the role of complement activation in phagocytosis and the release of cytokines and chemokines in response to two clinical isolates: Borrelia afzelii K78, which is resistant to complement-mediated lysis, and Borrelia garinii LU59, which is complement-sensitive. Methods: Borrelia spirochetes were incubated in hirudin plasma, or hirudin-anticoagulated whole blood. Complement activation was measured as the generation of C3a and sC5b-9. Binding of the complement components C3, factor H, C4, and C4BP to the bacterial surfaces was analyzed. The importance of complement activation on phagocytosis, and on the release of cytokines and chemokines, was investigated using inhibitors acting at different levels of the complement cascade. Results: 1) Borrelia garinii LU59 induced significantly higher complement activation than did Borrelia afzelii K78. 2) Borrelia afzelii K78 recruited higher amounts of factor H resulting in significantly lower C3 binding. 3) Both Borrelia strains were efficiently phagocytized by granulocytes and monocytes, with substantial inhibition by complement blockade at the levels of C3 and C5. 4) The release of the pro-inflammatory cytokines and chemokines IL-1 beta, IL-6, TNF, CCL20, and CXCL8, together with the anti-inflammatory IL-10, were increased the most (by>10-fold after exposure to Borrelia). 5) Both strains induced a similar release of cytokines and chemokines, which in contrast to the phagocytosis, was almost totally unaffected by complement blockade. Conclusions: Our results show that complement activation plays an important role in the process of phagocytosis but not in the subsequent cytokine release in response to live Borrelia spirochetes.

  • 204.
    Sandholm, Kerstin
    et al.
    Linnéuniversitetet, Fakulteten för Hälso- och livsvetenskap (FHL), Institutionen för kemi och biomedicin (KOB).
    Persson, Barbro
    Uppsala University.
    Skattum, Lillemor
    Lund University.
    Eggertsen, Gösta
    Karolinska Institutet;Karolinska University Hospital.
    Nyman, Dag
    Aland Cent Hosp, Finland.
    Gunnarsson, Iva
    Karolinska Institutet;Karolinska University Hospital.
    Svenungson, Elisabet
    Karolinska Institutet;Karolinska University Hospital.
    Nilsson, Bo
    Uppsala University.
    Nilsson Ekdahl, Kristina
    Linnéuniversitetet, Fakulteten för Hälso- och livsvetenskap (FHL), Institutionen för kemi och biomedicin (KOB). Uppsala University.
    Evaluation of a Novel Immunoassay for Quantification of C1q for Clinical Diagnostic Use2019Ingår i: Frontiers in Immunology, ISSN 1664-3224, E-ISSN 1664-3224, Vol. 10, artikel-id 7Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Objectives: C1q is a valuable biomarker of disease activity in systemic lupus erythematosus (SLE). The "gold standard" assay, rocket immunoelectrophoresis (RIE), is time-consuming, and thus a shift to soluble immune precipitation techniques such as nephelometry has occurred. However, quantification of C1q with these techniques has been questioned as a result of the antibody binding properties of C1q. In the present work, we have compared results using various techniques (RIE, nephelometry, and ELISA) and have developed and validated a new magnetic bead-based sandwich immunoassay (MBSI). Methods: C1q was quantified by nephelometry and the new sandwich immunoassay in 45 serum samples analyzed using RIE. C1q was also assessed in plasma using RIE and sandwich immunoassay in samples from SLE patients with nephritis (n = 69), SLE patients without nephritis (n = 310) as classified by BILAG score, and matched controls (n = 322). In addition, cerebrospinal fluid (CSF) samples from 31 patients, previously analyzed with ELISA, were also analyzed with the MBSI to test the behavior of this new assay in the lower detection range. Results: We found a strong correlation between the new MBSI, RIE, and ELISA, but not with nephelometry. The MBSI demonstrated lower levels of C1q in SLE patients than in matched controls (p < 0.0001), and patients with nephritis had lower levels than patients without nephritis (p < 0.01). Similarily, RIE showed significant differences between the patient groups (p < 0.0001). An association was also found between the levels of C1q and the SLE disease activity index (SLEDAI). Furthermore, there was good correlation between the values obtained by MBSI and ELISA, in both serum (r = 0.960) and CSF (r = 0.786), underscoring the ability of both techniques to measure low concentrations of C1q with high accuracy. Conclusion: The sandwich immunoassay correlated well with RIE, but soluble immune precipitation techniques, such as nephelometry, did not appear suitable alternatives, since C1q itself, and possibly anti-C1q antibodies, interfered with the measurements. The new sandwich immunoassay is therefore a good replacement for RIE in monitoring SLE disease activity.

