| Helicobacter pylori Dampens Gut Epithelial Self-Renewal by Inhibiting Apoptosis, a Bacterial Strategy to Enhance Colonization of the Stomach Cell Host & Microbe, Volume 2, Issue 4, 11 October 2007, Pages 250-263 Hitomi Mimuro, Toshihiko Suzuki, Shigenori Nagai, Gabriele Rieder, Masato Suzuki, Takeshi Nagai, Yukihiro Fujita, Kanna Nagamatsu, Nozomi Ishijima, Shigeo Koyasu, Rainer Haas and Chihiro Sasakawa Summary Colonization of the gastric pits in the stomach by (Hp) is a major risk factor for gastritis, gastric ulcers, and cancer. Normally, rapid self-renewal of gut epithelia, which occurs by a balance of progenitor proliferation and pit cell apoptosis, serves as a host defense mechanism to limit bacterial colonization. To investigate how Hp overcomes this host defense, we use the Mongolian gerbil model of Hp infection. Apoptotic loss of pit cells induced by a proapoptotic agent is suppressed by Hp. The ability of Hp to suppress apoptosis contributed to pit hyperplasia and persistent bacterial colonization of the stomach. Infection with WT Hp but not with a mutant in the virulence effector increased levels of the prosurvival factor phospho-ERK and antiapoptotic protein MCL1 in the gastric pits. Thus, CagA activates host cell survival and antiapoptotic pathways to overcome self-renewal of the gastric epithelium and help sustain Hp infection. Summary | Full Text | PDF (952 kb) |
| Gastric autoimmunity: the role of Helicobacter pylori and molecular mimicry Trends in Molecular Medicine, Volume 10, Issue 7, 1 July 2004, Pages 316-323 Mario M. D'Elios, Ben J. Appelmelk, Amedeo Amedei, Mathijs P. Bergman and Gianfranco Del Prete Abstract Pathogens can induce autoreactive T cells to initiate autoimmune disease by several mechanisms. Pathogen-induced inflammation results in the enhanced presentation of self antigens, which causes the expansion of the activated autoreactive T cells that are required for disease onset. Alternatively, a pathogen might express antigens with epitopes that are structurally similar to epitopes of autoantigens, resulting in a mechanism of molecular mimicry. This is the case for -associated human autoimmune gastritis, in which the activated CD4 Th1 cells that infiltrate the gastric mucosa cross-recognize the epitopes of self gastric parietal cell HK-ATPase and of various proteins. Therefore, in genetically susceptible individuals, infection can start or worsen gastric autoimmunity, leading to atrophic gastritis. Abstract | Full Text | PDF (548 kb) |
| A possible molecular basis for the effect of gastric anti-ulcerogenic drugs Trends in Pharmacological Sciences, Volume 19, Issue 10, 1 October 1998, Pages 401-403 G.A Balint Full Text | PDF (132 kb) |
Copyright © 1970 The Biophysical Society. All rights reserved.
Biophysical Journal, Volume 10, Issue 3, 215-236, 1 March 1970
doi:10.1016/S0006-3495(70)86295-6
Articles
George W. Kidder and W.S. Rehm
Upon passing a step current through the frog gastric mucosa, a transient response in voltage is observed, which can formally be represented by several types of model systems, although some models require elements which are hard to visualize in terms of the known morphology of the mucosa. A physically reasonable model can be constructed by considering the changes in intracellular ionic composition which arise due to current flow, and the consequent changes in diffusion potentials across the two cell membranes. A simple model has been developed which fits the observed long time-constant portion of the transient at low current densities, and predicts departures from exponential behavior at larger currents. Since reasonable values for membrane resistance and cell volume give a fit, it is proposed that this model may account for the long time-constant portion of the transient response. There is no reason to expect that similar considerations do not hold for epithelial tissues in general.