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Prostate epithelial cells can act as early sensors of infection by up‐regulating TLR4 expression and proinflammatory mediators upon LPS stimulation
Author(s) -
Gatti Gerardo,
Rivero Virginia,
Motrich Rubén Darío,
Maccioni Mariana
Publication year - 2006
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 - 10.1189/jlb.1005597
Subject(s) - proinflammatory cytokine , tlr4 , biology , stimulation , microbiology and biotechnology , immunology , cancer research , inflammation , signal transduction , endocrinology
Despite the prevalence of prostate disease, little is known about the immunobiology of the prostate and its contribution to disease. The main goal of this work was to investigate how prostate epithelial cells deal with inflammatory stimuli. To this aim, we stimulated a rat prostate epithelial cell line [metastasis‐lung (MAT‐LU)] or rat primary epithelial cells with lipopolysaccharide (LPS). Prostate epithelial cells constitutively express significant levels of Toll‐like receptor 4 (TLR4) and CD14 mRNA. TLR2 transcription could also be demonstrated, suggesting that these cells could recognize a broader spectrum of microbial molecular patterns. TLR4, TLR2, and CD14 proteins were also detected, although not at the cell surface but intracellularly. Prostate epithelial cells not only express these receptors, but they are also able to respond to LPS, and LPS‐stimulated MAT‐LU cells activate nuclear factor‐κB transcription factor, induce the expression of inducible nitric oxide (NO) synthase, and secrete NO. Even more, numerous chemokine genes are up‐regulated or induced in this response. Our results clearly demonstrate that prostate epithelial cells are fully competent to respond. The fact that they express TLR4 and TLR2 intracellularly suggests the presence of regulatory mechanisms, which once overcome, could turn these cells into active players of the innate immunity, capable of initiating an inflammatory response.