  • 205.
    Sandholm, Kerstin
    et al.
    Linnéuniversitetet, Fakulteten för Hälso- och livsvetenskap (FHL), Institutionen för kemi och biomedicin (KOB).
    Wijkstrom, Elisabeth
    University Hospital, Uppsala.
    Skattum, Lillemor
    Lund University.
    Nilsson, Bo
    Uppsala University.
    Nilsson Ekdahl, Kristina
    Linnéuniversitetet, Fakulteten för Hälso- och livsvetenskap (FHL), Institutionen för kemi och biomedicin (KOB). Uppsala University.
    Validations of assays for the evaluation of C1q in inflammatory diseases and thromboinflammation2015Ingår i: Molecular Immunology, ISSN 0161-5890, E-ISSN 1872-9142, Vol. 67, nr 1, s. 176-177Artikel i tidskrift (Övrigt vetenskapligt)
  • 206. Sartz, Lisa
    et al.
    Olin, Anders
    Kristoffersson, AC
    Ståhl, AL
    Johansson, ME
    Westman, K
    Fremeaux-Bacchi, V
    Nilsson Ekdahl, Kristina
    Linnéuniversitetet, Fakultetsnämnden för naturvetenskap och teknik, Institutionen för naturvetenskap, NV.
    Karpman, Diana
    A novel C3 mutation causing increased formation of the C3 convertase in familial atypical hemolytic uremic syndrome.2012Ingår i: Journal of Immunology, ISSN 0022-1767, E-ISSN 1550-6606, Vol. 188, nr 4, s. 2030-2037Artikel, forskningsöversikt (Refereegranskat)
    Abstract [en]

    Atypical hemolytic uremic syndrome has been associated with dysregulation of the alternative complement pathway. In this study, a novel heterozygous C3 mutation was identified in a factor B-binding region in exon 41, V1636A (4973 T > C). The mutation was found in three family members affected with late-onset atypical hemolytic uremic syndrome and symptoms of glomerulonephritis. All three patients exhibited increased complement activation detected by decreased C3 levels and glomerular C3 deposits. Platelets from two of the patients had C3 and C9 deposits on the cell surface. Patient sera exhibited more C3 cleavage and higher levels of C3a. The C3 mutation resulted in increased C3 binding to factor B and increased net formation of the C3 convertase, even after decay induced by decay-accelerating factor and factor H, as assayed by surface plasmon resonance. Patient sera incubated with washed human platelets induced more C3 and C9 deposition on the cell surface in comparison with normal sera. More C3a was released into serum over time when washed platelets were exposed to patient sera. Results regarding C3 and C9 deposition on washed platelets were confirmed using purified patient C3 in C3-depleted serum. The results indicated enhanced convertase formation leading to increased complement activation on cell surfaces. Previously described C3 mutations showed loss of function with regard to C3 binding to complement regulators. To our knowledge, this study presents the first known C3 mutation inducing increased formation of the C3 convertase, thus explaining enhanced activation of the alternative pathway of complement.

  • 207.
    Seisenbaeva, Gulaim A.
    et al.
    Swedish University of Agricultural Sciences.
    Fromell, Karin
    Uppsala University.
    Vinogradov, Vasiliy V.
    ITMO Univ Kronverksky, Russia.
    Terekhov, Aleksey N.
    Ivanovo State Med Acad, Russia.
    Pakhomov, Andrey V.
    Ivanovo State Med Acad, Russia.
    Nilsson, Bo
    Uppsala University.
    Nilsson Ekdahl, Kristina
    Linnéuniversitetet, Fakulteten för Hälso- och livsvetenskap (FHL), Institutionen för kemi och biomedicin (KOB). Uppsala University.
    Vinogradov, Vladimir V.
    ITMO Univ Kronverksky, Russia.
    Kessler, Vadim G.
    Swedish University of Agricultural Sciences.
    Dispersion of TiO2 nanoparticles improves burn wound healing and tissue regeneration through specific interaction with blood serum proteins2017Ingår i: Scientific Reports, ISSN 2045-2322, E-ISSN 2045-2322, Vol. 7, artikel-id 15448Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Burn wounds are one of the most important causes of mortality and especially morbidity around the world. Burn wound healing and skin tissue regeneration remain thus one of the most important challenges facing the mankind. In the present study we have addressed this challenge, applying a solution-stabilized dispersion TiO2 nanoparticles, hypothesizing that their ability to adsorb proteins will render them a strong capacity in inducing body fluid coagulation and create a protective hybrid material coating. The in vitro study of interaction between human blood and titania resulted at enhanced TiO2 concentrations in formation of rather dense gel composite materials and even at lower content revealed specific adsorption pattern initiating the cascade response, promising to facilitate the regrowth of the skin. The subsequent in vivo study of the healing of burn wounds in rats demonstrated formation of a strongly adherent crust of a nanocomposite, preventing infection and inflammation with quicker reduction of wound area compared to untreated control. The most important result in applying the TiO2 dispersion was the apparently improved regeneration of damaged tissues with appreciable decrease in scar formation and skin color anomalies.

