Tags

Type your tag names separated by a space and hit enter

Low pH and Helicobacter pylori increase nuclear factor kappa B binding in gastric epithelial cells: a common pathway for epithelial cell injury?
J Cell Biochem. 2005 Oct 15; 96(3):589-98.JC

Abstract

Helicobacter pylori infection results in peptic ulceration and chronic gastritis through mechanisms which are not fully elucidated. Live H. pylori activate the pro-inflammatory transcription factor NF-kappaB in gastric epithelial cells. Patients may have peptic ulcer disease in the absence of H. pylori infection; therefore other factors contribute to the inflammatory process. Maximal acid output in patients with H. pylori infection and duodenal ulceration is significantly increased indicating a role for acid in the pathogenesis of mucosal ulceration. The effect of low pH on NF-kappaB activation in gastric epithelial cells has not been studied. Human gastric epithelial cells (AGS) were exposed to a range of pH changes in the presence or absence of H. pylori. NF-kappaB DNA-binding and cytosolic IkappaB-alpha were measured using electrophoretic mobility shift assay and Western blotting. NF-kappaB DNA-binding in gastric epithelial cells dramatically increased when the pH of the culture medium decreased. Increases in NF-kappaB nuclear binding were paralleled by decreasing amounts of cytosolic IkappaB-alpha. These findings were similar but less potent than those observed when cells were exposed to H. pylori. Low pH resulted in enhancement of H. pylori-induced NF-kappaB nuclear binding. DNA binding of NF-kappaB activation secondary to low pH was attenuated by PD98059 but not by SB203580. Similar to H. pylori, low pH potently and independently augments NF-kappaB nuclear binding in AGS cells and such activation appears to be mediated through MEK1-dependant signaling pathways.

Authors+Show Affiliations

Department of Clinical Medicine, Trinity Centre for Health Sciences, St. James's Hospital, Dublin 8, Ireland.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

16088959

Citation

O'Toole, Dermot, et al. "Low pH and Helicobacter Pylori Increase Nuclear Factor Kappa B Binding in Gastric Epithelial Cells: a Common Pathway for Epithelial Cell Injury?" Journal of Cellular Biochemistry, vol. 96, no. 3, 2005, pp. 589-98.
O'Toole D, Abdel-Latif MM, Long A, et al. Low pH and Helicobacter pylori increase nuclear factor kappa B binding in gastric epithelial cells: a common pathway for epithelial cell injury? J Cell Biochem. 2005;96(3):589-98.
O'Toole, D., Abdel-Latif, M. M., Long, A., Windle, H. J., Murphy, A. M., Bowie, A., O'Neill, L. A., Weir, D. G., & Kelleher, D. (2005). Low pH and Helicobacter pylori increase nuclear factor kappa B binding in gastric epithelial cells: a common pathway for epithelial cell injury? Journal of Cellular Biochemistry, 96(3), 589-98.
O'Toole D, et al. Low pH and Helicobacter Pylori Increase Nuclear Factor Kappa B Binding in Gastric Epithelial Cells: a Common Pathway for Epithelial Cell Injury. J Cell Biochem. 2005 Oct 15;96(3):589-98. PubMed PMID: 16088959.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Low pH and Helicobacter pylori increase nuclear factor kappa B binding in gastric epithelial cells: a common pathway for epithelial cell injury? AU - O'Toole,Dermot, AU - Abdel-Latif,Mohamed M M, AU - Long,Aideen, AU - Windle,Henry J, AU - Murphy,Anne M, AU - Bowie,Andrew, AU - O'Neill,Luke A J, AU - Weir,Donald G, AU - Kelleher,Dermot, PY - 2005/8/10/pubmed PY - 2005/12/13/medline PY - 2005/8/10/entrez SP - 589 EP - 98 JF - Journal of cellular biochemistry JO - J Cell Biochem VL - 96 IS - 3 N2 - Helicobacter pylori infection results in peptic ulceration and chronic gastritis through mechanisms which are not fully elucidated. Live H. pylori activate the pro-inflammatory transcription factor NF-kappaB in gastric epithelial cells. Patients may have peptic ulcer disease in the absence of H. pylori infection; therefore other factors contribute to the inflammatory process. Maximal acid output in patients with H. pylori infection and duodenal ulceration is significantly increased indicating a role for acid in the pathogenesis of mucosal ulceration. The effect of low pH on NF-kappaB activation in gastric epithelial cells has not been studied. Human gastric epithelial cells (AGS) were exposed to a range of pH changes in the presence or absence of H. pylori. NF-kappaB DNA-binding and cytosolic IkappaB-alpha were measured using electrophoretic mobility shift assay and Western blotting. NF-kappaB DNA-binding in gastric epithelial cells dramatically increased when the pH of the culture medium decreased. Increases in NF-kappaB nuclear binding were paralleled by decreasing amounts of cytosolic IkappaB-alpha. These findings were similar but less potent than those observed when cells were exposed to H. pylori. Low pH resulted in enhancement of H. pylori-induced NF-kappaB nuclear binding. DNA binding of NF-kappaB activation secondary to low pH was attenuated by PD98059 but not by SB203580. Similar to H. pylori, low pH potently and independently augments NF-kappaB nuclear binding in AGS cells and such activation appears to be mediated through MEK1-dependant signaling pathways. SN - 0730-2312 UR - https://www.unboundmedicine.com/medline/citation/16088959/Low_pH_and_Helicobacter_pylori_increase_nuclear_factor_kappa_B_binding_in_gastric_epithelial_cells:_a_common_pathway_for_epithelial_cell_injury L2 - https://doi.org/10.1002/jcb.20539 DB - PRIME DP - Unbound Medicine ER -