ArticleMicrobiome2024
Systemic antibody responses against gut microbiota flagellins implicate shared and divergent immune reactivity in Crohn's disease and chronic fatigue syndrome.
Article in Microbiome, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers, 1 of them a synthesis that pooled it.
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Who cites it
13 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Biomarkers of post-acute infection syndrome: a systematic literature review.Frontiers in immunology · 2026Pooled it
- Systemic antibody responses against bacterial and viral antigens associate with fatigue in patients with inflammatory bowel disease.iScience · 2026Article
- Article
- Phage-Display Immunoprecipitation Sequencing Reveals Distinct Antibody Signatures Against Bacterial Flagellins Associated With Treatment Response in Crohn's Disease.Clinical and translational gastroenterology · 2026Article
- Mapping adaptive immune responses toward fungal antigens in inflammatory bowel disease using T cell repertoire sequencing and phage-immunoprecipitation sequencing.Journal of Crohn's & colitis · 2026Article
- High throughput profiling of the B cell repertoire identifies systematic changes in the repertoire of individuals with Crohn's disease.Frontiers in immunology · 2026Article
- Causes of symptoms and symptom persistence in long COVID and myalgic encephalomyelitis/chronic fatigue syndrome.Cell reports. Medicine · 2025Review
- Unraveling the gut microbiota's role in obesity: key metabolites, microbial species, and therapeutic insights.Journal of bacteriology · 2025Review
- Role of the gut microbiome in psychological symptoms associated with inflammatory bowel diseases.Seminars in immunopathology · 2025Review
- Profiling Antibody Reactivity to Gut Microbes in ME/CFS Patients.Methods in molecular biology (Clifton, N.J.) · 2025Article
- The microbiota-gut-brain axis in mental and neurodegenerative disorders: opportunities for prevention and intervention.Frontiers in aging neuroscience · 2025Review
- Advances in the research of intestinal fungi in Crohn's disease.World journal of gastroenterology · 2024Article
- Gut Microbiome and Paediatric Inflammatory Bowel Disease: Emerging Mechanistic and Therapeutic Insights Into Pathogenesis and Microbiota-Based Approaches.IET systems biologyReview
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Authors and funding
5 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundElevated systemic antibody responses against gut microbiota flagellins are observed in both Crohn's disease (CD) and myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS), suggesting potential serological biomarkers for diagnosis. However, flagellin-specific antibody repertoires and functional roles in the diseases remain incompletely understood. Bacterial flagellins can be categorized into three types depending on their interaction with toll-like receptor 5 (TLR5): (1) "stimulator" and (2) "silent" flagellins, which bind TLR5 through a conserved N-terminal motif, with only stimulators activating TLR5 (involving a C-terminal domain); (3) "evader" flagellins of pathogens, which entirely circumvent TLR5 activation via mutations in the N-terminal TLR5 binding motif.
resultsHere, we show that both CD and ME/CFS patients exhibit elevated antibody responses against distinct regions of flagellins compared to healthy individuals. N-terminal binding to Lachnospiraceae flagellins was comparable in both diseases, while C-terminal binding was more prevalent in CD. N-terminal antibody-bound flagellin sequences were similar across CD and ME/CFS, resembling "stimulator" and "silent" flagellins more than evaders. However, C-terminal antibody-bound flagellins showed a higher resemblance to the stimulator than to silent flagellins in CD, which was not observed in ME/CFS.
conclusionsThese findings suggest that antibody binding to the N-terminal domain of stimulator and silent flagellins may impact TLR5 activation in both CD and ME/CFS patients. Blocking this interaction could lead commensal bacteria to be recognized as pathogenic evaders, potentially contributing to dysregulation in both diseases. Furthermore, elevated antibody binding to the C-terminal domain of stimulator flagellins in CD may explain pathophysiological differences between the diseases. Overall, these results highlight the diagnostic potential of these antibody responses and lay a foundation for deeper mechanistic studies of flagellin/TLR5 interactions and their impact on innate/adaptive immunity balance.
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