Campylobacter jejuni induces transcellular translocation of commensal bacteria via lipid rafts.
Campylobacter jejuni induces transcellular translocation of commensal bacteria via lipid rafts.
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DOI：
10.1186/1757-4749-1-2
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发表时间：
2009-02-03
期刊：
影响因子：
4.2
通讯作者：
Buret AG
中科院分区：
文献类型：
--
作者：
Kalischuk LD;Inglis GD;Buret AG
弯曲杆菌肠炎代表了通过未知机制发展炎症性肠病（IBD）的风险因素。由于IBD患者表现出对肠道菌群的炎症反应，诱导肠道细菌穿过肠上皮移位的因素可能有助于IBD的发病机制。本研究旨在确定弯曲杆菌是否诱导非侵入性肠道细菌移位，并表征潜在机制。小鼠感染C.空肠和肠道细菌移位通过肠系膜淋巴结（MLN）、肝和脾的定量细菌培养来评估。为了研究弯曲杆菌诱导细菌移位的机制，将非侵袭性大肠杆菌HB 101 ±野生型弯曲杆菌或侵袭缺陷突变体接种到transwell生长的T84单层细胞中，并测量细菌内化和移位。通过测量3 kDa葡聚糖探针的通量来评估上皮渗透性。通过胆固醇耗竭和小窝蛋白共定位来评估脂筏的作用。C. jejuni 81-176可诱导肠道细菌移位至感染小鼠的MLN、肝脏和脾脏。在T84细胞单层中，弯曲杆菌诱导的E.大肠杆菌通过跨细胞途径发生，而不增加上皮通透性，并被上皮细胞质膜胆固醇耗尽所阻断。侵袭缺陷型突变体和弯曲菌条件培养基也能诱导E。coli易位，表明C.空肠不直接将细菌“穿梭"到肠上皮细胞中。In C. jejuni处理的单层，易位E.大肠杆菌与脂筏结合，这种现象被胆固醇耗竭所阻断。弯曲杆菌，不管其自身的侵袭性，促进非侵入性细菌通过脂质筏介导的跨细胞过程穿过肠上皮的易位。
Campylobacter enteritis represents a risk factor for the development of inflammatory bowel disease (IBD) via unknown mechanisms. As IBD patients exhibit inflammatory responses to their commensal intestinal microflora, factors that induce translocation of commensal bacteria across the intestinal epithelium may contribute to IBD pathogenesis. This study sought to determine whether Campylobacter induces translocation of non-invasive intestinal bacteria, and characterize underlying mechanisms. Mice were infected with C. jejuni and translocation of intestinal bacteria was assessed by quantitative bacterial culture of mesenteric lymph nodes (MLNs), liver, and spleen. To examine mechanisms of Campylobacter-induced bacterial translocation, transwell-grown T84 monolayers were inoculated with non-invasive Escherichia coli HB101 ± wild-type Campylobacter or invasion-defective mutants, and bacterial internalization and translocation were measured. Epithelial permeability was assessed by measuring flux of a 3 kDa dextran probe. The role of lipid rafts was assessed by cholesterol depletion and caveolin co-localization. C. jejuni 81–176 induced translocation of commensal intestinal bacteria to the MLNs, liver, and spleen of infected mice. In T84 monolayers, Campylobacter-induced internalization and translocation of E. coli occurred via a transcellular pathway, without increasing epithelial permeability, and was blocked by depletion of epithelial plasma membrane cholesterol. Invasion-defective mutants and Campylobacter-conditioned cell culture medium also induced E. coli translocation, indicating that C. jejuni does not directly 'shuttle' bacteria into enterocytes. In C. jejuni-treated monolayers, translocating E. coli associated with lipid rafts, and this phenomenon was blocked by cholesterol depletion. Campylobacter, regardless of its own invasiveness, promotes the translocation of non-invasive bacteria across the intestinal epithelium via a lipid raft-mediated transcellular process.
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影响因子：
3.1
作者：
Chen, Ming L.;Ge, Zhongming;Schauer, David B.
通讯作者：
Schauer, David B.
影响因子：
3.1
作者：
Medina, Freddy A.;de Almeida, Cecilia J.;Lisanti, Michael P.
通讯作者：
Lisanti, Michael P.
影响因子：
6.4
作者：
KORLATH, JA;OSTERHOLM, MT;ROBINSON, RA
通讯作者：
ROBINSON, RA
影响因子：
4.9
作者：
Halfvarson, Jonas;Jess, Tine;Jarnerot, Gunnar
通讯作者：
Jarnerot, Gunnar
影响因子：
29.4
作者：
Ferrier, L;Mazelin, L;Bueno, L
通讯作者：
Bueno, L