2009
DOI: 10.3109/08923970902838672
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Tigecycline attenuates staphylococcal superantigen-induced T-cell proliferation and production of cytokines and chemokines

Abstract: The purpose of this study is to examine the in vitro modulatory effect of tigecycline on staphylococcal superantigen-induced T-cell activation and cytokines and chemokines production by human peripheral blood mononuclear cells (PBMC). Isolated human PBMC from ten healthy volunteers were stimulated by staphylococcal enterotoxin B (SEB) and Staphylococcal toxic shock syndrome toxin-1 (TSST-1) superantigens with varying concentrations of tigecycline. Cytokines IL-1 beta, IL-6, TNF-alpha, and chemokines MIP-1 alph… Show more

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Cited by 22 publications
(12 citation statements)
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“…Staphylococcal enterotoxins (SEs) and TSST-1 are intermediate molecular weight proteins (20–30 kDa) that cause food poisoning and toxic syndrome, respectively, in humans and other species [5]. Moreover, both SEs and TSST-1 can act as bacterial superantigens that bind to MHC class II molecules on antigen presenting cells and selectively stimulate T cells expressing appropriate Vβ gene segments on their T cell receptors (TCRs) [6]. The secretion of staphylococcal exotoxins is regulated in a growth-phase-dependent manner, predominantly occurring during the post-exponential phase [7].…”
Section: Introductionmentioning
confidence: 99%
“…Staphylococcal enterotoxins (SEs) and TSST-1 are intermediate molecular weight proteins (20–30 kDa) that cause food poisoning and toxic syndrome, respectively, in humans and other species [5]. Moreover, both SEs and TSST-1 can act as bacterial superantigens that bind to MHC class II molecules on antigen presenting cells and selectively stimulate T cells expressing appropriate Vβ gene segments on their T cell receptors (TCRs) [6]. The secretion of staphylococcal exotoxins is regulated in a growth-phase-dependent manner, predominantly occurring during the post-exponential phase [7].…”
Section: Introductionmentioning
confidence: 99%
“…[ 36 ] As an acute-phase reactant, fibrinogen biosynthesis is increased by interleukin (IL)-6-mediated increases in the transcription of the fibrinogen mRNA [ 37 ] ; IL-1 and tumor necrosis factor-alpha suppress fibrinogen synthesis. [ 38 ] There is, however, room for speculation that tigecycline may interfere with the production of fibrinogen by influencing the level of cytokines or by directly influencing the transcription of fibrinogen mRNA.…”
Section: Discussionmentioning
confidence: 99%
“…Indeed, PMIN does not inhibit the growth of minocycline-sensitive bacterial strains (Lertvorachon et al 2005;Bastos et al 2008), but does inhibit licking behaviour in mice to the same extent as those induced by minocycline (Bastos et al 2008). On the other hand, tigecycline, which differs from minocycline by the long side chain at the 9 position of carbon atom (9-tert-butyl-glycylamido moiety) and broader antibacterial spectrum, inhibits the production of inflammatory cytokines in different experimental settings, and this effects are unrelated to the antibacterial activity (Saliba et al 2009;Salvatore et al 2009). Both PMIN and tigecycline are equipotent to minocycline in reducing the microglial production of PGE 2 induced by LPS (L.F.S.…”
Section: Interaction Between Minocycline and Morphinementioning
confidence: 97%