  • 208.
    Sfyroera, Georgia
    et al.
    Univ Penn, USA.
    Ricklin, Daniel
    Univ Penn, USA.
    Reis, Edimara
    Univ Penn, USA.
    Chen, Hui
    Univ Penn, USA.
    Wu, Emilia
    Univ Minnesota, USA.
    Kaznessis, Yannis
    Univ Minnesota, USA.
    Nilsson Ekdahl, Kristina
    Linnéuniversitetet, Fakulteten för Hälso- och livsvetenskap (FHL), Institutionen för kemi och biomedicin (KOB). Uppsala University.
    Nilsson, Bo
    Linnéuniversitetet, Fakulteten för Hälso- och livsvetenskap (FHL), Institutionen för kemi och biomedicin (KOB).
    Lambris, John
    Univ Penn, USA.
    Rare loss-of-function mutation in complement component C3 provides insight into molecular and pathophysiological determinants of complement activity2015Ingår i: Journal of Immunology, ISSN 0022-1767, E-ISSN 1550-6606, Vol. 194, nr 7, s. 3305-3316Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    The plasma protein C3 is a central element in the activation and effector functions of the complement system. A hereditary dysfunction of C3 that prevents complement activation via the alternative pathway (AP) was described previously in a Swedish family, but its genetic cause and molecular consequences have remained elusive. In this study, we provide these missing links by pinpointing the dysfunction to a point mutation in the beta-chain of C3 (c.1180T > C; p.Met(373)Thr). In the patient's plasma, AP activity was completely abolished and could only be reconstituted with the addition of normal C3. The M373T mutation was localized to the macroglobulin domain 4 of C3, which contains a binding site for the complement inhibitor compstatin and is considered critical for the interaction of C3 with the AP C3 convertase. Structural analyses suggested that the mutation disturbs the integrity of macroglobulin domain 4 and induces conformational changes that propagate into adjacent regions. Indeed, C3 M373T showed an altered binding pattern for compstatin and surface-bound C3b, and the presence of Thr(373) in either the C3 substrate or convertase-affiliated C3b impaired C3 activation and opsonization. In contrast to known gain-of-function mutations in C3, patients affected by this loss-of-function mutation did not develop familial disease, but rather showed diverse and mostly episodic symptoms. Our study therefore reveals the molecular mechanism of a relevant loss-of-function mutation in C3 and provides insight into the function of the C3 convertase, the differential involvement of C3 activity in clinical conditions, and some potential implications of therapeutic complement inhibition.

  • 209.
    Speth, Cornelia
    et al.
    Med Univ Innsbruck, Austria.
    Rambach, Guenter
    Med Univ Innsbruck, Austria.
    Wuerzner, Reinhard
    Med Univ Innsbruck, Austria.
    Lass-Floerl, Cornelia
    Med Univ Innsbruck, Austria.
    Kozarcanin, Huda
    Uppsala University.
    Hamad, Osama A.
    Uppsala University.
    Nilsson, Bo
    Uppsala University.
    Nilsson Ekdahl, Kristina
    Linnéuniversitetet, Fakulteten för Hälso- och livsvetenskap (FHL), Institutionen för kemi och biomedicin (KOB). Uppsala University.
    Complement and platelets: Mutual interference in the immune network2015Ingår i: Molecular Immunology, ISSN 0161-5890, E-ISSN 1872-9142, Vol. 67, nr 1, s. 108-118Artikel, forskningsöversikt (Refereegranskat)
    Abstract [en]

    In recent years, the view of platelets has changed from mere elements of hemostasis to immunological multitaskers. They are connected in manifold ways to other cellular and humoral components of the immune network, one of which is the complement system, a potent player in soluble innate immunity. Our article reviews the crucial and complex interplay between platelets and complement, focusing on mutual regulation of these two interaction partners by their respective molecular mechanisms. Furthermore, the putative relevance of these processes to infectious diseases, inflammatory conditions, and autoimmune disorders, as well as the treatment of patients with biomaterials is highlighted. (C) 2015 Elsevier Ltd. All rights reserved.

  • 210. Tejde, A
    et al.
    Mathsson, L
    Nilsson Ekdahl, Kristina
    Högskolan i Kalmar, Naturvetenskapliga institutionen.
    Nilsson, Bo
    Rönnelid, J
    Immune complex stimulation of peripheral blood mononuclear cells result in enhancement or suppression of IL-12 production dependent on access to a functionally active complement system2004Ingår i: Clinical and experimental immunology, Vol. 137 (3), s. 521-528Artikel i tidskrift (Refereegranskat)
  • 211.
    Teramura, Yuji
    et al.
    Univ Tokyo, Japan.
    Asif, Sana
    Uppsala University.
    Gustafson, Elisabet
    Univ Uppsala Hosp.
    Nilsson Ekdahl, Kristina
    Linnéuniversitetet, Fakulteten för Hälso- och livsvetenskap (FHL), Institutionen för kemi och biomedicin (KOB). Uppsala University.
    Nilsson, Bo
    Uppsala University.
    Heparinzation of cell surfaces with a heparin-binding peptide-conjugated PEG-lipid for regulation of thromboinflammation in transplantation of human MSC and hepatocyte2015Ingår i: Xenotransplantation, ISSN 0908-665X, E-ISSN 1399-3089, Vol. 22, nr Supplement 1, s. S70-S70, artikel-id 561Artikel i tidskrift (Övrigt vetenskapligt)
  • 212.
    Teramura, Yuji
    et al.
    University of Tokyo, Japan;Uppsala University.
    Asif, Sana
    Uppsala University.
    Nilsson Ekdahl, Kristina
    Linnéuniversitetet, Fakulteten för Hälso- och livsvetenskap (FHL), Institutionen för kemi och biomedicin (KOB). Uppsala University.
    Gustafson, Elisabet
    Uppsala University Hospital.
    Nilsson, Bo
    Uppsala University.
    Cell Adhesion Induced Using Surface Modification with Cell-Penetrating Peptide-Conjugated Poly(ethylene glycol)-Lipid: A New Cell Glue for 3D Cell-Based Structures2017Ingår i: ACS Applied Materials and Interfaces, ISSN 1944-8244, E-ISSN 1944-8252, Vol. 9, nr 1, s. 244-254Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    We synthesized a novel material, cell-penetrating peptide conjugated poly(ethylene glycol)-lipid (CPP-PEG-lipid), that can induce the adhesion of floating cells. Firm cell adhesion with spreading could be induced by cell surface modification with the CPP-PEG-lipids. Cell adhesion was induced by CPPs but not by any other cationic short peptides we tested. Here, we demonstrated adherence using the floating cell line CCRF-CEM as well as primary human T cells, B cells, erythrocytes, and hepatocytes. As compared to cells grown in suspension, adherent cells were more rapidly induced to attach to substrates with the cell-surface modification. The critical factor for attachment was localization of CPPs at the cell membrane by PEG-lipids with PEG > 20 kDa. These cationic CPPs on PEG chains were able to interact with substrate surfaces such as polystyrene (PS) surfaces, glass surfaces, and PS microfibers that are negatively charged, inducing firm cell adhesion and cell spreading. Also, as opposed to normal cationic peptides that interact strongly with cell membranes, CPPs were less interactive with the cell surfaces because of their cell-penetrating property, making them more available for adhering cells to the substrate surface. No effects on cell viability or cell proliferation were observed after the induction of cell adhesion. With this technique, cells could be easily immobilized onto PS microfibers, an important step in fabricating 3D cell-based structures. Cells immobilized onto 3D PS microfibers were alive, and human hepatocytes showed normal production of urea and albumin on the microfibers. This method is novel in inducing firm cell adhesion-via a one-step treatment.

