Escherichia coli LF82
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA487828 | ENA |
REPOSITORIES: ENA
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Project description:LF82, an adherent invasive Escherichia coli (AIEC) pathobiont, is associated with Crohn’s disease, an inflammatory bowel disease of unknown etiology. No genetic features have been identified that distinguish AIEC strains, such as LF82, from “commensal” or pathogenic E. coli. We investigated an extremely rare single nucleotide polymorphism (SNP) within the highly conserved rpoD gene, encoding sigma70 [primary sigma factor, RNA polymerase (RNAP)]. We demonstrate that sigma70 D445V results in transcriptome and phenotypic changes consistent with LF82 phenotypes, including increased biofilm formation and antibiotic resistance. The position of D445V within RNAP is predicted to affect spacer interaction; in vitro transcriptions reveal that the variant increases transcription from several promoters with a 16 bp spacer and a -14G:C. Our work demonstrates that a single SNP within the bacterial primary sigma can lead to myriad gene expression changes/ new phenotypes and suggests an underrecognized mechanism by which pathobionts and other strain variants can emerge.
2024-09-30 | GSE253924 | GEO
Project description:Adherent-Invasive Escherichia coli Transcriptome
| PRJNA752090 | ENA
Project description:Imbalance in beneficial and harmful bacteria underlies gastrointestinal diseases, such as inflammatory bowel disease. Here, we demonstrated that certain E. coli strains, specifically adherent-invasive E. coli (AIEC), utilize a serine metabolism pathway to outcompete other E. coli strains in the inflamed gut. In contrast, amino acid metabolism has a minimal effect on their competitive fitness in the healthy gut. The availability of luminal serine used for the competition of E. coli is largely dependent on dietary intake, as the inflammation-induced blooms of AIEC are significantly blunted when amino acids, particularly serine, are removed from the diet. Thus, intestinal inflammation regulates the intraspecific competition between Enterobacteriaceae by eliciting their metabolic reprogramming.
2019-09-06 | GSE106412 | GEO
Project description:Current clinical antibiotics are largely broad-spectrum agents that promote intestinal dysbiosis and colonisation of Enterobacteriaceae, which are often drug-resistant. Indeed, dysbiosis creates an ideal niche for adherent-invasive Escherichia coli (AIEC) in patients with inflammatory bowel disease (IBD). There is an urgent and unmet need for novel narrow-spectrum and microbiome-sparing antibiotics. Here, we screened >10,000 molecules for antibacterial activity against AIEC and discovered enterololin, an antibacterial compound with targeted activity against Enterobacteriaceae species. Molecular substructure- and deep learning-guided mechanism of action investigations revealed that enterololin perturbs lipoprotein trafficking through a mechanism involving the LolCDE complex. Moreover, enterololin can suppress an AIEC infection in mouse models, while largely preserving the overall microbiome composition. This work highlights the utility of deep learning methods for predicting molecular interactions, thereby accelerating mechanism of action elucidation of novel molecules, and identifies a promising Enterobacteriaceae-specific antibacterial candidate for further development to treat challenging infections in IBD patients.
2025-08-27 | GSE300731 | GEO
Project description:Crohn’s disease (CD), an inflammatory bowel disease that arises from an immune attack of the GI tract, affects roughly 1.6 million Americans. The etiology of CD and the other major irritable bowel disease, ulcerative colitis, is not known, but host genetics and immunology, the gut microbiome, and environmental factors are all thought to be involved. In addition, Adherent Invasive Escherichia coli (AIEC) strains are frequently found to be associated with CD. Key features distinguish AIEC from commensal E. coli, including adherence/invasion of the intestinal epithelium, increased biofilm formation, increased antibiotic resistance, and survival/replication within macrophages. However, these pathobionts lack genetic features typical of frank pathogens. Thus, the potential role AIEC play in CD pathogenesis is not clear. The E. coli pathobiont LF82, isolated from ileum of a patient with CD, has been a well-studied, prototypic AIEC. Dozens of single nucleotide polymorphisms (SNPs) distinguish LF82 and other AIEC from commensal E. coli, suggesting that some of these genetic features might account for particular LF82 phenotypes. In this review, we summarize changes in the CD gut, the association of AIEC with CD, genes and SNPs associated with AIEC, and recent work connecting a specific SNP within a bacterial RNA polymerase gene to the expression of genes associated with the LF82 lifestyle.
