Hydrogen from intestinal bacteria is protective for Concanavalin A-induced hepatitis

• Published in: Biochemical and biophysical research communications Vol. 386; no. 2; pp. 316 - 321
• Main Authors: Kajiya, Mikihito, Sato, Kimihiro, Silva, Marcelo J.B., Ouhara, Kazuhisa, Do, Phi M., Shanmugam, K.T., Kawai, Toshihisa
• Format: Journal Article
• Language: English
• Published: United States Elsevier Inc 21.08.2009
• Subjects: Animals; Antibiotics; Bacteria; Biomarkers - analysis; Chemical and Drug Induced Liver Injury - pathology; Chemical and Drug Induced Liver Injury - prevention & control; Concanavalin A; Concanavalin A - toxicity; Disease Models, Animal; Escherichia coli; Escherichia coli - metabolism; Hepatitis; Hydrogen - metabolism; IFN-γ; Inflammation; Intestines - microbiology; Lymphocytes; Male; Mice; Mice, Inbred C57BL; Mitogens - toxicity; Molecular hydrogen; Mouse model; TNF-α; Molecular hydrogen; Hepatitis; IFN-γ; Antibiotics; TNF-α; Lymphocytes; Bacteria; Inflammation; Mouse model; Concanavalin A
• ISSN: 0006-291X; 1090-2104
• DOI: 10.1016/j.bbrc.2009.06.024

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-α and IFN-γ 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-α and IFN-γ 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.