NEUTROPHIL EMIGRATION IN THE SKIN, LUNGS, AND PERITONEUM - DIFFERENT REQUIREMENTS FOR CD11 CD18 REVEALED BY CD18-DEFICIENT MICE/

To determine the role of CD11/CD18 complexes in neutrophil emigration, inflammation was induced in the skin, lungs, or-peritoneum of mutant mice deficient in CD18 (CD18(-/-) mutants). Peripheral blood of CD18(- /-) contained 11-fold more neutrophils than did mutants blood of wild- type (WIT) mice. During irritant dermatitis induced by topical applica tion of croton oil, the number of emigrated neutrophils in histologica l sections of dermis was 98% less in CD18(-/-) mutants than in WT mice . During Streptococcus pneumonia pneumonia, neutrophil emigration in C D18(-/-) mutants was not reduced. These data are consistent with expec tations based on studies using blocking antibodies to inhibit CD11/CD1 8 complexes, and on observations of humans lacking CD11/CD18 complexes . The number of emigrated neutrophils in lung sections during Escheric hia coli pneumonia, or in peritoneal lavage fluid after 4 h of S. pneu moniae peritonitis, was not reduced in CD18(-/-) mutants, but rather w as greater than the WT values (240 +/- 30 and 220 +/- 30% WT, respecti vely). Also, there was no inhibition of neutrophil emigration during s terile peritonitis induced by intraperitoneal injection of thioglycoll ate (90 +/- 20% WT). These data contrast with expectations. Whereas CD 11/CD18 complexes are essential to the dermal emigration of neutrophil s during acute dermatitis, CD18(-/-) mutant mice demonstrate surprisin g alternative pathways for neutrophil emigration during pneumonia or p eritonitis.