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From the * Physiology Program, Harvard School of Public Health, Boston, Massachusetts 02115; and 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
Department of Molecular and Human Genetics, Baylor College of Medicine, Houston, Texas 77030
/
mutants). Peripheral blood of CD18
/
mutants contained 11-fold more neutrophils than did
blood of wild-type (WT) mice. During irritant dermatitis induced by topical application of
croton oil, the number of emigrated neutrophils in histological sections of dermis was 98% less
in CD18
/
mutants than in WT mice. During Streptococcus pneumoniae pneumonia, neutrophil
emigration in CD18
/
mutants was not reduced. These data are consistent with expectations based on studies using blocking antibodies to inhibit CD11/CD18 complexes, and on observations of humans lacking CD11/CD18 complexes. The number of emigrated neutrophils in
lung sections during Escherichia coli pneumonia, or in peritoneal lavage fluid after 4 h of S. pneumoniae peritonitis, was not reduced in CD18
/
mutants, but rather was greater than the WT
values (240 ± 30 and 220 ± 30% WT, respectively). Also, there was no inhibition of neutrophil emigration during sterile peritonitis induced by intraperitoneal injection of thioglycollate
(90 ± 20% WT). These data contrast with expectations. Whereas CD11/CD18 complexes are essential to the dermal emigration of neutrophils during acute dermatitis, CD18
/
mutant
mice demonstrate surprising alternative pathways for neutrophil emigration during pneumonia
or peritonitis.
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