Innate immune receptor genetic polymorphisms in pouchitis: is CARD15 a susceptibility factor?
Innate immune receptor genetic polymorphisms in pouchitis: is CARD15 a susceptibility factor?
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储袋炎先天免疫受体基因多态性：CARD15是易感因素吗？
DOI：
10.1097/01.mib.0000186407.25694.cf
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发表时间：
2005
影响因子：
4.9
通讯作者：
Plevy,ScottE
中科院分区：
文献类型：
--
作者：
Meier,CarmenB;Hegazi,RefaatA;Aisenberg,James;Legnani,PeterE;Nilubol,Naris;Cobrin,GenaM;Duerr,RichardH;Gorfine,StephenR;Bauer,JoelJ;Sachar,DavidB;Plevy,ScottE
结肠袋炎是溃疡性结肠炎（UC）回肠袋-肛门吻合术（IPAA）后常见的并发症。本研究的目的是确定先天免疫受体样受体（TLR）4和半胱天冬酶激活和募集结构域家族成员15（CARD 15）基因的遗传多态性是否与结肠袋炎有关。每年发作1 - 2次（n = 11），每年发作2次以上（n = 38）。tlr 4基因的单核苷酸多态性（D299 G，T399 I）通过实时荧光探针聚合酶链反应（PCR）技术进行测定;卡15个多态性（L1007 fsinsC，R702 W，G908 R）通过焦磷酸测序进行测定。结肠袋炎与TLR 4基因多态性之间没有相关性，结肠袋炎患者携带CARD 15基因突变的患者比例显著高于无结肠袋炎患者（18%比8%;P< 0.05）; 24%每年发作2次以上的结肠袋炎患者携带CARD 15基因突变（与无结肠袋炎组相比P< 0.01）。CARD 15插入突变L1007 fsinsC在结肠袋炎患者中的检出率为14%，而在非结肠袋炎患者中的检出率为0%（P< 0.05）。所有携带L1007 fsinsC的患者每年发生2次以上。结论CARD 15多态性在IPAA治疗UC后发生结肠袋炎的患者中更常见。这些发现，如果在前瞻性分析中得到证实，则表明CARD 15突变，特别是L1007 fsinsC，可能易导致UC IPAA后发生结肠袋炎。
BackgroundPouchitis is a frequent complication after ileal pouch-anal anastamosis (IPAA) for ulcerative colitis (UC). The aim of this study was to determine whether genetic polymorphisms in the innate immune receptorstoll-like receptor(TLR)4andcaspase activation and recruitment domain family member 15(CARD15) genes are associated with pouchitis.MethodsFrom a retrospectively ascertained cohort of patients with UC 5 to 12 years after IPAA (n = 101), subjects were classified into 3 groups: no pouchitis (n = 52); 1 to 2 episodes per year (n = 11), and more than 2 episodes per year (n = 38). Single nucleotide polymorphisms in thetlr4gene (D299G, T399I) were determined by a real-time polymerase chain reaction-based fluorogenic probe technique; andcard15polymorphisms (L1007fsinsC, R702W, G908R) were determined by pyrosequencing.ResultsPouchitis affected 49% (49/101) of the study population. No correlation between pouchitis and the presence ofTLR4polymorphisms was found. The percentage of patients who harboredCARD15mutations was significantly higher in patients with pouchitis than in patients without pouchitis (18% versus 8%;P< 0.05); 24% of pouchitis patients with more than 2 episodes per year harboredCARD15mutations (P< 0.01 compared with the no pouchitis group). TheCARD15insertion mutation L1007fsinsC was present in 14% of patients with pouchitis and in 0% without pouchitis (P< 0.05). All patients who carried L1007fsinsC developed more than 2 episodes per year.ConclusionsCARD15polymorphisms are seen in greater frequency in patients with pouchitis after IPAA for UC. These findings, if borne out in prospective analyses, suggest thatCARD15mutations, particularly L1007fsinsC, may predispose to the development of pouchitis after IPAA for UC.
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