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Abstract
The adherent-invasive Escherichia coli (AIEC) pathotype has been implicated in the pathogenesis of inflammatory bowel diseases in general and in Crohn’s disease (CD) in particular. AIEC strains are primarily characterized by their ability to adhere to and invade intestinal epithelial cells. However, the genetic and phenotypic features of AIEC isolates vary greatly as a function of the strain’s clonality, host factors, and the gut microenvironment. It is thus essential to identify the determinants of AIEC pathogenicity and understand their role in intestinal epithelial barrier dysfunction and inflammation. We reasoned that soil nematode Caenorhabditis elegans (a simple but powerful model of host-bacterium interactions) could be used to study the virulence of AIEC vs. non- AIEC E. coli strains. Indeed, we found that the colonization of C. elegans (strain N2) by E. coli impacted survival in a strain-specific manner. Moreover, the AIEC strains’ ability to invade cells in vitro was linked to the median lifespan in C. elegans (strain PX627). However, neither the E. coli intrinsic invasiveness (i.e., the fact for an individual strain to be characterized as invasive or not) nor AIEC’s virulence levels (i.e., the intensity of invasion, established in % from the infectious inoculum) in intestinal epithelial cells was correlated with C. elegans’ lifespan in the killing assay. Nevertheless, AIEC longevity of C. elegans might be a relevant model for screening anti-adhesion drugs and anti-invasive probiotics.
Highlights
The uracil auxotroph OP50 is the “gold-standard” control strain routinely used in C. elegans survival assays [40]
MG1655 is a prototype non-invasive, non-pathogenic, human-commensal-derived E. coli K-12 strain used as a model in bacterial genetics, molecular biology, and biotechnology [42]
In a first set of experiments, we evaluated C. elegans’ lifespan upon infection with three non-invasive non-pathogenic E. coli strains (OP50, MG1655, and the probiotic-like EcN), and three adherent-invasive Escherichia coli (AIEC) strains (LF82, EC-06362, and NRG857c) (Figure 1)
Summary
Inflammatory bowel diseases (IBDs, including Crohn’s disease (CD) and ulcerative colitis (UC)) are caused by intricate genetic and environmental factors that alter intestinal homeostasis [1,2]. This inflammatory contexts results in dysbiosis [3], which is characterized by specific changes in the symbiont/pathobiont ratio of the gut microbiota [4]. Along with a significant reduction in overall microbial diversity, microbial imbalance leads to a fall in the abundance of beneficial bacteria and an increase in the abundance of potentially pathogenic bacteria The latter include certain mucosa-associated bacteria (such as the Enterobacterales [5]) that might trigger or exacerbate IBDs in susceptible individuals
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