Shock : molecular, cellular, and systemic pathobiological aspects and therapeutic approaches : the official journal the Shock Society, the European Shock Society, the Brazilian Shock Society, the International Federation of Shock Societies
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The influence of gut fungi in chronic colitis was investigated by repeated oral administration of Candida albicans in a 3% dextran sulfate solution (DSS) induced-colitis mouse model. Candida administration in the DSS (DSS+Candida) model enhanced the mortality rate and induced bacteremia (without candidemia) resulting from a gut perm-selectivity defect despite similar diarrheal severity in mice treated with DSS alone. The dominant fecal bacteria in DSS+Candida and DSS alone mice were Pseudomonas spp. and Enterobacter spp., respectively, implying that Candida induced gut dysbiosis. ⋯ In conclusion, gut Candida induced bacteremia in the DSS model through an inflammation-induced gut perm-selectivity defect and facilitated the growth of some gut bacteria. Treatment strategies aimed at reducing gut fungi could attenuate disease severity. Further investigation of gut fungi in inflammatory bowel disease is warranted.
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This study investigated the therapeutic benefits of neuromuscular electrical stimulation (NMES). C57BL/6 mice were administered lipopolysaccharide (LPS; 20 mg/kg body weight) by intraperitoneal injection and divided into control (C) and NMES groups (n = 10-12 each). The latter received NMES to the bilateral gastrocnemius muscle for 1 h at low or high frequency (LF = 2 Hz and HF = 50 Hz, respectively) and low or high voltage (LV = 10 V and HV = 50 V, respectively). ⋯ Fatty acid oxidation (FAO) was slightly increased in these two groups, whereas carbohydrate oxidation (CHO) was decreased or not changed. Significant upregulation of PGC-1α in muscle as well as a decrease in plasma IL-6 level were also observed in these two groups (P < 0.05). Thus, NMES exerts therapeutic effects under conditions that induce a mild switch in energy metabolism from glucose to lipid predominant metabolism through PGC-1α upregulation and suppression of inflammation, and may be an effective early intervention even in hemodynamically unstable patients.
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The aim of this study was to investigate the changes of bile acids in the liver during hemorrhagic shock (HS) and their potential to attenuate liver injury via activation of SIRT1 (sirtuin 1)-FXR (farnesoid X receptor) signaling. ⋯ TUDCA in the liver decreased during HS. TUDCA supplementation might attenuate HS-induced liver injury by upregulating SIRT1-FXR signaling.
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Aging is a grave problem in sepsis, and T cell exhaustion is the main cause of sepsis-induced immunosuppression. Sepsis- and aging-induced T cell exhaustion is related to secondary infection with a poor long-term outcome in the elderly. However, the trend, impact, and mechanism of T cell exhaustion are still unclear. ⋯ Sepsis-induced T cell exhaustion was significantly severe in aged mice than in young mice and was accompanied with decreased naive CD4 and CD8 T cells (P < 0.01) and increased expression of program death 1 on T cell (P < 0.01) and regulatory T cell population (P < 0.01). IL-15 significantly improved sepsis-induced T exhaustion, with significantly increased numbers of natural killer cells and macrophages, and significantly enhanced phagocytosis activity in aged septic mice (P < 0.05). It decreased the long-term mortality associated with sepsis survivors by improving T cell exhaustion over an extended duration and also ameliorated aging-induced persistent T cell exhaustion in septic mice.