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Reduced inflammatory cell recruitment and plasma exudation in mice deficient in the laminin alpha‐4 chain
Author(s) -
Kenne Ellinor Maria,
Lindbom Lennart
Publication year - 2007
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.21.6.lb71-a
Subject(s) - extravasation , laminin , inflammation , basement membrane , chemistry , blood proteins , extracellular matrix , immunology , pathology , microbiology and biotechnology , medicine , biology , biochemistry
Leukocyte recruitment and plasma extravasation are critical events in inflammatory reactions. Leukocytes have to penetrate the endothelial lining and subendothelial basement membrane (BM) to reach the site of injury or infection. During emigration, the leukocytes trigger alterations in endothelial barrier function leading to increased vascular permeability. Laminin matrix proteins (laminins 8 and 10) are major constituents of the vascular BM. The laminin alpha‐4 chain is a component of laminin‐8, and serves roles as a structure protein and as a signaling molecule. The object of this study was to elucidate the importance of vessel wall laminin 8 in inflammatory cell recruitment and plasma extravasation. A mouse model of pleurisy was used to assess neutrophil recruitment and plasma exudation in laminin alpha‐4 chain deficient (Lam−/−) and wild‐type mice. Pleurisy was induced by intrapleural injection of thioglycolate, and neutrophil accumulation and plasma extravasation in the thoracic cavity was assessed after 4 hours. There was a suppression in both neutrophil recruitment (50% reduction) and plasma exudation (65% reduction) in Lam−/− compared to wild‐type mice at 4 hours. The results indicate an important role of interaction with BM laminin‐8 in leukocyte trafficking in inflammation.