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Effects of Helicobacter pylori on intracellular Ca2+ signaling in normal human gastric mucous epithelial cells
Authors:Marlink Katie L  Bacon Kathy D  Sheppard Brett C  Ashktorab Hassan  Smoot Duane T  Cover Timothy L  Deveney Clifford W  Rutten Michael J
Institution:Department of Surgery, Oregon Health Sciences University, 3181 Sam Jackson Park Road, Portland, OR 97201, USA.
Abstract:In stomach, Helicobacter pylori (Hp) adheres to gastric mucous epithelial cells (GMEC) and initiates several different signal transduction events. Alteration of intracellular Ca2+ concentration (Ca2+]i) is an important signaling mechanism in numerous bacteria-host model systems. Changes in Ca2+]i induced by Hp in normal human GMEC have not yet been described; therefore, we examined effects of Hp on Ca2+]i in normal human GMEC and a nontransformed GMEC line (HFE-145). Cultured cells were grown on glass slides, porous filters, or 96-well plates and loaded with fura 2 or fluo 4. Hp wild-type strain 60190 and vacA-, cagA-, and picB-/cagE- isogenic mutants were incubated with cells. Changes in Ca2+]i were recorded with a fluorimeter or fluorescence plate reader. Wild-type Hp produced dose-dependent biphasic transient Ca2+]i peak and plateau changes in both cell lines. Hp vacA- isogenic mutant produced changes in Ca2+]i similar to those produced by wild type. Compared with wild type, cagA- and picB-/cagE- isogenic mutants produced lower peak changes and did not generate a plateau change. Preloading cultures with intracellular Ca2+ chelator BAPTA blocked all Hp-induced Ca2+]i changes. Thapsigargin pretreatment of cultures to release Ca2+ from internal stores reduced peak change. Extracellular Ca2+ removal reduced plateau response. Hp-induced peak response was sensitive to G proteins and PLC inhibitors. Hp-induced plateau change was sensitive to G protein inhibitors, src kinases, and PLA2. These findings are the first to show that H. pylori alters Ca2+]i in normal GMEC through a Ca2+ release/influx mechanism that depends on expression of cagA and picB/cagE genes.
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