  • 213.
    Teramura, Yuji
    et al.
    University of Tokyo, Japan.
    Asif, Sana
    Uppsala University.
    Nilsson Ekdahl, Kristina
    Linnéuniversitetet, Fakulteten för Hälso- och livsvetenskap (FHL), Institutionen för kemi och biomedicin (KOB). Uppsala University.
    Nilsson, Bo
    Uppsala University.
    Cell surface engineering for regulation of immune reactions in cell therapy2015Ingår i: Immune Responses to Biosurfaces: Mechanisms and Therapeutic Interventions / [ed] John D. Lambris, Kristina Nilsson-Ekdahl, Daniel Ricklin, Bo Nilsson, Springer, 2015, s. 189-209Kapitel i bok, del av antologi (Refereegranskat)
    Abstract [en]

    Transplantation of the pancreatic islets of Langerhans (islets) is a promising cell therapy for treating insulin-dependent type 1 diabetes mellitus. Islet transplantation is a minimally-invasive technique involving relatively simple surgery. However, after intraportal transplantation, the transplanted islets are attacked by the recipient’s immune system, because they activate a number of systems, including coagulation, complement response, inflammation, immune rejection, and recurrence of autoimmune disease. We have developed a surface modification and microencapsulation technique that protects cells and islets with biomaterials and bioactive substances, which may be useful in clinical settings. This approach employs amphiphilic polymers, which can interact with lipid bilayer membranes, without increasing cell volume. Molecules attached to these polymers can protect transplanted cells and islets from attack by the host immune system. We expect that this surface modification technique will improve graft survival in clinical islet transplantation.

  • 214.
    Teramura, Yuji
    et al.
    The University of Tokyo, Japan;Uppsala University.
    Nilsson Ekdahl, Kristina
    Linnéuniversitetet, Fakulteten för Hälso- och livsvetenskap (FHL), Institutionen för kemi och biomedicin (KOB). Uppsala University.
    Barbu, Andreea
    Uppsala University.
    A hybrid of cells and pancreatic islets toward a new bioartificial pancreas.2016Ingår i: Regenerative Therapy, ISSN 2352-3204, Vol. 3, nr Special Issue, s. 68-74Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Cell surface engineering using single-stranded DNA–poly(ethylene glycol)-conjugated phospholipid (ssDNA–PEG-lipid) is useful for inducing cell–cell attachment two and three dimensionally. In this review, we summarize our recent techniques for cell surface engineering and their applications to islet transplantation. Because any DNA sequence can be immobilized onto the cell surface by hydrophobic interactions between ssDNA–PEG-lipid and the cellular membrane without impairing cell function, a cell–cell hybrid can be formed through the DNA hybridization. With this technique, it would be possible to create three-dimensional hybrid structures of pancreatic islets coated with various accessory cells, such as patients’ own cells, mesenchymal and adipose-derived stem cells, endothelial progenitor cells, neural crest stem cells or regulatory T cells, which might significantly improve the outcome of islet transplantation in diabetic patients.

