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Gastritis II: Pathophysiology

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The pathophysiology of gastritis begins with the colonization of the stomach lining by Helicobacter pylori (H. pylori). This bacterium spreads mainly via the oral-oral route through saliva or shared utensils, and can also be transmitted in overcrowded or unhygienic environments through contaminated water, despite its brief survival outside the body.ColonizationOnce ingested, H. pylori enters the stomach and begins colonization by navigating through the mucus layer lining the stomach wall. It...

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Related Experiment Video

Updated: Jul 13, 2026

Mucin Agarose Gel Electrophoresis: Western Blotting for High-molecular-weight Glycoproteins

Mucin Agarose Gel Electrophoresis: Western Blotting for High-molecular-weight Glycoproteins

Published on: June 14, 2016

Histamine induces MUC5AC expression via a hCLCA1 pathway.

Yong Min Kim¹, Tae-Bin Won, Si Whan Kim

¹Department of Otorhinolaryngology-Head and Neck Surgery, Chungnam National University College of Medicine, Daejeon, Korea.

|July 12, 2007

Summary

Histamine increases MUC5AC production via human chloride channel 1 (hCLCA1) upregulation in airway cells. Antihistamines and hCLCA1 blockers may reduce this response in allergic diseases.

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Establishment of a Mouse Model with Cough Hypersensitivity via Inhalation of Citric Acid

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Last Updated: Jul 13, 2026

Mucin Agarose Gel Electrophoresis: Western Blotting for High-molecular-weight Glycoproteins

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Published on: June 14, 2016

Establishment of a Mouse Model with Cough Hypersensitivity via Inhalation of Citric Acid

Establishment of a Mouse Model with Cough Hypersensitivity via Inhalation of Citric Acid

Published on: January 10, 2025

Area of Science:

Immunology
Cell Biology
Respiratory Medicine

Background:

Histamine is a key mediator in allergic responses.
Histamine's role in mucin gene expression and production remains unclear.

Purpose of the Study:

To determine if histamine stimulates MUC5AC production in NCI-H292 cells.
To identify the specific pathway involved in histamine-induced mucin production.

Main Methods:

Quantitative analysis of MUC5AC production using RT-PCR, immunoassay, and immunocytochemistry.
Assessment of histamine's effects on MUC5AC and hCLCA1 expression over time and concentration.
Evaluation of antihistamine and hCLCA1 blocker (niflumic acid) effects on MUC5AC production.

Main Results:

Histamine significantly increased MUC5AC gene expression and protein production in a dose- and time-dependent manner.
Histamine elevated hCLCA1 mRNA levels, correlating with concentration.
Antihistamine (chlorpheniramine) and hCLCA1 blocker (NFA) pretreatment reduced histamine-induced MUC5AC expression and production.

Conclusions:

Histamine-induced MUC5AC production is mediated by the upregulation of hCLCA1.
Antihistamines and hCLCA1 channel blockers show potential for partially inhibiting histamine-driven MUC5AC production in allergic conditions like allergic rhinitis.