Proteomics Analysis Revealed that Crosstalk betweenHelicobacter pyloriandStreptococcus mitisMay Enhance Bacterial Survival and Reduces Carcinogenesis.
Helicobacter pyloriis the dominant species of the human gastric microbiota and is present in the stomach of more than half of the human population worldwide. Colonization byH. pyloricauses persistent inflammatory response andH. pylori-induced gastritis is the strongest singular risk factor for the development of gastric adenocarcinoma. However, only a small proportion of infected individuals develop malignancy. BesidesH. pylori, other microbial species have also been shown to be related to gastritis. We previously reported that interspecies microbial interaction betweenH. pyloriandS. mitisresulted in alteration of their metabolite profiles. In this study, we followed up by analyzing the changing protein profiles ofH. pyloriandS. mitisby LC/Q-TOF mass spectrometry to understand the different response of the two bacterial species in a multi-species micro-environment. Differentially-expressed proteins in mono- and co-cultures could be mapped into 18 biological pathways. The number of proteins involve in RNA degradation, nucleotide excision repair, mismatch repair, and lipopolysaccharide (LPS) biosynthesis were increased in co-culturedH. pylori. On the other hand, fewer proteins involve in citrate cycle, glycolysis/ gluconeogenesis, aminoacyl-tRNA biosynthesis, translation, metabolism, and cell signaling were detected in co-culturedH. pylori. This is consistent with our previous observation that in the presence ofS. mitis, H. pyloriwas transformed to coccoid. Interestingly, phosphoglycerate kinase (PGK), a major enzyme used in glycolysis, was found in abundance in co-culturedS. mitisand this may have enhanced the survival ofS. mitisin the multi-species microenvironment. On the other hand, thioredoxin (TrxA) and other redox-regulating enzymes ofH. pyloriwere less abundant in co-culture possibly suggesting reduced oxidative stress. Oxidative stress plays an important role in tissue damage and carcinogenesis. Using thein vitroco-culture model, this study emphasized the possibility that pathogen-microbiota interaction may have a protective effect againstH. pylori-associated carcinogenesis.
Department of Medical Microbiology, Faculty of Medicine, University of Malaya Kuala Lumpur, Malaysia.
Yalda
Y
Khosravi
Department of Medical Microbiology, Faculty of Medicine, University of Malaya Kuala Lumpur, Malaysia.
Mun Fai
MF
Loke
Department of Medicine, Faculty of Medicine, University of Malaya Kuala Lumpur, Malaysia.
Khean Lee
KL
Goh
Department of Medical Microbiology, Faculty of Medicine, University of Malaya Kuala Lumpur, Malaysia.
Jamuna
J
Vadivelu
Helicobacter pylori; LC/Q-TOF mass spectrometry; Streptococcus mitis; phosphoglycerate kinase (PGK); thioredoxin (TrxA)
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