Division of Gastroenterology and Hepatology, Department of Medicine, Karolinska University Hospital, Karolinska Institutet, Huddinge, Stockholm, Sweden.
Neurogastroenterol Motil. 2011 Oct;23(10):928-34. doi: 10.1111/j.1365-2982.2011.01765.x. Epub 2011 Aug 21.
Irritable bowel syndrome (IBS) is a widespread gastrointestinal disorder of unknown etiology. Recently, our group detected chlamydial antigens in enteroendocrine cells (EEC) of jejunum biopsies from patients with IBS. Impairment of EEC secretion upon Chlamydia infection might lead to disturbances of gut functions. We have therefore studied the interaction between Chlamydia and EEC in vitro.
Two different human enteroendocrine cell lines were studied: LCC-18 from a neuroendocrine colonic tumour and CNDT2 from a small intestinal carcinoid. Cell lines were infected with C. trachomatis serovar LGV II strain 434. We used Penicillin G for inducing persistent infection. The ultrastructure of infected cells was studied using transmission electron microscopy and immunofluorescence and we used RT-PCR analysis for studying changes in gene expression at different stages of infection.
We found that both cell lines could be infected with C. trachomatis yielding productive infections and persistence could be induced using penicillin G. Immunofluorescence showed different cellular distributions of serotonin and chromogranin A in non-infected (cytoplasmatic distribution) compared with infected cells (serotonin and chromogranin mostly in chlamydial inclusions). In line with the microscopical findings, we found a significant down-regulation of the gene coding for the vesicular monoamine transporter (VMAT1) in infected compared with non-infected EEC (P<0.05).
CONCLUSIONS & INFERENCES: Altered protein distributions together with down-regulation of VMAT1 suggest that chlamydial infection may influence vesicular transport. It is therefore possible that such an infection in vivo could lead to disturbances in the regulation of gut functions.
肠易激综合征（IBS）是一种病因不明的广泛的胃肠道疾病。最近，我们的研究小组在 IBS 患者的空肠活检肠内分泌细胞（EEC）中检测到衣原体抗原。衣原体感染后 EEC 分泌功能的损伤可能导致肠道功能紊乱。因此，我们在体外研究了衣原体与 EEC 的相互作用。
研究了两种不同的人肠内分泌细胞系：来源于神经内分泌结肠肿瘤的 LCC-18 和来源于小肠类癌的 CNDT2。细胞系用沙眼衣原体血清型 LGV II 株 434 感染。我们使用青霉素 G 诱导持续感染。使用透射电子显微镜和免疫荧光研究感染细胞的超微结构，并用 RT-PCR 分析研究感染不同阶段基因表达的变化。
我们发现两种细胞系均可被沙眼衣原体感染，产生有活力的感染，使用青霉素 G 可诱导持续感染。免疫荧光显示，与未感染细胞相比（细胞质分布），非感染细胞（5-羟色胺和嗜铬粒蛋白 A 主要在衣原体包涵体中）的 5-羟色胺和嗜铬粒蛋白 A 存在不同的细胞分布。与显微镜观察结果一致，我们发现感染的 EEC 中编码囊泡单胺转运体（VMAT1）的基因显著下调（与未感染 EEC 相比，P<0.05）。
蛋白分布的改变和 VMAT1 的下调提示衣原体感染可能影响囊泡转运。因此，体内这种感染可能导致肠道功能调节紊乱。
