Acta Scientific Microbiology

Editorial Volume 9 Issue 10

Hydrogen Sulfide (H2S) Physiology with Crosstalk with GIT Sulfate-Reducing Bacteria (SRB) and Other Bacteria in Therapy of Obesity, Inflammatory Bowel Disease Along with Colorectal Cancer

Kulvinder Kochar Kaur*

Scientific Director Cum Owner Dr Kulvinder Kaur Centre for Human Reproduction, Jalandhar, Punjab, India

*Corresponding Author: Kulvinder Kochar Kaur, Scientific Director Cum Owner Dr Kulvinder Kaur Centre for Human Reproduction, Jalandhar, Punjab, India.

Received: August 27, 2026; Published: September 28, 2026

Abstract

H2S delineate’s a pivotal molecule for living organisms inclusive of humans. Enrichment of empirical corroborations are present which point a part of H2S in physiology as well as pathophysiology. The biological parts of H2S with plethora of concentrating on its part in the gastrointestinal tract (GIT) has been reviewed extensively. H2S is believed to be the third gasotransmitter, along with nitric oxide (NO) as well as carbon monoxide (CO), in addition to is implicated in i) inflammation, ii) gut motility, iii) oxidative stress (OS), iv) ulcer repair, v) vascular tone, vi) neuromodulation, vii) cryoprotection, viii) memory generation, ix) hormone liberation, x) apoptosis along with x) several other vital biologic working. Certain of such events are further targets for CO as well as NO despite the mechanistic modes of actions of such other gaseous signaling molecules might be variable. H2S in the GIT is generated apart from by the enzymes cystathionine-β-synthase (CBS), as well as cystathionine-γ-lyase (CSE) of the host however further by sulfate-reducing bacteria (SRB) which are resident microbes utilizing the fermentation by-product hydrogen in the form of the substrate. H2S in the intestine is further generated by certain members that reside in the form of gut bacteria. Of the maximum pronouncedgenerators of H2S are sulfate- reducing bacteria (SRB). Dependence on the of the prevalence of methane excretors, sulfate reduction is the predominant Figure 1: Courtesy ref no- 4 Biogeneration of H2S by mammalian cells. hydrogenotrophic pathway in equivalent to 60% of humans. Enumeration of SRB by culture based methods documented a variety of 103–1011 bacteria per gm of human feces. SRB belong to the class δ-Proteobacteria in addition to generate H2S utilizing the enzyme complex dissimilatory sulfite reductases (DSR) (Figure 2). The maximum pronounced genus in such category is Desulfovibrio, that use lactate as well as hydrogen in the form of a substrate. Other genera being Desulfobacter, Desulfomonas, Desulfobulbus, in addition to Desulfotomaculum. The SRB utilize sulfate in the form of a terminal electron acceptor (TEA) for respiration, with the concurrent generation of H2S. Other bacterial species affiliated to variable genera, for instance i) Streptococcus, ii) Fusobacterium, iii) Salmonella, iv) Enterobacter, along with v) Helicobacter further generate H2S from L-cysteine, by the actions of cysteine desulfhydrase. In an extra diet- dependent assessment, once obese subjects were fed diets to balance their gut microbes, weight reduction was associated with a reduction in H2S-generating families Desulfovibrionaceae as well as Enterobacteriaceae (i) Escherichia, ii) Shigella, iii) Klebsiella, along with iv) Citrobacter), in addition to a diminishing in proinflammatory i) Tumor necrosis factor (TNF-α) along with ii) Interleukin (IL-6) cytokines. There are conflicting reports inclusive of an extra study illustrating that Desulfovibrio quantities were substantially lesser in obese/overweight children in contrast to controls. Hence, the part of SRB in addition to SRB obtained H2S in the pathogenesis of a disease situation, for instance obesity, continue to be uncharted. Despite, mounting corroboration points that SRB is associated with inflammatory situations, it is not clear if such is a side derivative or SRB are the causative factors of the disease. Apart from SRB, other H2S-generating gut bacteria, for instance Fusobacterium, have further been observed to be associated with IBD. The communication amongst H2S-generating gut bacteria in addition to inflammation was further embraced by the observations that Bilophila wadsworthia, a sulfite-reducing bacteria which forms H2S analogous to Desulfovibrio was higher in quantity in mice fed with high fat diet (HFD), along with this was correlated with proinflammatory reactions in genetically vulnerable mice. Additional question is are SRB advantageous or inimical ? Does this knowledge possess the capacity of being used to generate innovative treatments to address inflammatory diseases dependent on targeting SRB? Thus H2S can be utilized in Ischemia/Reperfusion damage, H2S in Intestinal Inflammation, H2S in Ulcer repair, and H2S in Intestinal Motility. Thereby utilized for therapy of IBD (inclusive of UC, CD) and CRC [1-4]

References

  1. Chan MV and Wallace JL. “Hydrogen sulfide-based therapeutics and gastrointestinal diseases: Translating physiology to treatments”. American Journal of Physiology-Gastrointestinal and Liver Physiology 305 (2013): G467-G473.
  2. Stepién PP and Pieniazek NJ. “The use of the L-serine sulfhydrylase assay for the estimation of cystathionine beta-synthase”. Analytical Biochemistry 54 (1973): 294-249.
  3. Radcliffe BC and Egan AR. “A survey of methionine adenosyltransferase and cystathionine gamma-lyase activities in ruminant tissues”. Australian Journal of Biological Sciences 27 (1974): 465-471.
  4. Singh SB and Lin HC. “Hydrogen Sulfide in Physiology and Diseases of the Digestive Tract”. Microorganisms4 (2015): 866-889.

Citation

Citation: Kulvinder Kochar Kaur. “Hydrogen Sulfide (H2S) Physiology with Crosstalk with GIT Sulfate-Reducing Bacteria (SRB) and Other Bacteria in Therapy of Obesity, Inflammatory Bowel Disease Along with Colorectal Cancer". Acta Scientific Microbiology 9.10 (2026): 01-02.

Copyright

Copyright: © 2026 Kulvinder Kochar Kaur. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.




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