Hydrogen from intestinal bacteria is protective for Concanavalin A-induced hepatitis
Hydrogen from intestinal bacteria is protective for Concanavalin A-induced hepatitis
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DOI：
10.1016/j.bbrc.2009.06.024
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发表时间：
2009-08-21
影响因子：
3.1
通讯作者：
Kawai, Toshihisa
中科院分区：
文献类型：
--
作者：
Kajiya, Mikihito;Sato, Kimihiro;Kawai, Toshihisa
众所周知，一些肠道细菌，如大肠杆菌，可以产生大量的氢分子（H-2）。虽然H-2的抗氧化作用已被充分证明，但本研究调查了肠道定植细菌释放的H-2是否会影响ConA诱导的小鼠肝炎。全身抗生素显著降低肝脏和肠道H-2水平，抑制肠道细菌。血清中AST、ALT、tnf - α和ifn - γ水平的测定表明，抗生素抑制肠道菌群增加了cona诱导肝炎的严重程度，而用产h -2的大肠杆菌重建肠道菌群，而不是用h -2缺陷突变型大肠杆菌重建肠道菌群，可以下调cona诱导的肝脏炎症。此外，引入H-2可显著抑制cona刺激的脾淋巴细胞体外产生tnf - α和ifn - γ。这些结果表明，肠道细菌释放的H-2可以抑制ConA引起的肝脏炎症。(C) 2009爱思唯尔公司版权所有。
It is well known that some intestinal bacteria, such as Escherichia coli, can produce a remarkable amount of molecular hydrogen (H-2). Although the antioxidant effects of H-2 are well documented, the present study examined whether H-2 released from intestinally colonized bacteria could affect Concanavalin A (ConA)-induced mouse hepatitis. Systemic antibiotics significantly decreased the level of H-2 in both liver and intestines along with suppression of intestinal bacteria. As determined by the levels of AST, ALT, TNF-alpha and IFN-gamma in serum, suppression of intestinal bacterial flora by antibiotics increased the severity of ConA-induced hepatitis, while reconstitution of intestinal flora with H-2-producing E. coli, but not H-2-deficient mutant E. coli, down-regulated the ConA-induced liver inflammation. Furthermore, in vitro production of both TNF-alpha and IFN-gamma by ConA-stimulated spleen lymphocytes was significantly inhibited by the introduction of H-2. These results indicate that H-2 released from intestinal bacteria can suppress inflammation induced in liver by ConA. (C) 2009 Elsevier Inc. All rights reserved.