Suppression of human immunodeficiency virus type 1 replication in macrophages by commensal bacteria preferentially stimulating Toll-like receptor 4

Ahmed, Nursarat; Hayashi, T.; Hasegawa, Atsuhiko; Furukawa, Hiroyuki; Okamura, Noboru; Chida, Toshio; Masuda, Tohru; Kannagi, Mari

doi:10.1099/vir.0.022442-0

Cited by 33 publications

(28 citation statements)

References 44 publications

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“…This indicates that NR signaling, in addition to directly repressing virus expression in infected cells, is capable of dampening the proinflammatory cytokine response that activates HIV-1 expression in an autocrine or paracrine fashion. , it is not surprising that a number of TLR ligands activate HIV-1 expression in immune cells (3,11,34,36,114,145,161). In agreement with other reports (3,11,36,98,114,145,161), we show that signaling through TLR2 activates HIV-1 expression in macrophages and DCs ( Fig.…”

Section: Nr Ligands Inhibit Hiv-1 Replication In Primary Macrophagessupporting

confidence: 81%

Nuclear Receptor Signaling Inhibits HIV-1 Replication in Macrophages through Multipletrans-Repression Mechanisms

Hanley

Viglianti

2011

J Virol

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Section: Nr Ligands Inhibit Hiv-1 Replication In Primary Macrophagessupporting

confidence: 81%

Nuclear Receptor Signaling Inhibits HIV-1 Replication in Macrophages through Multipletrans-Repression Mechanisms

Hanley

Viglianti

2011

J Virol

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“…Based on our results, and on previous reports, 57 we propose that the role of TLRs during HIV-1 infection could be dual. During the initial phase of infection, TLR signaling could promote antiviral activity through IFN-a/b release, 58 whereas during the chronic phase, TLR stimulation could induce a strong inflammatory response that would increase HIV-1 replication.…”

mentioning

confidence: 76%

HIV Type 1 Infection Up-Regulates TLR2 and TLR4 Expression and Function in Vivo and in Vitro

Hernández

Stevenson

Latz

et al. 2012

AIDS Research and Human Retroviruses

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Toll-like receptors (TLRs) play a critical role in innate immunity against pathogens. Their stimulation induces the activation of NF-jB, an important inducer of HIV-1 replication. In recent years, an increasing number of studies using several cells types from HIV-infected patients indicate that TLRs play a key role in regulating the expression of proinflammatory cytokines and viral pathogenesis. In the present study, the effect of HIV-1 stimulation of monocyte-derived macrophage (MDM) and peripheral blood mononuclear cell (PBMC) subpopulations from healthy donors on the expression and functions of TLR2 and TLR4 was examined. In addition, and to complete the in vitro study, the expression pattern of TLR2 and TLR4 in 49 HIV-1-infected patients, classified according to viral load and the use of HAART, was determined and compared with 25 healthy subjects. An increase of TLR expression and production of proinflammatory cytokines were observed in MDMs and PBMCs infected with HIV-1 in vitro and in response to TLR stimulation, compared to the mock. In addition, an association between TLR expression and up-regulation of CD80 in plasmacytoid dendritic cells (pDCs) was observed. The ex vivo analysis indicated increased expression of TLR2 and TLR4 in myeloid dendritic cells (mDCs), but only of TLR2 in monocytes obtained from HIV-1-infected patients, compared to healthy subjects. Remarkably, the expression was higher in cells from patients who do not use HAART. In monocytes, there was a positive correlation between both TLRs and viral load, but not CD4 + T cell numbers. Together, our in vitro and ex vivo results suggest that TLR expression and function can be up-regulated in response to HIV-1 infection and could affect the inflammatory response. We propose that modulation of TLRs represents a mechanism to promote HIV-1 replication or AIDS progression in HIV-1-infected patients.

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“…In contrast, BV-associated bacteria could increase HIV-infection risk and HIV replication in the genital mucosa of HIV-infected women, by provoking local immune activation and/or disruption of the vaginal epithelium (Sha et al, 2005;Marconi et al, 2013;Mitchell et al, 2013;Petrova et al, 2013). In vitro studies have indeed shown that some BV-associated bacteria can enhance HIV expression, translation and/or replication (Klebanoff and Coombs, 1991;Hashemi et al, 1999;Ahmed et al, 2010).…”

Section: Discussionmentioning

confidence: 99%

Lactobacillus-dominated cervicovaginal microbiota associated with reduced HIV/STI prevalence and genital HIV viral load in African women

Tsivtsivadze²,

et al. 2014

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Cervicovaginal microbiota not dominated by lactobacilli may facilitate transmission of HIV and other sexually transmitted infections (STIs), as well as miscarriages, preterm births and sepsis in pregnant women. However, little is known about the exact nature of the microbiological changes that cause these adverse outcomes. In this study, cervical samples of 174 Rwandan female sex workers were analyzed cross-sectionally using a phylogenetic microarray. Furthermore, HIV-1 RNA concentrations were measured in cervicovaginal lavages of 58 HIV-positive women among them. We identified six microbiome clusters, representing a gradient from low semi-quantitative abundance and diversity dominated by Lactobacillus crispatus (cluster R-I, with R denoting 'Rwanda') and L. iners (R-II) to intermediate (R-V) and high abundance and diversity (R-III, R-IV and R-VI) dominated by a mixture of anaerobes, including Gardnerella, Atopobium and Prevotella species. Women in cluster R-I were less likely to have HIV (P ¼ 0.03), herpes simplex virus type 2 (HSV-2; Po0.01), and high-risk human papillomavirus (HPV; Po0.01) and had no bacterial STIs (P ¼ 0.15). Statistically significant trends in prevalence of viral STIs were found from low prevalence in cluster R-I, to higher prevalence in clusters R-II and R-V, and highest prevalence in clusters R-III/R-IV/R-VI. Furthermore, only 10% of HIV-positive women in clusters R-I/R-II, compared with 40% in cluster R-V, and 42% in clusters R-III/ R-IV/R-VI had detectable cervicovaginal HIV-1 RNA (P trend ¼ 0.03). We conclude that L. crispatusdominated, and to a lesser extent L. iners-dominated, cervicovaginal microbiota are associated with a lower prevalence of HIV/STIs and a lower likelihood of genital HIV-1 RNA shedding.

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Suppression of human immunodeficiency virus type 1 replication in macrophages by commensal bacteria preferentially stimulating Toll-like receptor 4

Cited by 33 publications

References 44 publications

Nuclear Receptor Signaling Inhibits HIV-1 Replication in Macrophages through Multipletrans-Repression Mechanisms

Nuclear Receptor Signaling Inhibits HIV-1 Replication in Macrophages through Multipletrans-Repression Mechanisms

HIV Type 1 Infection Up-Regulates TLR2 and TLR4 Expression and Function in Vivo and in Vitro

Lactobacillus-dominated cervicovaginal microbiota associated with reduced HIV/STI prevalence and genital HIV viral load in African women

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