Hydrogen Gas Reduces Inflammation and Prevents Fever in Sepsis Study
- Authors
- Eduardo A. Saramago, Gabriela S. Borges, Carlitos G. Singolani-Jr, Jonatas E. Nogueira, Renato N. Soriano, Evelin C. Cárnio, Luiz G.S. Branco
- Journal
- Brain, Behavior, and Immunity
- Year
- 2019
- DOI
- 10.1016/j.bbi.2018.09.027
- Study Type
- Rat
- Outcome
- Positive
- Peer Reviewed
- Yes
- Country
- Brazil
- Health Condition
- Sepsis
- Body System
- Immune System
TL;DR
Inflammation and fever in rats were reduced by inhaling molecular hydrogen, which also helped to balance immune responses and body temperature during severe infection.
Key Finding
Inhaled molecular hydrogen reduced inflammatory markers and prevented fever in mild inflammation, while preventing dangerous drops in blood pressure during severe inflammation in rats exposed to bacterial toxins.
Summary
Researchers tested whether inhaled molecular hydrogen (H2) could help rats' bodies respond better to a severe bacterial toxin (lipopolysaccharide) that triggers whole-body inflammation. They found that hydrogen inhalation reduced inflammatory chemicals in the blood, prevented fever in mild cases, and prevented dangerous drops in blood pressure during severe inflammation—likely by reducing the production of certain signaling molecules in the body.
Practical Takeaway
This is an animal study only, so results cannot yet be applied to humans. Early evidence suggests hydrogen may influence inflammatory responses and fever regulation, but human studies would be needed to determine if these effects occur in people or have any clinical benefit for sepsis or inflammatory conditions.
Abstract
Molecular hydrogen (H2) exerts anti-oxidative, anti-apoptotic, and anti-inflammatory effects. Here we tested the hypothesis that H2 modulates cardiovascular, inflammatory, and thermoregulatory changes in systemic inflammation (SI) induced by lipopolysaccharide (LPS) at different doses (0.1 or 1.5 mg/kg, intravenously, to induce mild or severe SI) in male Wistar rats (250-300 g). LPS or saline was injected immediately before the beginning of 360-minute inhalation of H2 (2% H2, 21% O2, balanced with nitrogen) or room air (21% O2, balanced with nitrogen). Deep body temperature (Tb) was measured by dataloggers pre-implanted in the peritoneal cavity. H2 caused no change in cardiovascular, inflammatory parameters, and Tb of control rats (treated with saline). During mild SI, H2 reduced plasma surges of proinflammatory cytokines (TNF-α and IL-6) while caused an increase in plasma IL-10 (anti-inflammatory cytokine) and prevented fever. During severe SI, H2 potentiated hypothermia, and prevented fever and hypotension, which coincided with reduced plasma nitric oxide (NO) production. Moreover, H2 caused a reduction in surges of proinflammatory cytokines (plasma TNF-α and IL-1β) and prostaglandin E2 [(PGE2), in plasma and hypothalamus], and an increase in plasma IL-10. These data are consistent with the notion that H2 blunts fever in mild SI, and during severe SI potentiates hypothermia, prevents hypotension reducing plasma NO production, and exerts anti-inflammatory effects strong enough to prevent fever by altering febrigenic signaling and ultimately down-modulating hypothalamic PGE2 production.