Open AccessLactic acid stimulates interleukin‐23 production by peripheral blood mononuclear cells exposed to bacterial lipopolysaccharide
Author(s) -
Witkin Steven S.,
Alvi Shaheen,
Bongiovanni Ann Marie,
Linhares Iara M.,
Ledger William J.
Publication year - 2011
Publication title -
fems immunology & medical microbiology
Language(s) - English
Resource type - Journals
eISSN - 1574-695X
pISSN - 0928-8244
DOI - 10.1111/j.1574-695x.2010.00757.x
Subject(s) - lactic acid , lipopolysaccharide , peripheral blood mononuclear cell , biology , tumor necrosis factor alpha , cytokine , interleukin , microbiology and biotechnology , bacteria , biochemistry , endocrinology , immunology , in vitro , genetics
Lactic acid is the predominant acid present in the vagina. We evaluated the consequences of lactic acid, at physiological levels present in the vagina, on cytokine responses of peripheral blood mononuclear cells (PBMCs) obtained from 10 individuals in the presence or absence of bacterial lipopolysaccharide. Preincubation of PBMCs in 15 mM lactic acid before the addition of lipopolysaccharide resulted in a 246% mean increase in interleukin‐23 (IL‐23) secretion over that released in the presence of lipopolysaccharide alone ( P =0.0068). The lipopolysaccharide‐induced production of tumor necrosis factor‐α, IL‐6, IL‐10 and IL‐12 was unaffected by lactic acid. IL‐23 stimulation was not observed if the lactic acid was neutralized before its addition to the culture medium or if hydrochloric acid was substituted for lactic acid. In the absence of lipopolysaccharide, lactic acid did not stimulate the production of IL‐23 or any of the other cytokines. The increase in IL‐23 production was proportional to the lactic acid concentration over a 15–60 mM range. We conclude that at body sites characterized by lactic acid accumulation, such as in the human vagina, exposure to gram‐negative bacteria results in selective IL‐23 production, leading to a subsequent preferential stimulation of the Th17 T lymphocyte pathway.