Helicobacter pylori induces an array of pro-inflammatory cytokines in human gastric epithelial cells: quantification of mRNA for interleukin-8, -1 alpha/beta, granulocyte-macrophage colony-stimulating factor, monocyte chemoattractant protein-1 and tumour necrosis factor-alpha.
Despite the fact that Helicobacter pylori is known to be non-invasive, mucosal infiltration of inflammatory cells have been observed in the gastric mucosa. The exact pathogenesis of such an inflammatory reaction has not been well defined. We explored the repertoire of cytokine genes expressed in human gastric epithelial cells in response to coculture with H. pylori. After gastric epithelial cells, SNU-5 and KATO III, were infected with H. pylori, expression of several cytokine genes was assessed using quantitative reverse transcription polymerase chain reaction. Interleukin (IL)-8, -1 alpha and -1 beta mRNA were expressed in both gastric epithelial cells throughout the entire infection period. In SNU-5, IL-1 alpha and IL-8 mRNA were expressed at 1 h, reached a peak level at 4 h and then decreased. Interleukin-1 beta mRNA was expressed less frequently than IL-1 alpha, or IL-8 mRNA. In SNU-5 cells, granulocyte-macrophage colony-stimulating factor (GM-CSF), monocyte chemoattractant protein-1 (MCP-1), and tumour necrosis factor-alpha (TNF-alpha) mRNA were expressed at 9 h, but was not expressed in KATO III. Gene expression paralleled the amount of IL-8 protein measured by enzyme-linked immunoabsorbent assay (ELISA). Interleukin-8 mRNA expression was not observed in KATO III cells infected with Campylobacter fetus ssp. fetus, Campylobacter jejuni or Escherichia coli. IL-8 mRNA expression was increased not only in gastric epithelial cells but also in non-gastric cells infected with H. pylori. These results suggest that an inflammatory reaction induced by H. pylori may be initially triggered by an array of pro-inflammatory cytokines expressed by infected gastric epithelial cells.
Jung
H C
HC
Department of Internal Medicine, Seoul National University College of Medicine, Korea.
Kim
J M
JM
Song
I S
IS
Kim
C Y
CY
D002169:Campylobacter Infections / Q000378:metabolism; D002478:Cells, Cultured; D018932:Chemokine CCL2 / Q000032:analysis / Q000235:genetics; D018920:Coculture Techniques; D016207:Cytokines / Q000032:analysis* / Q000235:genetics; D004848:Epithelium / Q000737:chemistry; D004927:Escherichia coli Infections / Q000378:metabolism; D016178:Granulocyte-Macrophage Colony-Stimulating Factor / Q000032:analysis / Q000235:genetics; D016481:Helicobacter Infections / Q000378:metabolism*; D016480:Helicobacter pylori; D006801:Humans; D007375:Interleukin-1 / Q000032:analysis / Q000235:genetics; D016209:Interleukin-8 / Q000032:analysis / Q000235:genetics; D016133:Polymerase Chain Reaction; D012333:RNA, Messenger / Q000032:analysis; D013270:Stomach / Q000737:chemistry*; D013997:Time Factors; D014409:Tumor Necrosis Factor-alpha / Q000235:genetics
D018932:Chemokine CCL2; D016207:Cytokines; D007375:Interleukin-1; D016209:Interleukin-8; D012333:RNA, Messenger; D014409:Tumor Necrosis Factor-alpha; D016178:Granulocyte-Macrophage Colony-Stimulating Factor