PRIMING DIFFERENTIALLY REGULATES NEUTROPHIL ADHESION MOLECULE EXPRESSION FUNCTION/

Lung injury in a variety of disease stales is critically dependent on neutrophil-mediated inflammatory responses. Neutrophil recruitment to sites of infection or tissue damage requires coordinated regulation of neutrophil adhesion and activation status. We have examined the effec ts of treatment of human peripheral blood neutrophils with priming age nts [lipopolysaccharide (LPS), tumour necrosis factor-alpha (TNF-alpha ) and platelet-activating factor (PAF)] upon expression of CD11a, CD11 b, CD11c, CD35 and CD62-L and CD11b function to assess whether subtle regulation of neutrophil adhesion potential accompanies augmented form yl-methionyl-leucyl-phenylalanine-stimulated superoxide production. We have found that there are differential effects of 'priming' concentra tions of these agents. For LPS, CD62L loss occurs in the absence of ch anges in CD11b, whereas for PAF, CD11b up-regulation occurs in the abs ence of detectable loss of CD62-L. However, for TNF-alpha, decreased e xpression of CD62-L occurs concomitantly with increased expression of CD11b. In addition: we have shown that priming agents augment CD11b fu nctional activity in a manner that parallels the priming of the respir atory burst. Thus, priming agents may differentially regulate neutroph il adhesive capacity and data presented in this manuscript suggest tha t the increased effector cell function observed in primed cells may be associated with a distinct repertoire of potential adhesive interacti ons.