Helicobacter pylori cag pathogenicity island (cagPAI) involved in bacterial internalization and IL-8 induced responses via NOD1- and MyD88-dependent mechanisms in human biliary epithelial cells.
Helicobacter pylori cag pathogenicity island (cagPAI) involved in bacterial internalization and IL-8 induced responses via NOD1- and MyD88-dependent mechanisms in human biliary epithelial cells.
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DOI：
10.1371/journal.pone.0077358
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发表时间：
2013
期刊：
影响因子：
3.7
通讯作者：
Ferrero RL
中科院分区：
文献类型：
--
作者：
Boonyanugomol W;Chomvarin C;Hahnvajanawong C;Sripa B;Kaparakis-Liaskos M;Ferrero RL
幽门螺杆菌感染已被提出与肝胆道的各种疾病有关，包括胆汁导管上皮细胞的癌（胆管癌，CCA）。鉴于胃皮细胞中的幽门螺杆菌发病机理需要调查。从CCA的病例中衍生的胆管上皮细胞系与良好的AGS胃癌细胞系的结果进行了比较。对于这些细胞，与肝细胞的先前研究一致，肌动蛋白聚合和α5β1整联蛋白可能与CCA细胞中的幽门螺杆菌内在化有关。与野生型细菌相比，用CAGA，CAGL或CAGPAI细菌刺激的CCA细胞产生。先天免疫信号分子的敲低，核寡聚结构域1（NOD1）和髓样分化反应基因88（MyD88），数据共同证明CAGPAI表明幽门螺杆菌在胆管病原体中至关重要，因此提供了潜在的潜力胆道疾病中幽门螺杆菌的因果关系。
Helicobacter pylori infection has been proposed to be associated with various diseases of the hepatobiliary tract, including cancer of the bile duct epithelial cells (cholangiocarcinoma, CCA). The ability of H. pylori bacteria to cause pathogenic effects in these cells has, however, yet to be investigated. Given that the cag pathogenicity island (cagPAI) is required for H. pylori pathogenesis in gastric epithelial cells, we investigated wild-type and cag mutant strains for their ability to adhere, be internalized and induce pro-inflammatory responses in two bile duct epithelial cell lines derived from cases of CCA. The findings from these experiments were compared to results obtained with the well-characterized AGS gastric cancer cell line. We showed that the cagPAI encodes factors involved in H. pylori internalization in CCA cells, but not for adhesion to these cells. Consistent with previous studies in hepatocytes, actin polymerization and α5β1 integrin may be involved in H. pylori internalization in CCA cells. As for AGS cells, we observed significantly reduced levels of NF-κB activation and IL-8 production in CCA cells stimulated with either cagA, cagL or cagPAI bacteria, when compared with wild-type bacteria. Importantly, these IL-8 responses could be inhibited via either pre-treatment of cells with antibodies to α5β1 integrins, or via siRNA-mediated knockdown of the innate immune signaling molecules, nucleotide oligomerization domain 1 (NOD1) and myeloid differentiation response gene 88 (MyD88). Taken together, the data demonstrate that the cagPAI is critical for H. pylori pathogenesis in bile duct cells, thus providing a potential causal link for H. pylori in biliary tract disease.
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DOI：
10.1111/j.1749-6632.1996.tb52983.x
发表时间：
1996-01-01
期刊：
MICROBIAL PATHOGENESIS AND IMMUNE RESPONSE II
影响因子：
--
作者：
Birkness, KA;Gold, BD;Quinn, FD
通讯作者：
Quinn, FD
影响因子：
3.1
作者：
Boonyanugomol, Wongwarut;Chomvarin, Chariya;Baik, Seung-Chul
通讯作者：
Baik, Seung-Chul
影响因子：
3.1
作者：
Ito, Kyoko;Yamaoka, Yoshio;Graham, David Y.
通讯作者：
Graham, David Y.
影响因子：
12.4
作者：
Correia, J. da Silva;Miranda, Y.;Ulevitch, R. J.
通讯作者：
Ulevitch, R. J.
DOI：
10.1073/pnas.93.25.14648
发表时间：
1996-12-10
影响因子：
11.1
作者：
Censini, S;Lange, C;Covacci, A
通讯作者：
Covacci, A