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...arensis does significantly stimulate TLR2 signaling resulting in proinflammatory cytokine production, and intracellular bacteria colocalize with TLR2 and MyD88 (Katz et al., 2006; Malik et al., 2006; =-=Cole et al., 2007-=-). In vivo, TLR2 does not seem to play a role in host protection during intradermal challenge, but is important in an intranasal model of infection (Collazo et al., 2006; Malik et al., 2006). However,...

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... to F. tularensis infection. Examples of these reports include studies of the involvement of Toll-like receptors 2 and 4 in tularemia induced in the mouse via the respiratory or the intradermal route =-=(6, 9, 10, 28)-=-, analysis of proinflammatory gene expression following murine intraperitoneal or intradermal infection (8), and research on the contributions of B and T lymphocytes to protection and response in expe...

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... contribute to the induction of host immune responses to the pathogen. In the case of F. tularensis, in vitro studies have shown that the innate immune response mediated by this bacterium is via TLR2 =-=[53, 71, 72]-=-, which is likely a result of immunodominant surface lipoproteins [73]. However, following infection, it is possible that cytosol-derived proteins, such as DnaK, “hidden” epitopes, or nucleic acids, a...

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...ly showed that Ft LVS-induced macrophage proinflammatory gene expression was entirely TLR2 dependent and that cytokines encoded by these genes were expressed in a highly reproducible temporal pattern =-=(17)-=-. Using LVSiglC, a mutant strain of Ft LVS that is retained within the phagosome, we now demonstrate that Ft LVS is capable of prolonged TLR2-dependent signaling from within the phagosome. We also sh...

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...macrophages with LVS�iglC leads to prolonged activation of downstream signaling intermediates We showed previously that Ft-induced macrophage proinflammatory gene expression was wholly TLR2-dependent =-=[17, 18]-=-, and using confocal microscopy, we demonstrated that phagosomal Ft LVS colocalized with TLR2 and MyD88 [17]. This suggested that Ft LVS was capable of intraphagosomal TLR2mediated signaling. To confi...

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...ning 6 short (12-14 carbon) fatty acids, whereas Francisellaslipid A has 4 fatty acids with longer carbon chains (16-18 carbon) (11,24). On the othershand, Francisella has been shown to activate TLR2 =-=(25,26)-=- that recognizes lipoproteins,sglycans and glycophospholipids more frequently present in Gram-positive bacteria,sfungi and protozoan parasites, respectively (27). Francisella also activates anothersco...

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... 2006, 2007; Katz et al., 2006; Li et al., 2006; Thakran et al., 2008; Abplanalp et al., 2009). Moreover, it has been demonstrated that Francisella colocalizes with TLR2 and MyD88 inside macrophages (=-=Cole et al., 2007-=-; Figure 3), signals through TLR2 from within the phagosome (Cole et al., 2008; Figure 2 | Signaling triggered by F. tularensis located in the cytosol. Host cell signaling occurs after F. tularensis ...

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... TLR2 was required for induction of a range of pro-inflammatory cytokine genes (e.g., TNF-α, IL-1β, KC, p40, RANTES, IFN-γ, IL-6, IFN-β, MCP-1, and iNOS) by peritoneal macrophages in response to LVS (=-=Cole et al., 2007-=-; Abplanalp et al., 2009). Full signaling via TLR2 in LVS-infected macrophages required the adaptor molecules MyD88 and TIRAP (Cole et al., 2010). Consistent with the membrane-bound nature of TLR2, LV...

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...counterparts, we next employed a biological assay to gauge the responses of naı̈ve macrophages to differentially cultivated bacteria. F. tularensis LVS grown in MHB or on Thayer-Martin plates induces =-=(9, 10, 21)-=- or, as described in one report, initially induces and then represses (42) the production of proinflammatory cytokines (TNF-, IL-12p40, IL-6, etc.) by responding naı̈ve M. In contrast, M-grown Fran...