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| Author |
¿©¸»Èñ ( Mar Ie Yeo ) , ÇÔ±â¹é ( Ki Baik Hahm ) |
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| Title |
Helicobacter pylori ¿¬±¸µ¿Çâ ¹× Àü¸Á: Helicobacter pylori¿¡ ÀÇÇÑ À§Áúȯ ¹ß»ýÀÇ ºÐÀÚ»ý¹° ±âÀü |
| Publicationinfo |
Korean J Gastroenterol 2005 Sep; 046(03): 181-188. |
| Key_word |
Helicobacter pylori, Gastric carcinogenesis, CagA, VacA, Epithelial cell signaling |
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This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License
(http://creativecommons.org/licenses/by-nc/3.0/)
which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.
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| Abstract |
Helicobacter pylori (H. pylori) causes chronic gastritis in human stomach, a minority of which progress to peptic ulcer disease, atrophic gastritis, or gastric malignancies. Clinical outcomes of H. pylori infection has been shown to depend on the variability of H. pylori virulence factors, host susceptibility, environmental factors and their interactions. This review provides an update on the molecular pathogenesis of H. pylori infection, focused on H. pylori virulence factors, H. pylori-gastric epithelium interactions, and modulation of host cell signaling. Understanding of H. pylori molecular pathogenic mechanism will facilitate the development of novel treatment strategies for eradication of the bacterium and prevention of H. pylori-induced gastropathy. (Korean J Gastroenterol 2005;46: 181-188) |
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