Modulation of human polymorphonuclear leukocyte chemotaxis and superoxide anion production by Pseudomonas aeruginosa exoproducts, IL-1 beta and piroxicam.
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.
Fontán
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Departamento de Microbiología, Parasitología e Inmunología, Facultad de Medicina, Universidad de Buenos Aires, Argentina.
Amura
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Buzzola
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Sordelli
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D036002:ADP Ribose Transferases; D001427:Bacterial Toxins; D002634:Chemotaxis, Leukocyte / Q000187:drug effects*; D005098:Exotoxins / Q000633:toxicity*; D006801:Humans; D007375:Interleukin-1 / Q000494:pharmacology*; D009504:Neutrophils / Q000187:drug effects* / Q000276:immunology / Q000378:metabolism; D010894:Piroxicam / Q000494:pharmacology*; D011550:Pseudomonas aeruginosa / Q000472:pathogenicity*; D011994:Recombinant Proteins / Q000494:pharmacology; D013481:Superoxides / Q000378:metabolism*; D037521:Virulence Factors; D000097668:Pseudomonas aeruginosa Exotoxin A
D036002:ADP Ribose Transferases; D001427:Bacterial Toxins; D005098:Exotoxins; D007375:Interleukin-1; D010894:Piroxicam; D011994:Recombinant Proteins; D013481:Superoxides; D037521:Virulence Factors; D000097668:Pseudomonas aeruginosa Exotoxin A