Abstract
Helicobacter pylori, is an invariably commensal resident of the gut microbiome associated with gastric ulcer in adults. In addition, these patients also suffered from a low grade inflammation that activates the immune system and thus increased shunting of energy to host defense mechanisms. To assess whether a H. pylori infection could affect growth in early life, we determined the expression levels of selected metabolic gut hormones in germ free (GF) and specific pathogen-free (SPF) mice with and without the presence of H. pylori. Despite H. pylori-infected (SPFH) mice display alteration in host metabolism (elevated levels of leptin, insulin and peptide YY) compared to non-infected SPF mice, their growth curves remained the same. SPFH mice also displayed increased level of eotaxin-1. Interestingly, GF mice infected with H. pylori (GFH) also displayed increased levels of ghrelin and PYY. However, in contrast to SPFH mice, GFH showed reduced weight gain and malnutrition. These preliminary findings show that exposure to H. pylori alters host metabolism early in life; but the commensal microbiota in SPF mice can attenuate the growth retarding effect from H. pylori observed in GF mice. Further investigations of possible additional side effects of H. pylori are highly warranted.
Highlights
Helicobacter pylori, is an invariably commensal resident of the gut microbiome associated with gastric ulcer in adults
In contrast to SPFH mice, GFH showed reduced weight gain and malnutrition. These preliminary findings show that exposure to H. pylori alters host metabolism early in life; but the commensal microbiota in specific pathogen-free (SPF) mice can attenuate the growth retarding effect from H. pylori observed in germ free (GF) mice
None of the SPF and GF mice was positive for H. pylori
Summary
Helicobacter pylori, is an invariably commensal resident of the gut microbiome associated with gastric ulcer in adults. To assess whether a H. pylori infection could affect growth in early life, we determined the expression levels of selected metabolic gut hormones in germ free (GF) and specific pathogen-free (SPF) mice with and without the presence of H. pylori. In contrast to SPFH mice, GFH showed reduced weight gain and malnutrition These preliminary findings show that exposure to H. pylori alters host metabolism early in life; but the commensal microbiota in SPF mice can attenuate the growth retarding effect from H. pylori observed in GF mice. In the same study, the authors demonstrated that GF mice inoculated with normal gut microbiota early in life displayed similar characteristics as SPF mice. The ancient gastric pathogen, Helicobacter pylori, is a key member of the human gastric microbiome It coevolved with the human race and our association with H. pylori could be traced as early back as 60,000 years ago[9]. Many factors, including H. pylori, gut microbiota, the host and the environment, may contribute to the development of H. pylori-associated diseases
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