2025-12-10 | GSE313173 | GEO
Project description:Adherent-invasive Escherichia coli (AIEC) are associated with Crohn’s disease through their ability to invade, survive, and replicate within intestinal macrophages. To characterize the host response, we performed RNA-seq profiling of THP-1–derived macrophages infected for 24 h with five distinct AIEC strains, compared to uninfected controls. Transcriptomic analysis revealed extensive reprogramming of macrophage gene expression, marked by activation of pro-inflammatory signaling pathways (NF-κB, JAK–STAT, TNF) and concomitant suppression of lysosome-, phagosome-, and peroxisome-associated programs. Although pro-death signals were induced, execution modules of apoptosis and ferroptosis remained restrained, consistent with macrophage survival and thus permissive for bacterial replication. A conserved transcriptional signature emerged across strains, characterized by sustained inflammation coupled with diminished antimicrobial capacity. In parallel, we observed strain-specific differences in cytokine expression, lysosomal function, and lipid metabolism, highlighting that macrophage responses vary depending on the infecting AIEC strain. Overall, these data reveal that AIEC sustain macrophage inflammatory responses yet restrain cell death and antimicrobial mechanisms, establishing conditions that favor their replication and long-term survival within the host.
2026-03-04 | GSE307944 | GEO
Project description:Our aim was to identify candidate transcripts that distinguish AIEC from non-invasive E. coli (NIEC) strains and might be useful for rapid and accurate identification of AIEC by culture-independent technology. We performed comparative RNA-Sequence (RNASeq) analysis using AIEC strain LF82 and NIEC strain HS during exponential and stationary growth.
2017-02-09 | GSE69020 | GEO
Project description:The complex reservoir of metabolite-producing bacteria in the gastrointestinal tract contributes tremendously to human health and disease. Bacterial composition, and by extension gut metabolomic composition, is undoubtably influenced by the use of modern antibiotics. Herein, we demonstrate that polymyxin B, a last resort antibiotic used for chronic multidrug resistant infections infections, influences the production of the genotoxic metabolite colibactin from adherent-invasive Escherichia coli (AIEC) NC101. Colibactin can augment colorectal cancer (CRC) through DNA double stranded breaks and interstrand crosslinks. While the structure and biosynthesis of colibactin has been elucidated, chemical-induced regulation of its biosynthetic gene cluster and subsequent production of the genotoxin by pathogenic E. coli are largely unexplored. This research highlights the regulation of the colibactin-producing biosynthetic gene cluster under polymyxin stress. Using a multi-omic approach, we have identified that polymyxin stress enhances the abundance of colibactin biosynthesis proteins (Clb’s) in multiple pks+ E. coli strains, including pro-carcinogenic AIEC: NC101, the probiotic strain: E. coli Nissle 1917, and the antibiotic testing strain: E. coli ATCC 25922. Expression analysis via qPCR revealed that increased transcription of clb genes likely contributes to elevated Clb protein levels in NC101. Enhanced production of Clb’s by NC101 under polymyxin stress matched an increased production of the colibactin prodrug motif, a proxy for the mature genotoxic metabolite. Furthermore, E. coli with heightened tolerance for polymyxin antibiotics induced greater DNA damage, assessed by quantification of γH2AX staining in cultured intestinal epithelial cells. This study establishes a key link between the polymyxin B stress response and colibactin production in pks+ E. coli. Ultimately, our findings will inform future studies investigating colibactin regulation, the microbial response to antibiotics in the gut, and the ability of seemingly innocuous commensal microbes to induce host disease.
2021-07-15 | PXD025088 | Pride