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Influence of Mid‐Trimester Amniotic Fluid on Endogenous and Lipopolysaccharide‐Mediated Responses of Mononuclear Lymphoid Cells
Author(s) -
Witkin Steven S.,
Chervenak Joseph,
Bongiovanni Ann Marie,
Herway Catherine,
Linhares Iara M.,
Skupski Daniel
Publication year - 2012
Publication title -
american journal of reproductive immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.071
H-Index - 97
eISSN - 1600-0897
pISSN - 1046-7408
DOI - 10.1111/j.1600-0897.2011.01032.x
Subject(s) - peripheral blood mononuclear cell , lipopolysaccharide , tumor necrosis factor alpha , amniotic fluid , endogeny , monocyte , immune system , immunology , cytokine , interleukin , mediator , chemistry , biology , endocrinology , pregnancy , fetus , in vitro , biochemistry , genetics
Citation Witkin SS, Chervenak J, Bongiovanni AM, Herway C, Linhares IM, Skupski D. Influence of mid‐trimester amniotic fluid on endogenous and lipopolysaccharide‐mediated responses of mononuclear lymphoid cells. Am J Reprod Immunol 2012; 67: 28–33 Problem We evaluated the influence of amniotic fluid (AF) on immune mediator production by mononuclear leukocytes. Method of study Thirty mid‐gestation AFs were incubated with peripheral blood mononuclear cells (PBMCs) in the presence or absence of lipopolysaccharide (LPS). Supernatants were tested for interleukin (IL) – 6, 10, 12, 23, tumor necrosis factor‐α (TNF‐α) and monocyte chemotactic protein (MCP)‐1. Results Endogenous mediator production was minimal or non‐detectable. AF stimulated endogenous MCP‐1, IL‐6 and TNF‐α release. In the presence of LPS, production of MCP‐1 and IL‐10 by PBMCs was enhanced eight‐ to ninefold by AF. Release of IL‐6 and IL‐23 was enhanced less than twofold by the addition of AF while TNF‐α production was unchanged. AF‐stimulated mediator production was similar irrespective of pregnancy outcome. Conclusion Selective AF stimulation of LPS‐mediated MCP‐1 and IL‐10 release may be a mechanism to promote antibody production and the influx of phagocytic cells to engulf pathogens while downregulating the production of pro‐inflammatory cytokines.