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LIBRIS Formathandbok  (Information om MARC21)
FältnamnIndikatorerMetadata
00005794naa a2200409 4500
001oai:lup.lub.lu.se:c6dd1a65-5bd0-4cd6-8550-64d535c42bb6
003SwePub
008160401s2015 | |||||||||||000 ||eng|
0247 a https://lup.lub.lu.se/record/51458932 URI
0247 a https://doi.org/10.4049/jimmunol.14024702 DOI
040 a (SwePub)lu
041 a engb eng
042 9 SwePub
072 7a art2 swepub-publicationtype
072 7a ref2 swepub-contenttype
1001 a Arvidsson, Idau Lund University,Lunds universitet,Pediatrik, Lund,Sektion V,Institutionen för kliniska vetenskaper, Lund,Medicinska fakulteten,Paediatrics (Lund),Section V,Department of Clinical Sciences, Lund,Faculty of Medicine4 aut0 (Swepub:lu)med-iaa
2451 0a Shiga toxin-induced complement-mediated hemolysis and release of complement-coated red blood cell-derived microvesicles in hemolytic uremic syndrome.
264 c 2015-03-01
264 1b The American Association of Immunologists,c 2015
520 a Shiga toxin (Stx)-producing Escherichia coli (STEC) cause hemolytic uremic syndrome (HUS). This study investigated whether Stx2 induces hemolysis and whether complement is involved in the hemolytic process. RBCs and/or RBC-derived microvesicles from patients with STEC-HUS (n = 25) were investigated for the presence of C3 and C9 by flow cytometry. Patients exhibited increased C3 deposition on RBCs compared with controls (p < 0.001), as well as high levels of C3- and C9-bearing RBC-derived microvesicles during the acute phase, which decreased after recovery. Stx2 bound to P1 (k) and P2 (k) phenotype RBCs, expressing high levels of the P(k) Ag (globotriaosylceramide), the known Stx receptor. Stx2 induced the release of hemoglobin and lactate dehydrogenase in whole blood, indicating hemolysis. Stx2-induced hemolysis was not demonstrated in the absence of plasma and was inhibited by heat inactivation, as well as by the terminal complement pathway Ab eculizumab, the purinergic P2 receptor antagonist suramin, and EDTA. In the presence of whole blood or plasma/serum, Stx2 induced the release of RBC-derived microvesicles coated with C5b-9, a process that was inhibited by EDTA, in the absence of factor B, and by purinergic P2 receptor antagonists. Thus, complement-coated RBC-derived microvesicles are elevated in HUS patients and induced in vitro by incubation of RBCs with Stx2, which also induced hemolysis. The role of complement in Stx2-mediated hemolysis was demonstrated by its occurrence only in the presence of plasma and its abrogation by heat inactivation, EDTA, and eculizumab. Complement activation on RBCs could play a role in the hemolytic process occurring during STEC-HUS.
650 7a MEDICIN OCH HÄLSOVETENSKAPx Medicinska och farmaceutiska grundvetenskaperx Immunologi inom det medicinska området0 (SwePub)301102 hsv//swe
650 7a MEDICAL AND HEALTH SCIENCESx Basic Medicinex Immunology in the medical area0 (SwePub)301102 hsv//eng
7001 a Ståhl, Anne-lieu Lund University,Lunds universitet,Pediatrik, Lund,Sektion V,Institutionen för kliniska vetenskaper, Lund,Medicinska fakulteten,Paediatrics (Lund),Section V,Department of Clinical Sciences, Lund,Faculty of Medicine4 aut0 (Swepub:lu)pedi-ast
7001 a Manea Hedström, Minolau Lund University,Lunds universitet,Pediatrik, Lund,Sektion V,Institutionen för kliniska vetenskaper, Lund,Medicinska fakulteten,Paediatrics (Lund),Section V,Department of Clinical Sciences, Lund,Faculty of Medicine4 aut0 (Swepub:lu)pedi-mm0
7001 a Kristoffersson, Ann-Charlotteu Lund University,Lunds universitet,Pediatrik, Lund,Sektion V,Institutionen för kliniska vetenskaper, Lund,Medicinska fakulteten,Paediatrics (Lund),Section V,Department of Clinical Sciences, Lund,Faculty of Medicine4 aut0 (Swepub:lu)pedi-ack
7001 a Rylander, Christian4 aut
7001 a Westman, Juliau Lund University,Lunds universitet,Avdelningen för hematologi och transfusionsmedicin,Institutionen för laboratoriemedicin,Medicinska fakulteten,Division of Hematology and Transfusion Medicine,Department of Laboratory Medicine,Faculty of Medicine4 aut0 (Swepub:lu)med-jlw
7001 a Storry, Jillu Lund University,Lunds universitet,Avdelningen för hematologi och transfusionsmedicin,Institutionen för laboratoriemedicin,Medicinska fakulteten,Division of Hematology and Transfusion Medicine,Department of Laboratory Medicine,Faculty of Medicine4 aut0 (Swepub:lu)tran-jst
7001 a Olsson, Martin Lu Lund University,Lunds universitet,Avdelningen för hematologi och transfusionsmedicin,Institutionen för laboratoriemedicin,Medicinska fakulteten,Transfusionsmedicin,Forskargrupper vid Lunds universitet,Division of Hematology and Transfusion Medicine,Department of Laboratory Medicine,Faculty of Medicine,Transfusion Medicine,Lund University Research Groups4 aut0 (Swepub:lu)labm-mol
7001 a Karpman, Dianau Lund University,Lunds universitet,Pediatrik, Lund,Sektion V,Institutionen för kliniska vetenskaper, Lund,Medicinska fakulteten,Pediatrisk nefrologi,Forskargrupper vid Lunds universitet,Paediatrics (Lund),Section V,Department of Clinical Sciences, Lund,Faculty of Medicine,Pediatric Nephrology,Lund University Research Groups4 aut0 (Swepub:lu)pedi-dka
7102 a Pediatrik, Lundb Sektion V4 org
7730 t Journal of Immunologyd : The American Association of Immunologistsg 194:5, s. 2309-2318q 194:5<2309-2318x 1550-6606x 0022-1767
8564 u http://www.ncbi.nlm.nih.gov/pubmed/25637016?dopt=Abstracty FULLTEXT
8564 u http://dx.doi.org/10.4049/jimmunol.1402470y FULLTEXT
8564 u https://www.jimmunol.org/content/jimmunol/194/5/2309.full.pdf
8564 8u https://lup.lub.lu.se/record/5145893
8564 8u https://doi.org/10.4049/jimmunol.1402470

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