Abstract
The in vitro effects of the water-soluble fraction of whole cigarette smoke (WSF) and two alpha, beta-unsaturated aldehydes of cigarette smoke (acrolein and crotonaldehyde) on polymorphonuclear leukocyte (PMNL) adherence were determined with nylon fiber columns. Each of these cigarette smoke constituents caused a dose-dependent inhibition of PMNL adherence. However, at least fivefold higher concentrations of these agents were necessary to inhibit adherence as compared with those necessary to achieve the same level of inhibition of PMNL chemotaxis. Furthermore, inhibition of adherence by WSF could be differentiated from its effects on chemotaxis in that reduced glutathione completely protected chemotaxis from the effects of WSF but only afforded partial protection to PMNL adherence. These data suggest that the inhibitory effects of WSF, acrolein, and crotonaldehyde on PMNL chemotaxis are not due to their inhibition of adherence. Finally, although PMNL adherence is considered to be an integral part of the chemotactic mechanism, differentiation between these two PMNL functions may be possible, since some inhibitors of chemotaxis do not have corresponding inhibitory effects on adherence.