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Heparin attenuates TNF-alpha induced inflammatory response through a CD11b dependent mechanism

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dc.creator Salas Martínez, Azucena
dc.creator Sans i Cuffí, Miquel
dc.creator Soriano Viladomiu, Alex
dc.creator Reverter Calatayud, Juan Carlos
dc.creator Anderson, D. C.
dc.creator Piqué, J. M. (Piqué Badía)
dc.creator Panés Díaz, Julià
dc.date 2011-07-07T11:32:58Z
dc.date 2011-07-07T11:32:58Z
dc.date 2000
dc.date.accessioned 2024-12-16T10:27:13Z
dc.date.available 2024-12-16T10:27:13Z
dc.identifier 0017-5749
dc.identifier http://hdl.handle.net/2445/18629
dc.identifier 176976
dc.identifier 10861269
dc.identifier.uri http://fima-docencia.ub.edu:8080/xmlui/handle/123456789/22087
dc.description Background In addition to its anticoagulant properties, heparin has anti-inflammatory effects, the molecular and mechanistic bases of which are incompletely defined. AIMS The current studies were designed to test the hypothesis that heparin abrogates the expression or function of leucocyte-endothelial adherence molecules which are fundamental to the acute inflammatory response. Methods The effects of heparin on tumour necrosis factor alpha (TNF-¿) induced leucocyte rolling, adhesion, and migration as well as vascular permeability were assessed in rat mesenteric venules using intravital microscopy. Expression of adhesion molecules was quantitated using a double radiolabelled monoclonal antibody (mAb) binding technique in vivo (P-selectin, intercellular cell adhesion molecule type 1 (ICAM-1), and vascular cell adhesion molecule 1 (VCAM-1)) or flow cytometry (CD11a, CD11b, and L-selectin). Ex vivo binding of heparin to neutrophils was assessed by flow cytometry. RESULTS TNF-alpha induced a significant increase in leucocyte rolling, adhesion, and migration, and vascular permeability, coincident with a significant increase in expression of P-selectin, ICAM-1, and VCAM-1. Ex vivo assessment of blood neutrophils showed significant upregulation of CD11a and CD11b and significant downregulation of L-selectin within five hours of TNF-¿ administration. Heparin pretreatment significantly attenuated leucocyte rolling, adhesion, and migration but did not affect expression of cell adhesion molecules or vascular permeability elicited by TNF-¿ administration. Binding of heparin was significantly increased on blood neutrophils obtained five hours after TNF-¿ administration. Preincubation with an anti-CD11b mAb but not with an anti-CD11a or anti-L-selectin antibody significantly diminished heparin binding ex vivo.
dc.format 9 p.
dc.format application/pdf
dc.language eng
dc.publisher BMJ Group
dc.relation Reproducció digital del document publicat a: http://dx.doi.org/10.1136/gut.47.1.88
dc.relation Gut, 2000, vol. 47, núm 1, p. 88-96
dc.relation http://dx.doi.org/10.1136/gut.47.1.88
dc.rights (c) BMJ Publishing Group Ltd and British Society of Gastroenterology, 2000
dc.rights info:eu-repo/semantics/openAccess
dc.source Articles publicats en revistes (Medicina)
dc.subject Heparina
dc.subject Malalties inflamatòries intestinals
dc.subject Heparin
dc.subject Inflammatory bowel diseases
dc.title Heparin attenuates TNF-alpha induced inflammatory response through a CD11b dependent mechanism
dc.type info:eu-repo/semantics/article
dc.type info:eu-repo/semantics/publishedVersion


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