MODULATION OF HUMAN POLYMORPHONUCLEAR LEUKOCYTE CHEMOTAXIS AND SUPEROXIDE ANION PRODUCTION BY PSEUDOMONAS-AERUGINOSA EXOPRODUCTS, IL-1-BETAAND PIROXICAM

Whereas addition of 200 ng ml(-1) exotoxin A (exoA) did not modify PMN L chemotaxis, 20 U ml(-1) human recombinant interleukin-1 beta (hrlL-1 beta) primed polymorphonuclear leukocytes (PMNL) for migration toward s Pseudomonas aeruginosa peptide chemotactins (PAPCs). Piroxicam (100 mu g ml(-1)), a non-steroidal anti-inflammatory agent (NSAIA), inhibit ed PMNL chemotaxis and abolished the priming effect of hrlL-1 beta. Bo th PAPCs and exoA induced PMNL superoxide anion production, but neithe r hrIL-1 beta nor piroxicam modified significantly PMNL superoxide ani on production induced by PAPCs. The fact that hrIL-1 beta can prime PM NL for chemotaxis towards PAPCs and that piroxicam can abolish activat ion by primed PMNL are findings relevant to the pharmacological contro l of lung tissue damage during P. aeruginosa pneumonia.