Premium
Induction of cyclooxygenase‐2 by human monocytes exposed to group B streptococci
Author(s) -
Maloney Christopher G.,
Thompson Samuel D.,
Hill Harry R.,
Bohnsack John F.,
McIntyre Thomas M.,
Zimmerman Guy A.
Publication year - 2000
Publication title -
journal of leukocyte biology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.819
H-Index - 191
eISSN - 1938-3673
pISSN - 0741-5400
DOI - 10.1002/jlb.67.5.615
Subject(s) - eicosanoid , eicosanoid metabolism , biology , cyclooxygenase , prostacyclin , thromboxane , pathogenesis , immunology , prostaglandin , group b , cytokine , microbiology and biotechnology , enzyme , medicine , endocrinology , biochemistry , platelet , arachidonic acid
Group B streptococcal (GBS) infections are associated with high morbidity and mortality. The molecular pathways mediating the pathophysiological events in GBS infection are not fully delineated. Cyclooxygenases (COX) are the enzymes that convert arachidonate to active eicosanoids. To identify the effects of GBS on eicosanoid metabolism and regulatory mechanisms, we exposed human monocytes to GBS and found that they secreted prostaglandin E 2 , prostacyclin, and thromboxane A 2 . Exposure to GBS caused monocytes to express COX‐2 mRNA and protein in both a time‐ and concentration‐dependent manner that correlated with eicosanoid production. COX‐1 protein was unchanged. Addition of the anti‐inflammatory cytokines interleukin (IL)‐4 or IL‐10 markedly attenuated GBS‐induced COX‐2 protein accumulation after GBS exposure, as did inhibition of p38 MAPK. Our experiments are the first to show that exposure of monocytes to a gram‐positive bacterium (GBS) results in induction of functional COX‐2, suggesting that eicosanoids may play important roles in the pathogenesis of GBS infections. J. Leukoc. Biol. 67: 615–621; 2000.