  • 215. Teramura, Yuji
    et al.
    Nilsson, Per H.
    Linnéuniversitetet, Fakultetsnämnden för naturvetenskap och teknik, Institutionen för naturvetenskap, NV.
    Nilsson Ekdahl, Kristina
    Linnéuniversitetet, Fakultetsnämnden för naturvetenskap och teknik, Institutionen för naturvetenskap, NV.
    Magnusson, Peetra U.
    Qu, Hongchang
    Ricklin, Daniel
    Hong, Jaan
    Lambris, John D.
    Nilsson, Bo
    Autoregulation of thromboinflammation on biomaterials and cells by a novel therapeutic coating technique2012Ingår i: Immunobiology, ISSN 0171-2985, E-ISSN 1878-3279, Vol. 217, nr 11, s. 1140-1140Artikel i tidskrift (Övrigt vetenskapligt)
  • 216.
    Tjernberg, Anna Rockert
    et al.
    Region Kalmar, Sweden;Örebro University, Sweden.
    Woksepp, Hanna
    Region Kalmar, Sweden.
    Sandholm, Kerstin
    Linnéuniversitetet, Fakulteten för Hälso- och livsvetenskap (FHL), Institutionen för kemi och biomedicin (KOB).
    Johansson, Marcus
    Region Kalmar, SwedenRegion Kalmar, Sweden;Linköping University, Sweden.
    Dahle, Charlotte
    Linköping University, Sweden;Linköping University Hospital, Sweden.
    Ludvigsson, Jonas F.
    Karolinska Institutet, Sweden;Örebro University Hospital, Sweden.
    Bonnedahl, Jonas
    Linköping University, Sweden.
    Nilsson, Per H.
    Linnéuniversitetet, Fakulteten för Hälso- och livsvetenskap (FHL), Institutionen för kemi och biomedicin (KOB). Univ Oslo, Norway.
    Nilsson Ekdahl, Kristina
    Linnéuniversitetet, Fakulteten för Hälso- och livsvetenskap (FHL), Institutionen för kemi och biomedicin (KOB). Uppsala University, Sweden.
    Celiac disease and complement activation in response to Streptococcus pneumoniae2019Ingår i: European Journal of Pediatrics, ISSN 0340-6199, E-ISSN 1432-1076Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Individuals with celiac disease (CD) are at increased risk of invasive pneumococcal disease (IPD). The aim of this study was to explore whether the complement response to Streptococcus pneumoniae differed according to CD status, and could serve as an explanation for the excess risk of IPD in CD. Twenty-two children with CD and 18 controls, born 1999-2008, were included at Kalmar County Hospital, Sweden. The degree of complement activation was evaluated by comparing levels of activation products C3a and sC5b-9 in plasma incubated for 30 min with Streptococcus pneumoniae and in non-incubated plasma. Complement analyses were performed with enzyme-linked immunosorbent assay (ELISA). Pneumococcal stimulation caused a statistically significant increase in C3a as well as sC5b-9 in both children with CD and controls but there was no difference in response between the groups. After incubation, C3a increased on average 4.6 times and sC5b-9 22 times in both the CD and the control group (p = 0.497 and p = 0.724 respectively). Conclusion: Complement response to Streptococcus pneumoniae seems to be similar in children with and without CD and is thus unlikely to contribute to the increased susceptibility to invasive pneumococcal disease in CD.

  • 217.
    Tjernberg, Jenny
    et al.
    Rudbeck Laboratory, Uppsala.
    Nilsson Ekdahl, Kristina
    Högskolan i Kalmar, Naturvetenskapliga institutionen. Rudbeck Laboratory, Uppsala.
    Lambris, John
    University of Pennsylvania, USA.
    Korsgren, Olle
    Rudbeck Laboratory, Uppsala.
    Nilsson, Bo
    Rudbeck Laboratory, Uppsala.
    Acute antibody-mediated complement activation mediates lysis of pancreatic islets cells and may cause tissue loss in clinical islet transplantation2008Ingår i: Transplantation, ISSN 0041-1337, E-ISSN 1534-6080, Vol. 85, nr 8, s. 1193-1199Artikel i tidskrift (Refereegranskat)
  • 218.
    Toda, Shota
    et al.
    Shibaura Inst Technol, Japan.
    Fattah, Artin
    Uppsala University, Sweden.
    Asawa, Kenta
    Univ Tokyo, Japan.
    Nakamura, Naoko
    Shibaura Inst Technol, Japan.
    Nilsson Ekdahl, Kristina
    Linnéuniversitetet, Fakulteten för Hälso- och livsvetenskap (FHL), Institutionen för kemi och biomedicin (KOB). Uppsala University, Sweden.
    Nilsson, Bo
    Uppsala University, Sweden.
    Teramura, Yuji
    Uppsala University, Sweden;Univ Tokyo, Japan.
    Optimization of Islet Microencapsulation with Thin Polymer Membranes for Long-Term Stability2019Ingår i: Micromachines, ISSN 2072-666X, E-ISSN 2072-666X, Vol. 10, nr 11, s. 1-10, artikel-id 755Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Microencapsulation of islets can protect against immune reactions from the host immune system after transplantation. However, sufficient numbers of islets cannot be transplanted due to the increase of the size and total volume. Therefore, thin and stable polymer membranes are required for the microencapsulation. Here, we undertook the cell microencapsulation using poly(ethylene glycol)-conjugated phospholipid (PEG-lipid) and layer-by-layer membrane of multiple-arm PEG. In order to examine the membrane stability, we used different molecular weights of 4-arm PEG (10k, 20k and 40k)-Mal to examine the influence on the polymer membrane stability. We found that the polymer membrane made of 4-arm PEG(40k)-Mal showed the highest stability on the cell surface. Also, the polymer membrane did not disturb the insulin secretion from beta cells.

