Open AccessModulation of human polymorphonuclear leukocyte chemotaxis and superoxide anion production by Pseudomonas aeruginosa exoproducts, IL‐1β and piroxicam
Author(s) -
Fontán Patricia A.,
Amura Claudia R.,
Buzzola Fernanda R.,
Sordelli Daniel O.
Publication year - 1995
Publication title -
fems immunology & medical microbiology
Language(s) - English
Resource type - Journals
eISSN - 1574-695X
pISSN - 0928-8244
DOI - 10.1111/j.1574-695x.1995.tb00023.x
Subject(s) - superoxide , piroxicam , chemotaxis , pseudomonas aeruginosa , microbiology and biotechnology , neutrophile , interleukin 8 , chemistry , biology , immunology , biochemistry , bacteria , medicine , inflammation , receptor , pathology , enzyme , alternative medicine , genetics
Whereas addition of 200 ng ml −1 exotoxin A (exoA) did not modify PMNL chemotaxis, 20 U ml −1 human recombinant interleukin‐1β (hrIL‐1β) primed polymorphonuclear leukocytes (PMNL) for migration towards Pseudomonas aeruginosa peptide chemotactins (PAPCs). Piroxicam (100 μg ml −1 ), a non‐steroidal anti‐inflammatory agent (NSAIA), inhibited PMNL chemotaxis and abolished the priming effect of hrIL‐1β. Both PAPCs and exoA induced PMNL superoxide anion production, but neither hrIL‐1β nor piroxicam modified significantly PMNL superoxide anion production induced by PAPCs. The fact that hrIL‐1β 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.