Association of Helicobacter pylori and iNOS production by macrophages and lymphocytes in the gastric mucosa in chronic gastritis

J Immunol Res. 2014:2014:762514. doi: 10.1155/2014/762514. Epub 2014 Sep 18.

Abstract

Helicobacter pylori is one of the most common causes of chronic gastritis. With the development of the disease cellular inflammatory infiltrates composed of lymphocytes, plasma cells, and macrophages are formed in epithelium and lamina propria of the stomach. These cells are capable of secreting a number of active substances, including inducible nitric oxide synthase (iNOS). We examined the relationship between H. pylori and secretion of iNOS by cells of inflammatory infiltrates in chronic gastritis by light microscopy and immunohistochemistry. The data obtained indicate that stimulation of H. pylori immune system cells of the host organism during development of chronic gastritis causes increase in number of macrophages and lymphocytes in the inflammatory infiltrate of the gastric mucosa. This is accompanied with increased expression of inducible NO-synthase with excess free radicals in the tissues, which leads to secondary alterations and exacerbates the inflammation with impaired regeneration processes.

MeSH terms

  • Cell Count
  • Chronic Disease
  • Gastric Mucosa / enzymology
  • Gastric Mucosa / immunology*
  • Gastric Mucosa / microbiology
  • Gastritis / enzymology
  • Gastritis / immunology*
  • Gastritis / microbiology
  • Helicobacter Infections / enzymology
  • Helicobacter Infections / immunology*
  • Helicobacter Infections / microbiology
  • Helicobacter pylori / immunology*
  • Helicobacter pylori / physiology
  • Host-Pathogen Interactions / immunology
  • Humans
  • Immunohistochemistry
  • Lymphocytes / enzymology
  • Lymphocytes / immunology*
  • Lymphocytes / microbiology
  • Macrophages / enzymology
  • Macrophages / immunology*
  • Macrophages / microbiology
  • Middle Aged
  • Nitric Oxide Synthase Type II / immunology*
  • Nitric Oxide Synthase Type II / metabolism

Substances

  • Nitric Oxide Synthase Type II