![]() ![]() Data are representative of at least 2 independent experiments and depicted as the mean ± sem. WT and TREM-2 −/− mice were injected intraperitonally with FITC-labeled bacteria, and the bacterial uptake by peritoneal exudate cells was analyzed 1 h later by FACS ( I). coli at 37☌, and the phagocytic uptake of bacteria was quantified by FACS ( H). ![]() Primary PMs of WT and TREM-2 −/− mice were incubated for 1 h with FITC-labeled E. WT and TREM-2 −/− mice ( n = 12 per group) were infected intraperitonally with 1 × 10 4 CFU E. Transaminase levels were detected in plasma ( F). MCP-1 and KC were measured in PLF ( D) and IL-6 in plasma samples ( E) by ELISA. At 16 h postinfection, bacterial counts in PLF, spleen, and blood ( B) and peritoneal cell numbers ( C) were determined. Peritoneal cell influx was accessed at 6 h postinfection ( A). WT and TREM-2 −/− mice ( n = 8 per group) were intraperitonally infected with 1 × 10 4 CFU E. TREM-2 dampens inflammation and promotes bacterial clearance in E. Inflammation macrophages negative regulator peritonitis. Our results illustrate TREM-2's effects on infection-triggered inflammation and identify TREM-2 as a potential target to prevent overwhelming inflammation while preserving antibacterial-effector functions. Significantly, we identified a high turnover rate because TREM-2 RNA is 25-fold down-regulated and the protein proteasomally degraded upon LPS encounter, thus ensuring a tightly regulated and versatile system that modulates inflammation. In line with this, TREM-2(-/-) peritoneal macrophages (PMs) exhibited augmented inflammation following TLR4 stimulation, demonstrating the presence and negative regulatory functionality of TREM-2 on primary PMs. Very rough version of the package right now but it works fairly well. ![]() Upon infection with Escherichia coli, the otherwise beneficial effect of an exaggerated early immune response in TREM-2(-/-) animals was counteracted by a 50% reduction in bacterial phagocytosis. finetune finetune contains some extra functions for model tuning that extend what is currently in the tune package. Augmented early inflammation in TREM-2(-/-) animals was followed by an accelerated resolution and ultimately improved survival, associated with the induction of the negative regulator A20. We investigated TREM-2's role in regulating TLR4-mediated inflammation by studying wild-type and TREM-2(-/-) mice challenged with LPS and found TREM-2 to dampen early inflammation. The triggering receptor expressed on myeloid cells (TREM)-2 negatively regulates inflammation by macrophages and impacts on phagocytosis, but the function of endogenous TREM-2 during infections is poorly understood. During infections, TLR-mediated responses require tight regulation to allow for pathogen removal, while preventing overwhelming inflammation and immunopathology. ![]()
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