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Human trophoblast responses to Porphyromonas gingivalis infection
Author(s) -
Riewe S.D.,
Mans J.J.,
Hirano T.,
Katz J.,
Shiverick K.T.,
Brown T.A.,
Lamont R.J.
Publication year - 2010
Publication title -
molecular oral microbiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.18
H-Index - 77
eISSN - 2041-1014
pISSN - 2041-1006
DOI - 10.1111/j.2041-1014.2010.00573.x
Subject(s) - porphyromonas gingivalis , signal transduction , trophoblast , biology , p38 mitogen activated protein kinases , cytokine , microbiology and biotechnology , immunology , placenta , mapk/erk pathway , bacteria , pregnancy , genetics , fetus
Summary Porphyromonas gingivalis is a periodontal pathogen that is also associated with preterm low‐birthweight delivery. We investigated the transcriptional responses of human extravillous trophoblasts (HTR‐8) to infection with P. gingivalis . Over 2000 genes were differentially regulated in HTR‐8 cells by P. gingivalis . In ontology analyses of regulated genes, overpopulated biological pathways included mitogen‐activated protein (MAP) kinase signaling and cytokine production. Immunoblots confirmed overexpression of the MAP kinase pathway components MEK3, p38 and Max. Furthermore, P. gingivalis infection induced phosphorylation and activation of MEK3 and p38. Increased production of interleukin (IL)‐1β and IL‐8 by HTR‐8 cells was demonstrated phenotypically by enzyme‐linked immunosorbent assay of HTR‐8 cell lysates and culture supernatants. Hence, infection of trophoblasts by P. gingivalis can impact signal transduction pathways and modulate cytokine expression, outcomes that could disrupt the maintenance of pregnancy.