À§¾Ï¿¡¼ Helicobacter pylori cagA À¯ÀüÀÚ¿Í ¼÷ÁÖ Interleukin-1 Beta ¹× Interleukin-1 ¼ö¿ëü ±æÇ×Á¦ À¯ÀüÀÚ ´ÙÇü¼º
Helicobacter pylori cagA Gene and Host Interleukin-1 Beta and Interleukin-1 Receptor Antagonist Gene Polymorphisms in Gastric Carcinoma
ÀÌÀç½Â, ±è±¤ÇÏ, ÇãÁ¤, ¹ÚµµÀ±, ÀüÀº¼÷, °´ëȯ, ¼Û±Ù¾Ï, Á¶¸ù, ¾ç¿õ¼®,
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ÀÌÀç½Â ( Lee Jae-Seung )
ºÎ»ê´ëÇб³ ÀÇ°ú´ëÇÐ ³»°úÇб³½Ç
±è±¤ÇÏ ( Kim Gwang-Ha )
ºÎ»ê´ëÇб³ ÀÇ°ú´ëÇÐ ³»°úÇб³½Ç
ÇãÁ¤ ( Heo Jeong )
ºÎ»ê´ëÇб³ ÀÇ°ú´ëÇÐ ³»°úÇб³½Ç
¹ÚµµÀ± ( Park Do-Youn )
ºÎ»ê´ëÇб³ ÀÇ°ú´ëÇÐ º´¸®Çб³½Ç
ÀüÀº¼÷ ( Jun Eun-Sook )
ºÎ»ê´ëÇб³ ÀÇ°ú´ëÇÐ ÀÇÇבּ¸¼Ò
°´ëȯ ( Kang Dae-Hwan )
ºÎ»ê´ëÇб³ ÀÇ°ú´ëÇÐ ³»°úÇб³½Ç
¼Û±Ù¾Ï ( Song Geun-Am )
ºÎ»ê´ëÇб³ ÀÇ°ú´ëÇÐ ³»°úÇб³½Ç
Á¶¸ù ( Cho Mong )
ºÎ»ê´ëÇб³ ÀÇ°ú´ëÇÐ ³»°úÇб³½Ç
¾ç¿õ¼® ( Yang Ung-Seok )
ºÎ»ê´ëÇб³ ÀÇ°ú´ëÇÐ ³»°úÇб³½Ç
KMID : 0614620030410060438
Abstract
¸ñÀû: H. pylori cagA À¯ÀüÀÚ¿Í ¼÷ÁÖÀÇ IL-1B ¹× IL-1RN À¯ÀüÀÚ ´ÙÇü¼ºÀº À§¾ÏÀÇ ¹ß»ý°ú ¹ÐÁ¢ÇÑ ¿¬°ü¼ºÀ» °¡Áø´Ù. º» ¿¬±¸¿¡¼´Â H. pylori ¾ç¼º À§¿° ¹× À§¾Ï ȯÀÚ¿¡¼ H. pylori cagA À¯ÀüÀÚ¿Í ¼÷ÁÖ IL-1B ¹× IL-1RN À¯ÀüÀÚ ´ÙÇü¼ºÀ» Á¶»çÇÏ¿© À§¾Ï ¹ß»ý°úÀÇ ¿¬°ü¼ºÀ» ºÐ¼®ÇÏ°íÀÚ ÇÏ¿´´Ù.
´ë»ó°ú ¹æ¹ý: H. pylori ¾ç¼º À§¿° 52¿¹¿Í À§¾Ï 82¿¹¸¦ ´ë»óÀ¸·Î ÇÏ¿© H. pylori cagA À¯ÀüÀÚÇüÀ» Á¶»çÇÏ¿´°í ¼÷ÁÖ IL-1B-511 À¯ÀüÀÚ ´ÙÇü¼ºÀº PCR-RFLP¹ýÀ¸·Î, IL-1RN À¯ÀüÀÚÀÇ ÀÎÆ®·ÐÀº 2 ´ÙÇü¼ºÀº PCR ÈÄ VNTR·Î ºÐ¼®ÇÏ¿´´Ù.