  • 219.
    Toomik, R
    et al.
    Uppsala University.
    Nilsson Ekdahl, Kristina
    Uppsala University.
    Ekman, P
    Uppsala University.
    Demonstration of the regulation of phosphorylase by reversible phosphorylation and allosteric effectors1994Ingår i: Biochemical Education, Vol. 22 (4), s. 205-207Artikel i tidskrift (Refereegranskat)
  • 220. Tsai, Jon A
    et al.
    Lund, Mikael
    Lundell, Lars
    Nilsson Ekdahl, Kristina
    Högskolan i Kalmar, Naturvetenskapliga institutionen.
    One-lung ventilation during thoracoabdominal esophagectomy elicits complement activation2009Ingår i: Journal of Surgical Research, ISSN 0022-4804, E-ISSN 1095-8673, Vol. 152, nr 2, s. 331-337Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Background. One-lung ventilation (OLV) during thoracoabdominal esophagectomy may induce an inflammatory response that can contribute to the induction and propagation of frequently occurring postoperative respiratory distress. Markers of such a response might be detected in the pulmonary as well as in the systemic circulation. Inflammation and tissue damage may be key pathogenetic pathways and we hypothesized that 1-lung ventilation may induce an inflammatory cascade reflected by markers for such a response. Materials and methods. Thirty patients with esophageal cancer were randomized to OLV (n = 16) or 2-lung ventilation (TLV; n = 14) during the thoracic part of the operation. Compounds involved in inflammation and coagulation were measured perioperatively and during the 1st, 2nd, 3rd, and 10th postoperative d. Results. During the perioperative phase, the proinflammatory cytokine interleukin-6 and thrombin, measured as thrombin-antithrombin complexes, started to increase. Thrombin, which can induce complement activation, peaked at the end of surgery and interleukin-6 at the 1st to 2nd postoperative d, but there were no differences between the OLV and TLV groups. C3a and terminal complement complex (TCC) started to increase on the 2nd postoperative d and continued to do so for the rest of the study period. The increase of TCC was significantly higher in the OLV group compared to the TLV group, whereas C3a attained similar levels in the 2 groups. Conclusions. OLV is associated with an augmented inflammatory response as reflected by the activation of the TCC. This may induce pulmonary tissue damage and recruitment of inflammatory cells.

  • 221.
    van Griensven, Martijn
    et al.
    Technical University of Munich, Germany.
    Ricklin, Daniel
    University of Pennsylvania, USA ; University of Basel, Switzerland.
    Denk, Stephanie
    University of Ulm, Germany.
    Halbgebauer, Rebecca
    University of Ulm, Germany.
    Braun, Christian K
    University of Ulm, Germany.
    Schultze, Anke
    University of Ulm, Germany.
    Hönes, Felix
    University of Ulm, Germany.
    Koutsogiannaki, Sofia
    University of Pennsylvania, USA.
    Primikyri, Alexandra
    University of Pennsylvania, USA.
    Reis, Edimara
    University of Pennsylvania, USA.
    Messerer, David
    University of Ulm, Germany.
    Hafner, Sebastian
    University of Ulm, Germany.
    Radermacher, Peter
    University of Ulm, Germany.
    Biglarnia, Ali-Reza
    Malmö University Hospital ; Lund University.
    Resuello, Ranillo R G
    Simian Conservation Breeding and Research Center (SICONBREC), Philippines.
    Tuplano, Joel V
    Simian Conservation Breeding and Research Center (SICONBREC), Philippines.
    Mayer, Benjamin
    University of Ulm, Germany.
    Nilsson Ekdahl, Kristina
    Uppsala University, Sweden.
    Nilsson, Bo
    Uppsala University, Sweden.
    Lambris, John D
    University of Pennsylvania, USA.
    Huber-Lang, Markus
    University of Ulm, Germany.
    Protective Effects of the Complement Inhibitor Compstatin CP40 in Hemorrhagic Shock2019Ingår i: Shock, ISSN 1073-2322, E-ISSN 1540-0514, Vol. 51, nr 1, s. 78-87Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Trauma-induced hemorrhagic shock (HS) plays a decisive role in the development of immune, coagulation, and organ dysfunction often resulting in a poor clinical outcome. Imbalanced complement activation is intricately associated with the molecular danger response and organ damage after HS. Thus, inhibition of the central complement component C3 as turnstile of both inflammation and coagulation is hypothesized as a rational strategy to improve the clinical course after HS.Applying intensive care conditions, anaesthetized, monitored, and protectively ventilated non-human primates (NHP; cynomolgus monkeys) received a pressure-controlled severe HS (60 min at MAP 30 mmHg) with subsequent volume resuscitation. Thirty min after HS, animals were randomly treated with either an analog of the C3 inhibitor compstatin (i.e., Cp40) in saline (n = 4) or with saline alone (n = 4). The observation period lasted 300 min after induction of HS.We observed improved kidney function in compstatin Cp40-treated animals after HS as determined by improved urine output, reduced damage markers and a tendency of less histopathological signs of acute kidney injury. Sham-treated animals revealed classical signs of mucosal edema, especially in the ileum and colon reflected by worsened microscopic intestinal injury scores. In contrast, Cp40-treated HS animals exhibited only minor signs of organ edema and significantly less intestinal damage. Furthermore, early systemic inflammation and coagulation dysfunction were both ameliorated by Cp40.The data suggest that therapeutic inhibition of C3 is capable to significantly improve immune, coagulation and organ function and to preserve organ-barrier integrity early after traumatic HS. C3-targeted complement inhibition may therefore reflect a promising therapeutic strategy in fighting fatal consequences of HS.

