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Combinatorial requirements for adhesion molecules in mediating neutrophil emigration during bacterial peritonitis in mice
Author(s) -
Mizgerd Joseph P.,
Quinlan William M.,
LeBlanc Brian W.,
Kutkoski Gregory J.,
Bullard Daniel C.,
Beaudet Arthur L.,
Doerschuk Claire M.
Publication year - 1998
Publication title -
journal of leukocyte biology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.819
H-Index - 191
eISSN - 1938-3673
pISSN - 0741-5400
DOI - 10.1002/jlb.64.3.291
Subject(s) - peritonitis , p selectin , biology , intercellular adhesion molecule 1 , icam 1 , cd18 , cell adhesion molecule , cd11a , mutant , immunology , inflammation , antibody , monoclonal antibody , biochemistry , platelet , genetics , platelet activation , gene
To investigate the requirements for adhesion molecules in neutrophil emigration during peritonitis, mice received intraperitoneal injections of Streptococcus pneumoniae while the functions of multiple adhesion molecules were blocked. Emigration after 4 h was compromised by antibodies against ICAM‐1 or genetic deficiency of ICAM‐1. Anti‐CD11a/CD18 antibodies decreased emigration in ICAM‐1 mutant mice, suggesting that ICAM‐1 independent emigration requires CD11/CD18 complexes. In contrast, mice mutant in ICAM‐1 plus E‐selectin showed no defect in emigration, suggesting that E‐selectin commits neutrophils to an ICAM‐1‐dependent pathway during streptococcal peritonitis. However, in mutant mice lacking the three endothelial adhesion molecules E‐selectin, P‐selectin, and ICAM‐1, emigration after 4 h was significantly compromised. Thus, P‐selectin is essential to ICAM‐1‐and E‐selectin‐independent acute peritoneal inflammation. After 24 h of peritonitis, there were no differences between WT and E‐selectin/P‐selectin/ICAM‐1 mutant mice, demonstrating that these endothelial adhesion molecules are not essential to neutrophil emigration during later stages of peritonitis. J. Leukoc. Biol . 64: 291–297; 1998.