Helicobacter pylori: beneficial for most?

FOSL2 promotes leptin gene expression in human and mouse adipocytes

“…The MULAN search algorithm identified a PPARγ binding motif in the 5′ end of UpE (265-288 bp), coinciding with a PPARγ peak at that locus determined by ChIP-Seq (ref. 29 and data not shown). PPARγ could act as an adipocyte-specific "pioneer" factor that opens up the FOSL2 binding site during differentiation, thereby making it accessible.…”

“…Cells from 6-8 donors were used; all were female, with a mean age of 44 years and an average BMI of 28.9 kg/m 2 . hASCs were isolated, cultured, and differentiated as described in Supplemental Methods and elsewhere (29). For stimulation, mature human adipocytes were incubated with either dexamethasone (10 nM) or vehicle for 16 hours, and gene expression was assessed with RT-qPCR.…”

“…We sought to determine whether the UpE region showed histone modifications consistent with a role as a differentiation-dependent enhancer in human adipocytes. To that end, we utilized chromatin state maps of human adipocytes in which multiple histone modifications were mapped using ChIP-Seq at several time points during the time course of differentiation (29). For the purposes of the current study, we focused on H3K4me3 (a promoter mark), H3K4me1 and H3K27ac (enhancer marks), and H3K36me3 (a mark of transcriptional elongation) (27).…”

The Rediscovery of H. pylori Bacteria in the Gastric Mucosa by Robin Warren, and Implications of this Finding for Human Biology and Disease

“…pylori as a beneficial commensal species? An inverse relationship of H. pylori with esophageal adenocarcinoma, eosinophilic esophagitis, asthma and inflammatory bowel disease highlights the possible adverse consequences of H. pylori's rapid disappearance from the human stomach for the first time, [24,25,28] prompting numerous other investigations of the gastrointestinal microbiota randomized trials [17] that have cemented the role of H. pylori as the dominant gastric carcinogen. The designation of H. pylori as a definite carcinogen in 1994 did, however, prevent the conduct of the large-randomized clinical trials that normally would have been required to support this hypothesis, due to ethical concerns regarding untreated controls.…”

“…H. pylori's disappearance from many human populations in the developed world has coincided with the emergence of certain conditions of increasing prevalence in fully industrialized nations, including some characterized by unrestrained extragastric inflammation such as childhood-onset asthma, inflammatory bowel disease, eosinophilic esophagitis, and even esophageal adenocarcinoma [24][25][26]. Although the mechanisms underlying these inverse relationships remain obscure in humans, recent studies of animal models have demonstrated that the acquisition of H. pylori infection early in life may enhance mucosal and systemic regulatory T cell function while suppressing auto-reactivity [27,28].…”