  • 222.
    Vijayaraghavan, Swetha
    et al.
    Karolinska Institutet.
    Karami, Azadeh
    Karolinska Institutet.
    Aeinehband, Shahin
    Karolinska Institutet.
    Behbahani, Homira
    Karolinska Institutet.
    Grandien, Alf
    Karolinska Institutet.
    Nilsson, Bo
    Uppsala University.
    Nilsson Ekdahl, Kristina
    Linnéuniversitetet, Fakulteten för Hälso- och livsvetenskap (FHL), Institutionen för kemi och biomedicin (KOB). Uppsala University.
    Lindblom, Rickard P. F.
    Karolinska Institutet.
    Piehl, Fredrik
    Karolinska Institutet.
    Darreh-Shori, Taher
    Karolinska Institutet.
    Regulated Extracellular Choline Acetyltransferase Activity: The Plausible Missing Link of the Distant Action of Acetylcholine in the Cholinergic Anti-Inflammatory Pathway2013Ingår i: PLoS ONE, ISSN 1932-6203, E-ISSN 1932-6203, Vol. 8, nr 6, artikel-id e65936Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Acetylcholine (ACh), the classical neurotransmitter, also affects a variety of nonexcitable cells, such as endothelia, microglia, astrocytes and lymphocytes in both the nervous system and secondary lymphoid organs. Most of these cells are very distant from cholinergic synapses. The action of ACh on these distant cells is unlikely to occur through diffusion, given that ACh is very short-lived in the presence of acetylcholinesterase (AChE) and butyrylcholinesterase (BuChE), two extremely efficient ACh-degrading enzymes abundantly present in extracellular fluids. In this study, we show compelling evidence for presence of a high concentration and activity of the ACh-synthesizing enzyme, choline-acetyltransferase (ChAT) in human cerebrospinal fluid (CSF) and plasma. We show that ChAT levels are physiologically balanced to the levels of its counteracting enzymes, AChE and BuChE in the human plasma and CSF. Equilibrium analyses show that soluble ChAT maintains a steady-state ACh level in the presence of physiological levels of fully active ACh-degrading enzymes. We show that ChAT is secreted by cultured human-brain astrocytes, and that activated spleen lymphocytes release ChAT itself rather than ACh. We further report differential CSF levels of ChAT in relation to Alzheimer's disease risk genotypes, as well as in patients with multiple sclerosis, a chronic neuroinflammatory disease, compared to controls. Interestingly, soluble CSF ChAT levels show strong correlation with soluble complement factor levels, supporting a role in inflammatory regulation. This study provides a plausible explanation for the long-distance action of ACh through continuous renewal of ACh in extracellular fluids by the soluble ChAT and thereby maintenance of steady-state equilibrium between hydrolysis and synthesis of this ubiquitous cholinergic signal substance in the brain and peripheral compartments. These findings may have important implications for the role of cholinergic signaling in states of inflammation in general and in neurodegenerative disease, such as Alzheimer's disease and multiple sclerosis in particular.

  • 223. Wennberg, L
    et al.
    Sundberg, B
    Nilsson Ekdahl, Kristina
    Högskolan i Kalmar, Naturvetenskapliga institutionen.
    Korsgren, O
    C-peptide determinations in islet xenotransplantation: A study in the pig-to-mouse model2001Ingår i: Cell transplantation, Vol. 10, s. 165-173Artikel i tidskrift (Refereegranskat)
  • 224.
    Wu, YQ
    et al.
    University of Pennsylvania, USA.
    Qu, H
    University of Pennsylvania, USA.
    Sfyroera, G
    University of Pennsylvania, USA.
    Tzekou, A
    University of Pennsylvania, USA.
    Kay, BK
    University of Illinois at Chicago, USA.
    Nilsson, Bo
    Uppsala University.
    Nilsson Ekdahl, Kristina
    Linnéuniversitetet, Fakultetsnämnden för naturvetenskap och teknik, Institutionen för naturvetenskap, NV. Uppsala University Hospital.
    Ricklin, D
    University of Pennsylvania, USA.
    Lambris, JD
    University of Pennsylvania, USA.
    Protection of Nonself Surfaces from Complement Attack by Factor H-Binding Peptides: Implications for Therapeutic Medicine2011Ingår i: Journal of Immunology, ISSN 0022-1767, E-ISSN 1550-6606, Vol. 186, nr 7, s. 4269-4277Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Exposure of nonself surfaces such as those of biomaterials or transplanted cells and organs to host blood frequently triggers innate immune responses, thereby affecting both their functionality and tolerability. Activation of the alternative pathway of complement plays a decisive role in this unfavorable reaction. Whereas previous studies demonstrated that immobilization of physiological regulators of complement activation (RCA) can attenuate this foreign body-induced activation, simple and efficient approaches for coating artificial surfaces with intact RCA are still missing. The conjugation of small molecular entities that capture RCA with high affinity is an intriguing alternative, as this creates a surface with autoregulatory activity upon exposure to blood. We therefore screened two variable cysteine-constrained phage-displayed peptide libraries for factor H-binding peptides. We discovered three peptide classes that differed with respect to their main target binding areas. Peptides binding to the broad middle region of factor H (domains 5–18) were of particular interest, as they do not interfere with either regulatory or binding activities. One peptide in this group (5C6) was further characterized and showed high factor H-capturing activity while retaining its functional integrity. Most importantly, when 5C6 was coated to a model polystyrene surface and exposed to human lepirudin-anticoagulated plasma, the bound peptide captured factor H and substantially inhibited complement activation by the alternative pathway. Our study therefore provides a promising and novel approach to produce therapeutic materials with enhanced biocompatibility.

