Mucosa-associated but not luminal Escherichia coli is augmented in Crohn's disease and ulcerative colitis.
Mucosa-associated but not luminal Escherichia coli is augmented in Crohn's disease and ulcerative colitis.
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DOI：
10.1186/1757-4749-4-21
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发表时间：
2012-12-13
期刊：
影响因子：
4.2
通讯作者：
Rodrigues J
中科院分区：
文献类型：
--
作者：
de Souza HL;de Carvalho VR;Romeiro FG;Sassaki LY;Keller R;Rodrigues J
大肠杆菌被认为参与了克罗恩病(CD)和可能的溃疡性结肠炎(UC)的病因学，至少部分原因是观察到CD和UC患者肠道微生物区系中这些细菌的数量增加。然而，这种数量变化是否同样地发生在整个肠道的粘膜和腔隙中，目前还不完全清楚。为了评估这个问题，对来自不同肠道部位的粪便和粘膜活检进行了培养，目的是确定它们的大肠杆菌浓度。此外，还对培养物中存在致病性大肠杆菌的某些毒力基因进行了筛选。对14例正常人(38例活检和14例粪便标本)、11例CD(25例活检和11例粪便标本)和7例UC患者(18例活检和7例粪便标本)的临床资料分析表明，粪便中的大肠埃希菌数量没有显著差异，但CD患者的回肠组织和CD和UC患者的乙状结肠和直肠组织中的大肠杆菌数量至少增加了1log10cfu/mg。对培养物进行细菌黏附和去除(EAE)、侵袭质粒抗原H(IPAH)、聚集性黏附转录激活因子(AggR)、志贺氏细胞毒素(STX)、不耐热肠毒素(ELT)和肠杆菌科丝氨酸蛋白酶自体转运蛋白(SPATE)基因的筛选：质粒编码毒素(PET)、分泌型自体转运蛋白(Sat)、志贺氏菌胞外蛋白(SepA)、肠道定植相关蛋白(PIC)和志贺氏菌IgA样蛋白酶同源基因(SIGA)。在总共调查的样本中，检测到了10个基因中的6个：aggR、EAE、pET、Sat、SepA和SIgA。在来自不同临床材料或患者组的培养中，没有观察到任何这些标志物的患病率有差异。用麦康基琼脂、厌氧菌的Wilkins Chalgren琼脂、大肠杆菌/大肠菌群染色琼脂和血液琼脂培养稀释液进行细菌定量。采用多重聚合酶链式反应技术，从麦康基原汁培养物中提取DNA，进行大肠杆菌毒力基因的筛选。在CD和UC患者中，只有粘膜相关的大肠埃希菌数量增加，CD和CD患者的回肠、直肠和乙状结肠的增殖明显，这两个部位都是病变的常见部位。这些部位的大肠杆菌种群数量增加，毒力标志物的数量很少，这可能意味着它们与疾病过程无关。
Escherichia coli is believed to participate in the etiology of Crohn’s disease (CD) and possibly of ulcerative colitis (UC), due at least in part to the observed rise in the number of these bacteria in the gut microbiota of CD and UC patients. Nevertheless, it is not fully understood whether this quantitative variation occurs equally throughout the mucosal and luminal spaces of the gut. To assess this question, stools and mucosa biopsies from distinct intestinal sites were cultured aiming at determining their E. coli concentration. The cultures were additionally screened for the presence of some virulence genes of pathogenic E. coli. Analyses of clinical materials from 14 controls (38 biopsies and 14 stools samples), 11 CD (25 biopsies and 11 stools samples) and 7 UC patients (18 biopsies and 7 stools samples) indicated no significant variation in the number of E. coli present in stools, but a rise of at least one log10 CFU/mg in biopsies from the ileum of CD patients and the sigmoid and rectum of CD and UC patients. The cultures were screened for the presence of E. coli attaching and effacing (eae), invasion plasmid antigen H (ipaH), aggregative adherence transcriptional activator (aggR), Shiga cytotoxins (stx), and heat labile enterotoxin (elt) and the following serine proteases autotransporters of Enterobacteriaceae (SPATE) genes: plasmid encoded toxin (pet), secreted autotransporter toxin (sat), Shigella extracellular protein (sepA), protein involved in intestinal colonization (pic) and Shigella IgA-like protease homolog (sigA). Six of the 10 genes screened were detected in the total of samples investigated: aggR, eae, pet, sat, sepA and sigA. No difference in the prevalence of any of these markers was observed in cultures from different clinical materials or groups of patients. Bacterial quantitation was carried out following cultures of diluted samples suspensions in MacConkey agar, Wilkins Chalgren agar for anaerobes, E. coli/coliform chromocult agar, and blood agar. Screening for E. coli virulence genes was performed by multiplex PCR of DNA purified from total MacConkey undiluted broth cultures. In CD and UC patients only the mucosa associated population of E. coli is augmented and the proliferation is prominent in the ileum of CD and rectum and sigmoid of both UC and CD patients which are sites where the lesions usually are observed. The augmented E. coli population in these sites presented a low number of the virulence markers, possibly meaning that they are not relevant for the disease process.
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