PMID- 11051346
OWN - NLM
STAT- MEDLINE
DCOM- 20001108
LR  - 20041117
IS  - 0002-9270 (Print)
IS  - 0002-9270 (Linking)
VI  - 95
IP  - 10
DP  - 2000 Oct
TI  - Implication of NF-kappaB in Helicobacter pylori-associated gastritis.
PG  - 2768-76
AB  - 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.
FAU - Isomoto, H
AU  - Isomoto H
AD  - The Second Department of Internal Medicine, Nagasaki University School of 
      Medicine, Japan.
FAU - Mizuta, Y
AU  - Mizuta Y
FAU - Miyazaki, M
AU  - Miyazaki M
FAU - Takeshima, F
AU  - Takeshima F
FAU - Omagari, K
AU  - Omagari K
FAU - Murase, K
AU  - Murase K
FAU - Nishiyama, T
AU  - Nishiyama T
FAU - Inoue, K
AU  - Inoue K
FAU - Murata, I
AU  - Murata I
FAU - Kohno, S
AU  - Kohno S
LA  - eng
PT  - Journal Article
PL  - United States
TA  - Am J Gastroenterol
JT  - The American journal of gastroenterology
JID - 0421030
RN  - 0 (Chemokines)
RN  - 0 (Cytokines)
RN  - 0 (NF-kappa B)
SB  - IM
MH  - Adult
MH  - Aged
MH  - Animals
MH  - Chemokines/*blood
MH  - Cytokines/*blood
MH  - Female
MH  - Gastric Mucosa/immunology/pathology
MH  - Gastritis/*immunology/pathology
MH  - Helicobacter Infections/*immunology/pathology
MH  - Helicobacter pylori/*immunology
MH  - Humans
MH  - Immunity, Cellular/immunology
MH  - Immunoenzyme Techniques
MH  - Male
MH  - Mice
MH  - Middle Aged
MH  - NF-kappa B/*physiology
EDAT- 2000/10/29 11:00
MHDA- 2001/02/28 10:01
CRDT- 2000/10/29 11:00
PHST- 2000/10/29 11:00 [pubmed]
PHST- 2001/02/28 10:01 [medline]
PHST- 2000/10/29 11:00 [entrez]
AID - S0002927000010960 [pii]
AID - 10.1111/j.1572-0241.2000.02304.x [doi]
PST - ppublish
SO  - Am J Gastroenterol. 2000 Oct;95(10):2768-76. doi: 
      10.1111/j.1572-0241.2000.02304.x.