°á°ú: cagA ¾ç¼º·üÀº À§¿° 84.6%, À§¾Ï 72.0%·Î À¯ÀÇÇÑ Â÷ÀÌ´Â ¾ø¾ú´Ù(p=0.098). IL-1B-511 T/TÇü°ú T carrierÀÇ OR(95% CI)´Â °¢°¢ 1.0(0.3-3.1), 0.7(0.3-1.7), IL-1RN *2 carrierÀÇ OR(95% CI)´Â 0.6(0.2-2.0)À¸·Î À§¾Ï À§Çèµµ°¡ Áõ°¡ÇÏÁö ¾Ê¾Ò´Ù. H. pylori cagA À¯ÀüÀÚÇü°ú ¼÷ÁÖ IL-1B-511 ¹× IL-1RN À¯ÀüÀÚÇüÀ» Á¶ÇÕÇÏ¿© ºñ±³ÇØ º¸¾ÒÀ» ¶§ cagA ¾ç¼º/IL-1B-511 T carrierÀÇ OR(95% CI)´Â 0.3(0.1-1.4), cagA ¾ç¼º/IL-1RN *2 carrierÀÇ OR(95% CI)´Â 0.2(0.0-1.3)·Î À§¾Ï À§Çèµµ°¡ Áõ°¡ÇÏÁö ¾Ê¾Ò´Ù. ÀåÇü°ú ¹Ì¸¸ÇüÀ¸·Î ±¸ºÐÇÏ¿© ºñ±³ÇÒ ¶§¿¡µµ À§Çèµµ°¡ Áõ°¡ÇÏÁö ¾Ê¾Ò´Ù.
°á·Ð: H. pylori cagA À¯ÀüÀÚÇü°ú ¼÷ÁÖ IL-1B-511 ¹× IL-1RN À¯ÀüÀÚ ´ÙÇü¼ºÀº À§¾Ï À§Çèµµ Áõ°¡¿Í ¿¬°üÀÌ ¾ø¾ú´Ù. ±×·¯¹Ç·Î ±¹³» À§¾ÏÀÇ ¹ß»ý¿¡´Â ¼±¸¿Í´Â ´Þ¸® H. pylori cagA À¯ÀüÀÚ¿Í ¼÷ÁÖ IL-1B ¹× IL-1RN À¯ÀüÀÚ ´ÙÇü¼º ¿Ü¿¡ ´Ù¸¥ ³»ºÎÀû ¹× ¿ÜºÎÀû ¿äÀÎÀÌ ´õ Å« ¿ªÇÒÀ» ÇÒ °ÍÀ¸·Î »ý°¢µÇ¸ç, ÃßÈÄ ÀÌ¿¡ ´ëÇÑ ¿¬±¸°¡ ÇÊ¿äÇÒ °ÍÀ¸·Î »ý°¢µÈ´Ù.
Backgournd/Aims: Both Helicobacter pylori (H. pylori) cagA genotype and host interleukin-1 beta/interleukin-1 receptor antagonist (IL-1B/IL-1RN) gene polymorphisms play a role in determining the clinical consequences of H. pylori infection. In this study, we investigated H. pylori cagA genotype and host IL-1B/IL-1RN polymorphisms in Korean patients to clarify their involvement in the occurrence of gastric carcinoma.
Methods: The population comprised of 134 patients with H. pylori infection: 82 with gastric carcinoma and 52 with gastritis. The DNA was isolated from gastric biopsy sample and H. pylori cagA genotype was determined by PCR. The IL-1B-511 polymorphism was genotyped by PCR-RFLP and the IL-1RN polymorphism was analyzed.
Results: Infection with cagA+ H. pylori was not associated with an increased risk for gastric carcinoma. The IL-1B-511 *T carriers and IL-1RN *2 carriers did not show an increased risk for gastric carcinoma. Combining bacterial/host genotypes, cagA+/IL-1B-511 *T carriers and cagA+/IL-1RN *2 carriers showed no increased risk of gastric carcinoma. Classifying of gastric carcinoma into intestinal and diffuse type, the bacterial/host genotypes were also not associated with increased risk of each type.
Conclusions: Combined H. pylori cagA gene and host IL-1B/IL-1RN polymorphisms showed no increased risk of gastric carcinoma. Therefore, it seems other endogenous or exogenous factors might play more important roles in the development of gastric carcinoma in Korean.
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