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Lactobacilli and Vaginal Host Defense: Activation of the Human Immunodeficiency Virus Type 1 Long Terminal Repeat, Cytokine Production, and NF‐κB
Author(s) -
Seymour J. Klebanoff,
D. Heather Watts,
Christopher Mehlin,
Catherine M. Headley
Publication year - 1999
Publication title -
the journal of infectious diseases
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.69
H-Index - 252
eISSN - 1537-6613
pISSN - 0022-1899
DOI - 10.1086/314644
Subject(s) - jurkat cells , biology , cytokine , tumor necrosis factor alpha , microbiology and biotechnology , long terminal repeat , macrophage , hiv long terminal repeat , immunology , t cell , in vitro , biochemistry , gene expression , immune system , gene
Lactobacilli, a component of the normal vaginal flora, can activate the human immunodeficiency virus (HIV)-1 long terminal repeat (LTR) in the Jurkat T lymphocyte and THP-1 macrophage cell lines. Activation of the LTR in Jurkat cells was strongly enhanced by vanadate and inhibited by catalase, implicating H2O2. In contrast, activation in THP-1 cells occurred in the absence of vanadate and was unaffected by catalase. The active material partitioned into the phenol layer on hot aqueous phenol extraction. Lactobacilli also increased tumor necrosis factor-alphaand interleukin-1betaproduction and activated NF-kappaB in THP-1 cells and increased tumor necrosis factor-alphaproduction by human monocytes. Human vaginal fluid specimens had comparable properties, which correlated with their bacterial content. These findings suggest the presence in vaginal fluid of agent(s) derived from indigenous bacteria that can activate the HIV-1 LTR, cytokine production, and NF-kappaB in cells of macrophage lineage, with possible influence on vaginal physiology and host defense.

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