ArticleInfection and immunity2001
Adherent invasive Escherichia coli strains from patients with Crohn's disease survive and replicate within macrophages without inducing host cell death.
Article in Infection and immunity, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 221 papers.
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Who cites it
221 citing papers in PubMed.
- Treatment-Specific Composition of the Gut Microbiota Is Associated With Disease Remission in a Pediatric Crohn's Disease Cohort.Inflammatory bowel diseases · 2019Trial
- Article
- Review
- Current and emerging therapeutic strategies targeting adherent-invasive Escherichia coli in Crohn's disease: a review.Gut pathogens · 2026Review
- Dietary emulsifiers and host inflammation synergistically drive genomic evolution of Crohn's disease-associated Escherichia coli toward enhanced pathogenicity.Journal of Crohn's & colitis · 2026Article
- Adherent-InvasiveMicroorganisms · 2026Article
- From inflammation to fibrosis and cancer: the emerging role of AIEC-derived metabolites in intestinal disease progression.Experimental & molecular medicine · 2026Review
- A host anti-amyloidogenic stomach-specific protein inhibits colonization and biofilm formation by adherent invasive Escherichia coli in the colon.Research square · 2026Article
- Intermittent antibiotic exposure of Escherichia coli biofilms drives resistance in catheter-associated infection models.NPJ biofilms and microbiomes · 2026Article
- Gut microbiota dysbiosis and immune responses: insights from IgA nephropathy and inflammatory bowel disease.Frontiers in immunology · 2026Review
- Pulmonary injury in inflammatory bowel disease: intestinal barrier disruption, gut-lung axis remodeling, and treatment-related lung toxicity.Frontiers in immunology · 2026Review
- The P2X7 Receptor Promotes Intestinal Fibrosis by Modulating the Gut Microbiota and the Inflammasome.Cellular and molecular gastroenterology and hepatology · 2026Article
- Gut microbiota dysbiosis: Pathogenic drivers and emerging phage-based therapeutics.AIMS microbiology · 2026Review
- Pathotype-specific antimicrobial resistance in diarrheagenicFrontiers in microbiology · 2026Review
- Persistence mechanisms of Crohn's disease-associated adherent invasiveGut microbes · 2025Article
- Pathogenesis of adherent-invasiveGut microbes · 2025Article
- Intestinal Goblet Cell-Expressed Reg4 Ameliorates Intestinal Inflammation Potentially by Restraining Pathogenic Escherichia coli Infection.Probiotics and antimicrobial proteins · 2025Article
- Gut microbiota and inflammatory bowel disease: mechanisms, clinical implications, and future directions.Molecular biology reports · 2025Review
- The assembly of a hybrid type IV secretion system by a Crohn's disease-associated Escherichia coli strain.Nature communications · 2025Article
- Pathogenic Potential of Invasive Mucosa-Associated Klebsiella pneumoniae Isolates in Ulcerative Colitis: Characterization of Virulence Factors and Inflammatory Response.Immunity, inflammation and disease · 2025Article
161 more citing papers are in PubMed but not listed here.
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Authors and funding
6 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Escherichia coli strains recovered from Crohn's disease (CD) lesions are able to adhere to and invade cultured intestinal epithelial cells. We analyzed the behavior within macrophages of adherent invasive E. coli (AIEC) strains isolated from patients with CD. All the 15 AIEC strains tested were able to replicate extensively within J774-A1 cells: the numbers of intracellular bacteria increased 2.2- to 74.2-fold at 48 h over that at 1 h postinfection. By use of murine peritoneal macrophages and human monocyte-derived-macrophages, the reference AIEC strain LF82 was confirmed to be able to survive intracellularly. Transmission electron micrographs of AIEC LF82-infected macrophages showed that at 24 h postinfection, infected cells harbored large vacuoles containing numerous bacteria, as a result of the fusion of several vacuoles occurring after 8 h postinfection. No lactate dehydrogenase (LDH) release, no sign of DNA fragmentation or degradation, and no binding to fluorescein isothlocyanate-labeled annexin V were observed with LF82-infected J774-A1 cells, even after 24 h postinfection. LF82-infected J774-A1 cells secreted 2.7-fold more tumor necrosis factor alpha (TNF-alpha) than cells stimulated with 1 microg of lipopolysaccharide (LPS)/ml. No release of interleukin-1beta was observed with LPS-prestimulated J774-A1 cells infected with AIEC LF82. These findings showed that (i) AIEC strains are able to survive and to replicate within macrophages, (ii) AIEC LF82 replication does not induce any cell death of the infected cells, and (iii) LF82-infected J774-A1 cells release high levels of TNF-alpha. These properties could be related to some features of CD and particularly to granuloma formation, one of the hallmarks of CD lesions.
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