vulnificus infection strongly suggests that signaling by other TL

vulnificus infection strongly suggests that signaling by other TLR(s) is necessary for triggering the antimicrobial defense needed to eradicate infection. While the TLR-mediated TNFα response is often critical to survive bacterial infections, dysregulated TNFα production can be selleck chemicals llc deleterious (Schluter & Deckert, 2000; Bradley,

2008). To directly examine the role of TNFα in the host defense to V. vulnificus, TNFα KO mice were infected intraperitoneally with V. vulnificus ATCC 27562 cells and survival of the mice was monitored for 48 h postinfection (Table 1). At a dose of 9 × 106V. vulnificus CFU, TNFα KO mice were significantly more resistant than WT mice (P=0.0045), but identical to TLR4 KO mice, to lethal infection.

Furthermore, V. vulnificus was rarely detected in cultures of the blood and spleen of the TNFα KO mice that survived upto 48 h postinfection, indicating that TNFα was not necessary for these mice to clear infection. The finding that TNFα deficiency is protective (1) shows that TNFα Apoptosis inhibitor plays a deleterious role in V. vulnificus infection, presumably via its contribution to the harmful inflammatory response; and (2) supports the results of Espat et al. (1996), who demonstrated that the mortality of V. vulnificus infected mice with chemically induced cirrhosis could be completely inhibited by pretreatment with a TNFα receptor antagonist. Despite the often serious nature of V. vulnificus infection, there is little information concerning the interaction of this bacterium with the innate immune system or how this affects the host response and the outcome of infection. The goal of this study was to investigate the role of TLR4 in Fludarabine price the host response to V. vulnificus. The major findings of the study are that (1) TLR4 signaling is MyD88 dependent and plays a key role in TNFα production by WT mouse blood and splenocytes

stimulated with inactivated V. vulnificus ATCC 27562 cells, (2) TLR4 signaling is deleterious in the mouse infection model, (3) signaling by TLR(s) other than TLR4 is needed to eradicate V. vulnificus infection, and (4) the TLR-mediated TNFα response plays a critical role in the outcome of infection. For several Gram-negative bacteria, lipopolysaccharide is the major TLR4 agonist (Takeda & Akira, 2005; Gerold et al., 2007; Spiller et al., 2008). This may be the case for V. vulnificus, but requires further investigation. Additional studies are also necessary to ascertain whether other V. vulnificus clinical isolates elicit a TLR4-mediated host response similar to that of V. vulnificus ATCC 27562. The observation that TLR4 deficiency is protective against lethal infection with V. vulnificus is intriguing. Several studies have shown that the effect of TLR4 signaling on the host response is dependent on the type of pathogen, the dose, and the route of infection (Gerold et al., 2007; Spiller et al., 2008).

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