Gut Bacteria Produce Hydrogen That Protects the Liver from Inflammation
- Authors
- Mikihito Kajiya, Kimihiro Sato, Marcelo J.B. Silva, Kazuhisa Ouhara, Phi M. Do, K.T. Shanmugam, Toshihisa Kawai
- Journal
- Biochemical and Biophysical Research Communications
- Year
- 2009
- DOI
- 10.1016/j.bbrc.2009.06.024
- Study Type
- Mouse
- Outcome
- Positive
- Peer Reviewed
- Yes
- Country
- United States
- Health Condition
- Hepatitis
- Body System
- Digestive System
TL;DR
Hydrogen gas produced by gut bacteria can reduce liver inflammation in mice.
Key Finding
Hydrogen gas produced by intestinal bacteria, particularly E. coli, reduced liver inflammation and suppressed inflammatory immune responses in mice with induced hepatitis.
Summary
This mouse study investigated whether hydrogen gas produced by gut bacteria could protect against liver inflammation. Researchers found that when they eliminated gut bacteria with antibiotics, mice developed worse liver inflammation. However, when they restored bacteria that produce hydrogen gas, the liver inflammation improved. The study suggests that hydrogen from these bacteria may help reduce harmful immune responses in the liver.
Practical Takeaway
This is an early-stage mouse study showing that hydrogen-producing gut bacteria may have protective effects against liver inflammation. However, it does not yet tell us whether consuming hydrogen water would have similar benefits in humans, as the hydrogen in this study came from living bacteria in the gut rather than from drinking hydrogen water. More research in humans would be needed to determine if there are practical health applications.
Abstract
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.