Document Detail


Modulating the cytokine response to treat Helicobacter gastritis.
MedLine Citation:
PMID:  15652228     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
The conventional view of gastric acid secretion is that a negative feedback mechanism arises in response to high acidity, such that somatostatin keeps G-cells and parietal cells from producing more gastrin and acid, respectively. When the stomach becomes infected, for example with Helicobacter pylori (H. pylori), the feedback mechanism is impaired. In animal models, our laboratory has demonstrated that other types of bacteria besides H. pylori can cause gastritis. For example, under conditions of low acidity, gastritis is secondary to bacterial overgrowth, not production of excessive acid, thus suggesting a new paradigm for the regulation of gastric acid secretion under inflammatory conditions. Cytokines, released during the gastric inflammatory response, including IFN gamma, TNF alpha and IL-1 beta stimulate the G-cell to produce gastrin. Gastrin in turn triggers the release of acid, and hypergastrinemia suppresses somatostatin, the inhibitor of acid. The overall response results in maximal gastric acid output that acts as the stomach's most important anti-microbial agent. The increased acid secretion by the stomach in the presence of H. pylori seems to be part of the innate immune response, in that gastrin and somatostatin are reciprocally regulated by Th1 or Th2 cytokines, respectively. In a mouse model, we showed that octreotide, a somatostatin, analog, is an efficacious treatment for Helicobacter gastritis. In humans, octreotide might accelerate recovery from H. pylori infection, reducing the duration of antibiotic therapy.
Authors:
Yana Zavros; Juanita L Merchant
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Publication Detail:
Type:  Journal Article; Research Support, U.S. Gov't, P.H.S.    
Journal Detail:
Title:  Biochemical pharmacology     Volume:  69     ISSN:  0006-2952     ISO Abbreviation:  Biochem. Pharmacol.     Publication Date:  2005 Feb 
Date Detail:
Created Date:  2005-01-17     Completed Date:  2005-03-01     Revised Date:  2007-11-14    
Medline Journal Info:
Nlm Unique ID:  0101032     Medline TA:  Biochem Pharmacol     Country:  England    
Other Details:
Languages:  eng     Pagination:  365-71     Citation Subset:  IM    
Affiliation:
Department of Internal Medicine, University of Michigan, Ann Arbor, MI 48109-0650, USA.
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MeSH Terms
Descriptor/Qualifier:
Cytokines / biosynthesis*
Feedback
Gastric Acid / secretion
Gastrins / blood
Gastritis / complications,  immunology*
Helicobacter Infections / complications,  drug therapy,  immunology*
Humans
Stomach Neoplasms / etiology
Grant Support
ID/Acronym/Agency:
DK-34933/DK/NIDDK NIH HHS; P01 DK62041/DK/NIDDK NIH HHS
Chemical
Reg. No./Substance:
0/Cytokines; 0/Gastrins

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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