ROLE OF CD11B IN FOCAL ACID-INDUCED PNEUMONIA AND CONTRALATERAL LUNG INJURY IN RATS

Neutrophil emigration in response to acid aspiration does not require the adhesion complex, CD11/CD18. This study examined the role of CD11b /CD18 using the anti-CD11b F(ab')(2), 1B6, in focal HCl-induced intrac apillary neutrophil sequestration and edema formation within rat lungs , as well as the effect of pretreatment with endotoxin on this injury. The results show that at the site of aspiration pneumonia, anti-CD11b F(ab')(2) did not inhibit neutrophil sequestration or edema formation , either with or without endotoxin pretreatment. In the contralateral lung, focal HCl aspiration induced neutrophil sequestration that was i nhibited by the anti-CD11b F(ab')(2), but no edema formation. The comb ined effect of endotoxin pretreatment and HCl aspiration induced CD11b /CD18-independent edema formation in the contralateral lung. These dat a indicate that CD11b/CD18-independent pathways mediate neutrophil seq uestration and edema formation at that pneumonic site with or without pretreatment with endotoxin. CD11b/CD18 mediates neutrophil sequestrat ion at distant sites when no endotoxin is present, although this CD11b /CD18-dependent sequestration is not association with edema formation. The combined effects of endotoxin and HCl aspiration induce edema for mation at distant sites that could not be prevented by inhibiting the function of the CD11b/CD18 prior to aspiration.