Induction of human β-defensin-2 mRNA expression by Helicobacter pylori in human gastric cell line MKN45 cells on cag Pathogenicity Island

被引:58
作者
Wada, A
Mori, N
Oishi, K
Hojo, H
Nakahara, Y
Hamanaka, Y
Nagashima, M
Sekine, I
Ogushi, K
Niidome, T
Nagatake, T
Moss, J
Hirayama, T [1 ]
机构
[1] Nagasaki Univ, Inst Trop Med, Dept Bacteriol, Nagasaki 8528523, Japan
[2] Nagasaki Univ, Inst Trop Med, Dept Internal Med, Nagasaki 8528523, Japan
[3] Tokai Univ, Dept Ind Chem, Hiratsuka, Kanagawa 2591292, Japan
[4] Nagasaki Univ, Sch Med, Dept Mol Pathol, Atom Bomb Dis Inst, Nagasaki 8528523, Japan
[5] Nagasaki Univ, Sch Med, Fac Engn, Dept Appl Chem, Nagasaki 8528523, Japan
[6] NHLBI, Pulm Crit Care Med Branch, NIH, Bethesda, MD 20892 USA
关键词
D O I
10.1006/bbrc.1999.1452
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Helicobacter pylori is an etiological agent of gastritis, peptic ulcer, and gastric cancer. Human beta-defensin-2 (hBD-2) is an antimicrobial peptide which belongs to one of the most important host defense systems against bacterial infection in several epithelial tissues. We studied the effect of H. pylori on the expression of hBD-2 mRNA in MKN45 gastric mucosal cells. H. pylori, but not culture filtrate, increased the hBD-2 mRNA level in MKN45 cells; the inductive effect of H. pylori was not detected with Intestine 407 cells. Among H. pylori strains, strain OHPC0002, which lacks a cag Pathogenicity Island (PAI), did not induce hBD-2 mRNA in MKN45 cells. These results suggested that H; pylori cag PAI is critical for the induction of hBD-2 mRNA in MKN45 cells. Exposure of MKN45 cells to Salmonella typhimurium, S. enteritidis, S. typhi, and S. dublin, but not Escherichia coli ML35, also resulted in induction of hBD-2 mRNA. (C) 1999 Academic Press.
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页码:770 / 774
页数:5
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