CXC chemokines Gro(alpha)/IL-8 and IP-10/MIG in Helicobacter pylori gastritis

Clin Exp Immunol. 2000 Nov;122(2):192-9. doi: 10.1046/j.1365-2249.2000.01374.x.


Infection with Helicobacter pylori causes chronic active gastritis, which is characterized by neutrophils infiltrating the gastric epithelial layer and the underlying lamina propria as well as by T, B lymphocytes and macrophages accumulating in the lamina propria. In this study, the chemokine profile responsible for the recruitment of these inflammatory cells is investigated. Using both RNA/RNA in situ hybridization and immunohistochemistry, the expression of the neutrophil and/or lymphocyte-attractant CXC chemokines growth-related oncogene alpha (Gro(alpha)), IL-8, interferon-gamma (IFN-gamma)-inducible protein-10 (IP-10), monokine induced by IFN-gamma (MIG) and the CC chemokines macrophage inflammatory protein-1alpha (MIP-1alpha), -1beta, regulated on activation normal T cell expressed and secreted (RANTES) and monocyte chemoattractant protein-1 (MCP-1) is studied and microanatomically localized in the gastric mucosa. Macrophages in the lamina propria at sites with neutrophil infiltration and gastric epithelium infiltrated by neutrophils highly expressed the neutrophil-attractant chemokines Gro(alpha) and IL-8. Additionally, Gro(alpha) and IL-8 were expressed by neutrophils themselves localized within gastric epithelium, in the foveolar lumen and in the cellular debris overlying mucosal erosion. IP-10 and to a lower extent MIG, both selectively chemotactic for inflammatory T cells, were expressed by endothelial cells of gastric mucosal vessels and by mononuclear cells at sites with T cell infiltration. Expression of all other CC chemokines tested was significantly lower. These in vivo data indicate that a set of predominantly CXC chemokines modulates the inflammation in H. pylori gastritis. Gro(alpha) and IL-8 may play an important role in neutrophil trafficking from the mucosal vessel into the gastric epithelium, whereas IP-10 and MIG contribute to the recruitment of inflammatory T cells into the mucosa.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Chemokine CCL2 / genetics
  • Chemokine CCL2 / metabolism
  • Chemokine CCL3
  • Chemokine CCL4
  • Chemokine CCL5 / genetics
  • Chemokine CCL5 / metabolism
  • Chemokine CXCL1
  • Chemokine CXCL10
  • Chemokine CXCL9
  • Chemokines, CXC / genetics*
  • Chemokines, CXC / metabolism*
  • Chemotactic Factors / genetics
  • Chemotactic Factors / metabolism
  • Gastric Mucosa / immunology
  • Gastric Mucosa / pathology
  • Gastritis / genetics
  • Gastritis / immunology*
  • Gastritis / pathology
  • Gene Expression
  • Growth Substances / genetics
  • Growth Substances / metabolism
  • Helicobacter Infections / genetics
  • Helicobacter Infections / immunology*
  • Helicobacter Infections / pathology
  • Helicobacter pylori*
  • Humans
  • In Situ Hybridization
  • Intercellular Signaling Peptides and Proteins*
  • Interleukin-8 / genetics
  • Interleukin-8 / metabolism
  • Macrophage Inflammatory Proteins / genetics
  • Macrophage Inflammatory Proteins / metabolism
  • Neutrophils / immunology
  • RNA, Messenger / genetics
  • RNA, Messenger / metabolism
  • T-Lymphocytes / immunology


  • CXCL1 protein, human
  • CXCL9 protein, human
  • Chemokine CCL2
  • Chemokine CCL3
  • Chemokine CCL4
  • Chemokine CCL5
  • Chemokine CXCL1
  • Chemokine CXCL10
  • Chemokine CXCL9
  • Chemokines, CXC
  • Chemotactic Factors
  • Growth Substances
  • Intercellular Signaling Peptides and Proteins
  • Interleukin-8
  • Macrophage Inflammatory Proteins
  • RNA, Messenger