Can hydrogen gas therapy help with sepsis?

This mouse study suggests hydrogen gas inhalation could help sepsis patients by reducing deadly inflammation and improving survival rates. The therapy nearly doubled survival rates from 40% to 75% in septic mice.

How does hydrogen gas reduce inflammation in sepsis?

Hydrogen gas appears to suppress key inflammatory pathways like STAT3 and acute phase response signaling in multiple organs. It reduces inflammatory chemicals like IL-6 and TNF-α that drive sepsis complications.

What concentration of hydrogen gas was used in this study?

Researchers used 7% hydrogen gas that mice inhaled continuously starting immediately after sepsis was induced. The therapy continued for the duration of the study period.

Is hydrogen gas therapy safe for sepsis patients?

While this mouse study showed promising results, human clinical trials are needed to confirm safety and effectiveness. Hydrogen gas has been used safely in some clinical applications.

What organs does hydrogen therapy protect in sepsis?

The study found hydrogen therapy affected inflammatory pathways in the liver, intestines, and lungs. This multi-organ protection may explain why survival rates improved so significantly.

Hydrogen Gas Therapy Improves Survival in Sepsis by Reducing Inflammation

Authors: Hiroshi Matsuura, Hisatake Matsumoto, Daisuke Okuzaki, Kentaro Shimizu, Hiroshi Ogura, Takeshi Ebihara, Tsunehiro Matsubara, Shin-Ichi Hirano, Takeshi Shimazu
Journal: Journal of Surgical Research
Year: 2021
DOI: 10.1016/j.jss.2021.01.022
Study Type: Mouse
Outcome: Positive
Peer Reviewed: Yes
Country: Japan
Health Condition: Sepsis
Body System: Immune System

TL;DR

Inhaling molecular hydrogen (H2) significantly improved survival and reduced inflammation in mice with sepsis.

Key Finding

Septic mice that inhaled hydrogen gas had a significantly higher survival rate (75% versus 40%) and showed reduced inflammatory markers and improved blood sugar control compared to untreated septic mice.

Summary

Researchers gave septic mice (mice with a severe bloodstream infection) inhaled hydrogen gas and compared their survival to mice that didn't receive it. Mice breathing hydrogen gas had a 75% survival rate compared to 40% in the control group. The hydrogen gas also reduced inflammatory markers (immune chemicals that cause damage) in the blood and helped maintain normal blood sugar levels. By analyzing gene activity in the liver, intestines, and lungs, researchers found that hydrogen gas turned off several inflammatory signaling pathways (communication systems between cells that trigger inflammation).

Practical Takeaway

This study provides early evidence that hydrogen gas inhalation may help reduce inflammation in sepsis, but it was conducted only in mice. Much more research, including human clinical trials, would be needed before hydrogen gas could be considered a sepsis treatment. The findings suggest a potential mechanism worth investigating further, but do not yet support any clinical use in humans.

Abstract

Background: Molecular hydrogen (H2) has been used in clinical cases. However, there are few studies of H2 therapy to treat sepsis, and anti-inflammatory mechanisms of H2 are mostly unknown. We aimed to confirm effects of H2 therapy on sepsis and reveal its therapeutic mechanism via RNA sequencing in multiple organs in septic mice. Methods: Nine-week-old C57BL/6 male mice underwent cecal ligation and puncture (CLP) or sham procedure. Subsequently, the CLP model received immediate ± continuous inhalation of 7% H2. Mice were observed for a week to assess survival rates. Serum inflammatory cytokines were evaluated at 24 h after CLP procedure. Liver, intestine, and lungs in CLP mice receiving 24-h ± H2 therapy were assessed by RNA sequencing. Data were analyzed with Ingenuity Pathways Analysis (QIAGEN Inc). Results: Seven-day survival rate in septic mice was significantly improved in the H2 inhalation group compared with that in the control group (75% versus 40%, P < 0.05). H2 treatment attenuated serum interleukin-6 and tumor necrosis factor-α levels at 24 h after CLP, and blood glucose levels were maintained in the H2-treated group. In RNA sequencing, canonical pathway analysis revealed inactivity of various inflammatory signaling pathways, for example, acute phase response signaling and STAT3 pathways, in the liver and intestine in the CLP model after 24-h H2 inhalation. We detected significantly decreased expressions of upstream regulator genes such as the CD14 antigen gene in the liver and various cytokine receptor genes in the intestine and lungs in the H2-treated group. Conclusions: These findings may contribute to clarifying the mechanism of action of H2 therapy in sepsis.