Lactobacilli and Vaginal Host Defense: Activation of the Human Immunodeficiency Virus Type 1 Long Terminal Repeat, Cytokine Production, and NF‐κB

Klebanoff, Seymour J.; Watts, D. Heather; Mehlin, Christopher; Headley, Catherine M.

doi:10.1086/314644

Cited by 43 publications

(22 citation statements)

References 31 publications

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“…Our results are in contrast with the report by Klebanoff et al [33], which shows that L. acidophilus (strain crispatus) activates HIV-LTR transcription. Variation among L. acidophilus (strain crispatus) and the 2 strains tested by our laboratory could explain the differences in HIV-LTR induction activities.…”

Section: Discussioncontrasting

confidence: 99%

Induction of Human Immunodeficiency Virus Type 1 Expression by Anaerobes Associated with Bacterial Vaginosis

et al. 2000

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Bacterial vaginosis (BV) is a common disorder characterized by increased levels of anaerobic bacteria in the genital tract. BV has been associated with an increased rate of sexual transmission of human immunodeficiency virus (HIV). The effects of BV-associated anaerobic bacteria on HIV expression in monocytoid cells and T cells were examined. Peptostreptococcus asaccharolyticus and Prevotella bivia stimulated HIV expression in monocytoid cells, whereas Bacteroides ureolyticus, Peptostreptococcus anaerobius, and Lactobacillus acidophilus did not enhance HIV expression. P. asaccharolyticus also enhanced HIV expression in T cells and activated HIV long-terminal-repeat transcription in U38 cells. This report suggests a mechanism by which disturbances in vaginal flora could lead to a higher rate of sexual transmission of HIV. Furthermore, this study supports the idea that treatment of BV might serve as a preventive measure to reduce the risk of HIV transmission.

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Section: Discussioncontrasting

confidence: 99%

Induction of Human Immunodeficiency Virus Type 1 Expression by Anaerobes Associated with Bacterial Vaginosis

et al. 2000

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“…In support of this hypothesis, Klebanoff et al (1999) have shown that L. crispatus, which is present in the normal vaginal flora, induces TNFα secretion and activation of NF κB and the HIV LTR.…”

Section: Discussionmentioning

confidence: 78%

TLR2-Mediated Cell Stimulation in Bacterial Vaginosis

Mares¹,

Simões²,

Novak³

et al. 2008

Journal of Lower Genital Tract Disease

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Bacterial vaginosis (BV) is associated with preterm labor, pelvic inflammatory disease and increased HIV acquisition, although the pathways that mediate these pathological effects have not been elucidated. To determine the presence of toll-like receptor (TLR)-ligands and their specificity in BV, genital tract fluids were collected from women with and without BV by cervicovaginal lavage (CVL). The CVL samples were evaluated for their ability to stimulate secretion of proinflammatory cytokines and to activate NF κB and the HIV long terminal repeat (LTR), indicators of TLR activation, in human monocytic cells. Stimulation with BV CVLs induced higher levels of IL-8 and TNFα secretion, as well as higher levels of HIV LTR and NF κB activation, than CVLs from women with normal healthy bacterial flora. To identify which TLRs were important in BV, 293 cells expressing specific TLRs were exposed to CVL samples. BV CVLs induced higher IL-8 secretion by cells expressing TLR2 than CVLs from women without BV. Surprisingly, BV CVLs did not stimulate cells expressing TLR4/MD2, although these cells responded to purified LPS, a TLR4 ligand. BV CVLs, in cells expressing TLR2, also activated the HIV LTR. Thus, these studies show that soluble factor(s) present in the lower genital tract of women with BV activate cells via TLR2, identifying a pathway through which BV may mediate adverse effects.

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“…In vitro, lactobacilli (constituents of the normal vaginal flora) and Gardnerella vaginalis have been shown to enhance HIV-1 expression in mononuclear cells by a mechanism involving nuclear factor kB and the HIV long-terminal repeat promoter [33,34]. This may be the result of TNF-a signal transduction [34].…”

Section: Discussionmentioning

confidence: 99%

Correlation between Human Immunodeficiency Virus Type 1 RNA Levels in the Female Genital Tract and Immune Activation Associated with Ulceration of the Cervix

et al. 2000

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To address the hypothesis that local immune activation resulting from genital ulceration enhances human immunodeficiency virus type 1 (HIV-1) replication and shedding into the genital tract, paired plasma and cervicovaginal lavage (CVL) samples were obtained from 12 HIV-infected women before and after treatment of cervical intraepithelial lesions. Two weeks after treatment, inflammation and ulceration of the cervix were accompanied by major increases in mean concentrations of HIV-1 RNA (200-fold), tumor necrosis factor-alpha, interleukin 6, and soluble markers shed by activated lymphocytes and macrophages (sCD25 and sCD14, respectively) in CVL samples (P<.01 for each), but not plasma. Strong temporal and quantitative correlations were observed between concentrations of immunological markers and HIV-1 load in this compartment during a 10-week follow-up. Furthermore, in the presence of genital ulceration, HIV-1 in CVL samples was more readily captured by antibodies directed against virion-associated HLA-DR, a marker of host-cell activation, compared with virus in plasma. We suggest that local immune activation increases HIV-1 load in genital secretions, potentially increasing the risk of HIV-1 transmission.

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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

Cited by 43 publications

References 31 publications

Induction of Human Immunodeficiency Virus Type 1 Expression by Anaerobes Associated with Bacterial Vaginosis

Induction of Human Immunodeficiency Virus Type 1 Expression by Anaerobes Associated with Bacterial Vaginosis

TLR2-Mediated Cell Stimulation in Bacterial Vaginosis

Correlation between Human Immunodeficiency Virus Type 1 RNA Levels in the Female Genital Tract and Immune Activation Associated with Ulceration of the Cervix

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