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Role of adhesion glycoproteins CD 18 and intercellular adhesion molecule‐1 in complement‐mediated reactions of rabbit skin

1 The role of the adhesion glycoproteins CD 18 and intercellular adhesion molecule‐1 (ICAM‐1) in inflammatory responses produced during a reversed passive Arthus (RPA) reaction and induced by zymosan and zymosan‐activated plasma (ZAP) were studied in rabbit skin. 2 Oedema formation and haemorrhage were quantified by measuring accumulation of 125I‐albumin and 111In‐labelled red blood cells (111In‐RBC) respectively. 3 Monoclonal antibody (mAb) R15.7 (anti‐CD18), administered intravenously, abolished accumulation of 125I‐albumin and 111In‐RBC in dermal RPA reactions and in response to locally injected zymosan and ZAP. 4 When administered intravenously, the mAb RR1/1 (anti‐ICAM‐1) suppressed 125I‐albumin and 111In‐RBC accumulation in dermal RPA reactions and at sites treated with zymosan and ZAP. 5 Oedema formation in response to platelet‐activating factor (PAF) and bradykinin (BK) either in the presence or absence of prostaglandin E2 (PGE2) were not affected by mAb R15.7 or by mAb RR1/1.1.1. 6 We conclude that oedema formation and haemorrhage associated with RPA reactions and in responses to zymosan and ZAP are completely CD 18‐dependent, and are mediated, at least in part, via ICAM‐1. Responses to the neutrophil‐independent oedema forming mediators, PAF and BK are not dependent upon CD 18 or ICAM‐1.