  • 225.
    Zhao, Fei
    et al.
    Leibniz Inst Nat Prod Res & Infect Biol, Germany.
    Afonso, Sara
    Leibniz Inst Nat Prod Res & Infect Biol, Germany.
    Lindner, Susanne
    Leibniz Inst Nat Prod Res & Infect Biol, Germany.
    Hartmann, Andrea
    Leibniz Inst Nat Prod Res & Infect Biol, Germany.
    Loeschmann, Ina
    Leibniz Inst Nat Prod Res & Infect Biol, Germany.
    Nilsson, Bo
    Uppsala University, Sweden.
    Nilsson Ekdahl, Kristina
    Linnéuniversitetet, Fakulteten för Hälso- och livsvetenskap (FHL), Institutionen för kemi och biomedicin (KOB). Linneaus Ctr Bomat Chem, Kalmar, Sweden..
    Weber, Lutz T.
    Univ Hosp Cologne, Germany.
    Habbig, Sandra
    Univ Hosp Cologne, Germany.
    Schalk, Gesa
    Univ Hosp Cologne, Germany.
    Kirschfink, Michael
    Heidelberg Univ, Germany.
    Zipfel, Peter F.
    Leibniz Inst Nat Prod Res & Infect Biol, Germany;Friedrich Schiller Univ Jena, Germany.
    Skerka, Christine
    Leibniz Inst Nat Prod Res & Infect Biol, Germany.
    C3-Glomerulopathy Autoantibodies Mediate Distinct Effects on Complement C3-and C5-Convertases2019Ingår i: Frontiers in Immunology, ISSN 1664-3224, E-ISSN 1664-3224, Vol. 10, s. 1-14, artikel-id 1030Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    C3 glomerulopathy (C3G) is a severe kidney disease, which is caused by defective regulation of the alternative complement pathway. Disease pathogenesis is heterogeneous and is caused by both autoimmune and genetic factors. Here we characterized IgG autoantibodies derived from 33 patients with autoimmune C3 glomerulopathy. Serum antibodies from all 33 patients as well as purified IgGs bound to the in vitro assembled C3-convertase. Noteworthy, two groups of antibodies were identified: group 1 with strong (12 patients) and group 2 with weak binding C3-convertase autoantibodies (22 patients). C3Nef, as evaluated in a standard C3Nef assay, was identified in serum from 19 patients, which included patients from group 1 as well as group 2. The C3-convertase binding profile was independent of C3Nef. Group 1 antibodies, but not the group 2 antibodies stabilized the C3-convertase, and protected the enzyme from dissociation by Factor H. Also, only group 1 antibodies induced C3a release. However, both group 1 and group 2 autoantibodies bound to the C5-convertase and induced C5a generation, which was inhibited by monoclonal anti-C5 antibody Eculizumab in vitro. In summary, group 1 antibodies are composed of C3Nef and C5Nef antibodies and likely over-activate the complement system, as seen in hemolytic assays. Group 2 antibodies show predominantly C5Nef like activities and stabilize the C5 but not the C3-convertase. Altogether, these different profiles not only reveal a heterogeneity of the autoimmune forms of C3G (MPGN), they also show that in diagnosis of C3G not all autoimmune forms are identified and thus more vigorous autoantibody testing should be performed.

  • 226.
    Özmen, Lisa
    et al.
    Rudbeck Laboratory, University Hospital, Uppsala.
    Nilsson Ekdahl, Kristina
    Högskolan i Kalmar, Naturvetenskapliga institutionen. Rudbeck Laboratory, University Hospital, Uppsala.
    Elgue, Graciela
    Rudbeck Laboratory, University Hospital, Uppsala.
    Larsson, Rolf
    Rudbeck Laboratory, University Hospital, Uppsala.
    Korsgren, Olle
    Rudbeck Laboratory, University Hospital, Uppsala.
    Nilsson, Bo
    Rudbeck Laboratory, University Hospital, Uppsala.
    Inhibition of Thrombin Abrogates the Instant Blood-Mediated Inflammatory Reaction Triggered by Isolated Human Islets: Possible application of the thrombin inhibitor melagatran in clinical islet transplantation2002Ingår i: Diabetes, ISSN 0012-1797, E-ISSN 1939-327X, Vol. 51, nr 6, s. 1779-1784Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    A thrombotic/inflammatory reaction is elicited when isolated islets of Langerhans come in contact with ABO-compatible blood. The detrimental effects of this instant blood-mediated inflammatory reaction (IBMIR) provide a reasonable explanation for the observation that an unexpectedly high number of islets, from several donors, are needed to produce normoglycemia in transplant patients with type 1 diabetes. In this study, the hypothesis that a specific thrombin inhibitor, Melagatran, could reduce IBMIR in an in vitro model in which human islets are exposed to ABO-compatible blood was tested. The administration of Melagatran abrogated IBMIR dose-dependently. Islets exposed to blood, in the absence or presence of 0.4 μmol/l Melagatran, exhibited a loss of integrity and were found to be trapped in macroscopic clots containing platelets and CD11b+ leukocytes. At concentrations from 1 to 10 μmol/l, Melagatran inhibited both coagulation and complement activation. Also, platelet and leukocyte activation and consumption were decreased. Islet morphology was maintained with almost no platelets adhering to the surface, and infiltration by CD11b+ leukocytes was considerably reduced. In conclusion, Melagatran significantly reduced IBMIR in this model system. This protective effect indicates that thrombin plays a pivotal role in IBMIR and suggests that thrombin inhibition can improve the outcome of clinical islet transplantation.

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