Modulation of human polymorphonuclear leukocyte chemotaxis and superoxide anion production by Pseudomonas aeruginosa exoproducts, IL-1 beta and piroxicam.

FONTAN PA; AMURA CR; BUZZOLA FR; SORDELLI DO

FEMS IMMUNOLOGY AND MEDICAL MICROBIOLOGY

Blackwell Publishers

Lugar: UK; Año: 1995 vol. 10 p. 139 - 144

0928-8244

Whereas addition of 200 ng ml-1 exotoxin A (exoA) did not modify PMNL chemotaxis, 20 U ml-1 human recombinant interleukin-1 beta (hrIL-1 beta) primed polymorphonuclear leukocytes (PMNL) for migration towards Pseudomonas aeruginosa peptide chemotactins (PAPCs). Piroxicam (100 micrograms ml-1), a non-steroidal anti-inflammatory agent (NSAIA), inhibited PMNL chemotaxis and abolished the priming effect of hrIL-1 beta. Both PAPCs and exoA induced PMNL superoxide anion production, but neither hrIL-1 beta nor piroxicam modified significantly PMNL superoxide anion production induced by PAPCs. The fact that hrIL-1 beta can prime PMNL for chemotaxis towards PAPCs and that piroxicam can abolish activation by primed PMNL are findings relevant to the pharmacological control of lung tissue damage during P. aeruginosa pneumonia