Study summary · research use only
Oral glutathione supplementation drastically reduces Helicobacter-induced gastric pathologies
Plain-language summary
Paraphrased from the published abstract below — not a verdict on whether anything works.
In this study, the metabolism of Helicobacter suis, a bacterium causing gastric disease in pigs and humans, was examined, showing depletion of glutamine (Gln) during culture and conversion of both Gln and glutathione (GSH) to glutamate via the bacterial enzyme γ-glutamyltranspeptidase (GGT) (species not specified for the culture experiments). The in vivo effect of oral Gln and GSH supplementation was assessed in Mongolian gerbils infected with H. suis. Oral Gln supplementation was associated with reduced gastritis and epithelial proliferation, and oral GSH supplementation was associated with inflammation and epithelial proliferation levels returning to those of uninfected control gerbils. The authors suggest Gln and GSH supplementation may help reduce Helicobacter-associated tissue damage in humans and pigs alongside eradication therapy.
Abstract
Helicobacter (H.) suis causes gastric pathologies in both pigs and humans. Very little is known on the metabolism of this bacterium and its impact on the host. In this study, we have revealed the importance of the glutamate-generating metabolism, as shown by a complete depletion of glutamine (Gln) in the medium during H. suis culture. Besides Gln, H. suis can also convert glutathione (GSH) to glutamate, and both reactions are catalyzed by the H. suis γ-glutamyltranspeptidase (GGT). Both for H. pylori and H. suis, it has been hypothesized that the degradation of Gln and GSH may lead to a deficiency for the host, possibly initiating or promoting several pathologies. Therefore the in vivo effect of oral supplementation with Gln and GSH was assessed. Oral supplementation with Gln was shown to temper H. suis induced gastritis and epithelial (hyper)proliferation in Mongolian gerbils. Astonishingly, supplementation of the feed with GSH, another GGT substrate, resulted in inflammation and epithelial proliferation levels returning to baseline levels of uninfected controls. This indicates that Gln and GSH supplementation may help reducing tissue damage caused by Helicobacter infection in both humans and pigs, highlighting their potential as a supportive therapy during and after Helicobacter eradication therapy.
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