Helicobacter pylori infection can affect energy modulating hormones and body weight in germ free mice.
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.
Department of Medical Microbiology, Faculty of Medicine, University of Malaya, Kuala Lumpur, Malaysia.
Yalda
Y
Khosravi
National Cancer Centre, Singapore, Singapore.
Shih Wee
SW
Seow
National Cancer Centre, Singapore, Singapore.
Arlaine Anne
AA
Amoyo
School of Chemical and Life Sciences, Singapore Polytechnic, Singapore.
Kher Hsin
KH
Chiow
School of Chemical and Life Sciences, Singapore Polytechnic, Singapore.
Tuan Lin
TL
Tan
School of Chemical and Life Sciences, Singapore Polytechnic, Singapore.
Whye Yen
WY
Wong
School of Chemical and Life Sciences, Singapore Polytechnic, Singapore.
Qian Hui
QH
Poh
School of Chemical and Life Sciences, Singapore Polytechnic, Singapore.
Ignatius Mario Doli
IM
Sentosa
Duke-NUS Graduate Medical School, Singapore.
Ralph M
RM
Bunte
1] Department of Microbiology, Tumor and Cell Biology (MTC), Karolinska Institutet, Stockholm, Sweden [2] LKC School of Medicine, Nanyang Technological University, Singapore, Singapore [3] SCELSE Microbiome Centre, Nanyang Technological University, Singapore, Singapore.
Sven
S
Pettersson
Department of Medical Microbiology, Faculty of Medicine, University of Malaya, Kuala Lumpur, Malaysia.
Mun Fai
MF
Loke
Department of Medical Microbiology, Faculty of Medicine, University of Malaya, Kuala Lumpur, Malaysia.
Jamuna
J
Vadivelu
D000818:Animals; D015992:Body Mass Index; D054413:Chemokine CCL11 / Q000378:metabolism; D004734:Energy Metabolism; D054439:Ghrelin / Q000378:metabolism; D016481:Helicobacter Infections / Q000378:metabolism* / Q000382:microbiology; D016480:Helicobacter pylori / Q000502:physiology; D054884:Host-Pathogen Interactions; D006801:Humans; D007328:Insulin / Q000378:metabolism; D007420:Intestine, Large / Q000378:metabolism* / Q000382:microbiology; D020738:Leptin / Q000378:metabolism; D008810:Mice, Inbred C57BL; D064307:Microbiota / Q000502:physiology; D008954:Models, Biological; D036361:Peptide Hormones / Q000378:metabolism*; D019894:Peptide YY / Q000378:metabolism; D013047:Specific Pathogen-Free Organisms; D015430:Weight Gain / Q000502:physiology
D054413:Chemokine CCL11; D054439:Ghrelin; D007328:Insulin; D020738:Leptin; D036361:Peptide Hormones; D019894:Peptide YY