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. 2000 Oct;95(10):2768-76.
doi: 10.1111/j.1572-0241.2000.02304.x.

Implication of NF-kappaB in Helicobacter pylori-associated gastritis

H Isomoto  1 , Y Mizuta, M Miyazaki, F Takeshima, K Omagari, K Murase, T Nishiyama, K Inoue, I Murata, S Kohno
Affiliations

Implication of NF-kappaB in Helicobacter pylori-associated gastritis

H Isomoto et al. Am J Gastroenterol. 2000 Oct.

Abstract

Objective: Transcription factor NF-kappaB plays a pivotal role in inflammatory responses by up-regulating mRNA expression of bioactive molecules such as chemokines and adhesion molecules. The present study was designed to elucidate the implication of NF-kappaB in Helicobacter pylori-associated gastritis (HAG).

Methods: We examined 41 patients with HAG and 18 H. pylori-negative control subjects. Expression of activated NF-kappaB was studied in situ by immunohistochemistry using alpha-p65 mouse monoclonal antibody (alpha-p65 mAb), which recognizes activated NF-kappaB. To identify the cell types in which NF-kappaB was activated, we performed immunohistochemical analysis using antibodies against vascular endothelial cells, macrophages, and B and T lymphocytes. We also examined the colocalization of activated NF-kappaB with the of intercellular expression adhesion molecule-1 (ICAM-1) on endothelial cells. We measured the levels of NF-kappaB-dependent chemokines including interleukin-8 (IL-8) and monocyte chemoattractant protein-1 (MCP-1), regulated on activation normal T-cell expressed and secreted (RANTES) and macrophage inflammatory protein-1alpha (MIP-1alpha) in antral mucosa by ELISA (ELISA).

Results: Activated NF-kappaB was detected in the nuclei of epithelial cells in antral mucosa, especially of patients with HAG. NF-kappaB positivity index (NF-kappaB PI), representing the percentages of epithelial cells with positive nuclear staining for activated NF-kappaB, was significantly higher in patients with HAG than in H. pylori-negative controls. NF-kappaB PI correlated significantly with histological scores of gastritis. Moreover, activated NF-kappaB was identified in the nuclei of vascular endothelial cells, macrophages, and B lymphocytes within the lamina propria in HAG. Colocalization of activated NF-kappaB with ICAM-1 expression in the same endothelial cells was demonstrated. The IL-8 levels significantly correlated with the NF-kappaB PI.

Conclusions: In addition to epithelial cells, macrophages, vascular endothelial cells, and B lymphocytes contained activated NF-kappaB. In these cells, activated NF-kappaB may be involved in the inflammation process in HAG through the up-regulation of chemokines or adhesion molecules.

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