Activation of the human immunodeficiency virus long terminal repeat in THP-1 cells by a staphylococcal extracellular product.

Klebanoff, Seymour J.; Kazazi, Farhad; Voorhis, W. C. Von; Schlechte, K. G.

doi:10.1073/pnas.91.22.10615

Cited by 20 publications

(20 citation statements)

References 26 publications

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“…Stable transfectants of the macrophage cell line THP-1 containing the luciferase reporter gene under the control of the HIV-1 LTR (THP-1 LTR luc ) were prepared as previously described [18]. IG5, a Jurkat T cell-derived cell line containing a stably integrated HIV-1 LTR-luciferase construct, was obtained through the Research and Reference Reagent Program (Division of AIDS, NIAID, NIH).…”

Section: Methodsmentioning

confidence: 99%

“…We have recently demonstrated the release of a factor or factors by staphylococcal strains that strongly activated the HIV-1 LTR in THP-1 cells but was without effect on the LTR in Jurkat T cells [18,19]. These properties are in contrast to the activation of the LTR by H 2 O 2 or H 2 O 2 plus vanadate, which was considerably stronger in Jurkat than in THP-1 cells [15].…”

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confidence: 93%

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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

et al. 1999

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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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Section: Methodsmentioning

confidence: 99%

mentioning

confidence: 93%

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

et al. 1999

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“…␦-Hemolysin can be formylated (see section on formylated peptides). PSM is released into the culture medium during overnight culture and is also detected in the supernatant fluid after vigorous vortexing of washed bacteria, suggesting that PSM is also partially bound to the cell surface (85).…”

Section: Vol 18 2005mentioning

confidence: 99%

Recognition ofStaphylococcus aureusby the Innate Immune System

2005

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The gram-positive bacterium Staphylococcus aureus is a major pathogen responsible for a variety of diseases ranging from minor skin infections to life-threatening conditions such as sepsis. Cell wall-associated and secreted proteins (e.g., protein A, hemolysins, and phenol-soluble modulin) and cell wall components (e.g., peptidoglycan and alanylated lipoteichoic acid) have been shown to be inflammatory, and these staphylococcal components may contribute to sepsis. On the host side, many host factors have been implicated in the innate detection of staphylococcal components. One class of pattern recognition molecules, Toll-like receptor 2, has been shown to function as the transmembrane component involved in the detection of staphylococcal lipoteichoic acid and phenol-soluble modulin and is involved in the synthesis of inflammatory cytokines by monocytes/macrophages in response to these components. Nod2 (nucleotide-binding oligomerization domain 2) is the intracellular sensor for muramyl dipeptide, the minimal bioactive structure of peptidoglycan, and it may contribute to the innate immune defense against S. aureus. The staphylococcal virulence factor protein A was recently shown to interact directly with tumor necrosis factor receptor 1 in airway epithelium and to reproduce the effects of tumor necrosis factor alpha. Finally, peptidoglycan recognition protein L is an amidase that inactivates the proinflammatory activities of peptidoglycan. However, peptidoglycan recognition protein L probably plays a minor role in the innate immune response to S. aureus. Thus, several innate immunity receptors may be implicated in host defense against S. aureus

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“…The luciferase reporter gene under the control of the HIV-1 LTR was introduced as a stable transfectant into the human macrophage cell line THP-1 as previously described (Klebanoff et al, 1994). The cells were incubated with the PSM components indicated in the legend to Fig.…”

Section: Activation Of the Hiv-1 Ltrmentioning

confidence: 99%

“…Cells were sedimented by centrifugation and an aliquot of the supernatant solution (0.7 ml) was removed and frozen at -70∞C for the subsequent measurement of TNFa. The remainder of the supernatant solution was removed, and the cells were lysed and luciferase activity was determined as previously described (Klebanoff et al, 1994) using a luciferase assay kit (Promega Biotec, Madison, WI) with a Monolight 1500 luminometer (Analytical Luminescence Laboratory, San Diego, CA). The photons counted over a 30 s period were designated as relative light units (RLU).…”

Section: Activation Of the Hiv-1 Ltrmentioning

confidence: 99%

Regulated expression of pathogen-associated molecular pattern molecules in Staphylococcus epidermidis: quorum-sensing determines pro-inflammatory capacity and production of phenol-soluble modulins

Vuong

Dürr

Carmody

et al. 2004

Cellular Microbiology

143

129

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SummaryPhenol-soluble modulin (PSM) is a peptide complex produced by the nosocomial pathogen Staphylococcus epidermidis that has a strong capacity to activate the human innate immune response. We developed a novel method based on liquid chromatography-mass spectrometry (LC-MS) to quantify the production of the individual PSM components. Each PSM peptide was abundant in most of the 76 S epidermidis strains tested. Importantly, none of the PSM components were secreted by an agr mutant strain, indicating that PSM synthesis is regulated strictly by the agr quorum-sensing system. Furthermore, the agr mutant strain failed to elicit production of TNF a a a a by human myeloid cells and induced significantly less neutrophil chemotaxis compared with the wild-type strain. Thus, quorum-sensing in S. epidermidis dramatically influenced activation of human host defence. We propose that an agr quorum-sensing mechanism facilitates growth and survival in infected hosts by adapting production of the pro-inflammatory PSMs to the stage of infection.

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Activation of the human immunodeficiency virus long terminal repeat in THP-1 cells by a staphylococcal extracellular product.

Abstract: ABSTRACT

Cited by 20 publications

References 26 publications

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

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

Recognition ofStaphylococcus aureusby the Innate Immune System

Regulated expression of pathogen-associated molecular pattern molecules in Staphylococcus epidermidis: quorum-sensing determines pro-inflammatory capacity and production of phenol-soluble modulins

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