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*
Department of Microbiology and Immunology, University of Adelaide, Adelaide, South Australia, Australia; and
Centre de Recherche en Rhumatologie et Immunologie, Centre de Recherche du Centre Hospitalier de lUniversité Laval and Department of Medicine, Faculty of Medicine, Université Laval, Ste-Foy, Quebec, Canada
Production of chemokines (chemotactic cytokines) by neutrophils is
likely to be important in the regulation of inflammation and the
control of infection. In this study we show that exposure of human
neutrophils to various microbial pathogens leads to the production of
both macrophage inflammatory protein 1
(MIP-1
) and IL-8. The
bacterial microbes, Salmonella typhimurium and
Pseudomonas aeruginosa, and Staphylococcus
aureus all strongly induced both IL-8 and MIP-1
secretion,
whereas Streptococcus pneumoniae, Staphylococcus
epidermidis, and the opportunistic yeast Candida
albicans were less potent. Saccharomyces cerevisiae
and zymosan both induced IL-8 secretion but failed to stimulate that of
MIP-1
. Coincubation of neutrophils with the proinflammatory cytokine
TNF-
and the micro-organisms also led to differential expression of
MIP-1
and IL-8. Significant enhancement of the induction of both
MIP-1
and IL-8 by S. typhimurium, P.
aeruginosa, and S. pneumoniae as well as by C.
albicans was observed. In contrast, while IL-8 production in
response to S. cerevisiae and zymosan was enhanced in the
presence of TNF-
, no MIP-1
was produced. These combined results
indicate that while neutrophils exposed to some micro-organisms alone
or in the presence of inflammatory cytokines such as TNF-
will
produce both MIP-1
and IL-8, resulting in generation of signals for
the recruitment of mononuclear leukocytes and neutrophils,
respectively, certain types of micro-organisms can skew this response
toward synthesis of IL-8.
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