粘附性侵袭性大肠杆菌(AIEC)与克罗恩病(CD)的发病机理密切相关。具有相似遗传背景和毒力基因谱的大肠杆菌菌株与其他肠道疾病有关,如溃疡性结肠炎(UC),结直肠癌(CRC),和乳糜泻(CeD),但AIEC在这些疾病中的作用仍有待探索。我们的目的是评估分布,丰度,以及UC中AIEC的致病特征,CRC,和CeD。
在从14名UC和15名CRC患者的回肠和结肠分离的4,233个大肠杆菌中以及从17名CeD和10名健康(H)儿童获得的38个粪便大肠杆菌菌株中研究了AIEC表型。将AIEC患病率和丰度与CD患者和H对照组的先前数据进行比较。克隆,毒力基因携带,并确定了鉴定的AIEC的系统发育起源。
在UC中,AIEC患病率介于CD和H受试者之间(UC:35.7%,CD:55.0%,H:21.4%),与结肠疾病的CD患者相似(C-CD:40.0%)。在CRC中,患病率低于这些组(6.7%).在AIEC患者中,所有肠道条件的估计丰度相似.从UC和CRC中分离出的所有AIEC菌株都属于B1系统组,除了一个A系,大多数(75%的克隆不同的AIEC)含有Afa/Dr操纵子和cdt基因。从CeD组群中分离的大肠杆菌都不是AIEC。尽管如此,从活性CeD患者分离的大肠杆菌菌株显示出比从H和非活性CeD儿科患者分离的大肠杆菌菌株更高的侵袭指数。
我们支持以下假设:AIEC样菌株不仅可以参与CD,还可以参与UC。需要进一步的工作来研究这些菌株组的毒力特性,并确定AIEC和UC之间是否存在因果关系。相比之下,我们排除了AIEC与CRC的可能关联。此外,进一步研究CeD中的大肠杆菌菌株可能的致病作用将是令人感兴趣的。
Adherent-invasive E. coli (AIEC) has largely been implicated in the pathogenesis of Crohn\'s disease (CD). E. coli strains with similar genetic backgrounds and virulence genes profiles have been associated with other intestinal disorders, such as ulcerative colitis (UC), colorectal cancer (CRC), and coeliac disease (CeD), but the role of AIEC in these diseases remains unexplored. We aimed to assess the distribution, abundance, and pathogenic features of AIEC in UC, CRC, and CeD.
The AIEC phenotype was investigated in 4,233 E. coli isolated from the ileum and colon of 14 UC and 15 CRC patients and in 38 fecal E. coli strains obtained from 17 CeD and 10 healthy (H) children. AIEC prevalence and abundance were compared with previous data from CD patients and H controls. Clonality, virulence gene carriage, and phylogenetic origin were determined for the AIEC identified.
In UC, AIEC prevalence was intermediate between CD and H subjects (UC: 35.7%, CD: 55.0%, H: 21.4%), and similar to CD patients with colonic disease (C-CD: 40.0%). In CRC, the prevalence was lower (6.7%) than these groups. In patients with AIEC, the estimated abundance was similar across all intestinal conditions. All AIEC strains isolated from UC and CRC belonged to the B1 phylogroup, except for a strain of the A phylogroup, and the majority (75% of clonally distinct AIEC) harbored the Afa/Dr operon and the cdt gene. None of the E. coli isolated from the CeD cohort were AIEC. Nonetheless, E. coli strains isolated from active CeD patients showed higher invasion indices than those isolated from H and inactive CeD pediatric patients.
We support the hypothesis that AIEC-like strains can be involved not only in CD but also in UC. Further works are needed to study the virulence particularities of these groups of strains and to determine if there is a causative link between AIEC and UC. In contrast, we rule out the possible association of AIEC with CRC. In addition, to further study the E. coli strains in CeD for their possible pathogenic role would be of interest.