ArticlePLoS pathogens2023
TRPV1 controls innate immunity during Citrobacter rodentium enteric infection.
Article in PLoS pathogens, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 9 citations in OpenAlex.
- TRPV1 from the TRP family: Structure, function, implication in autoimmune diseases and potential therapies.Channels (Austin, Tex.) · 2026Review
- Tac1 deficiency reduces the severity of enteric bacterial infection.PLoS pathogens · 2026Article
- The sympathetic nervous system enhances host immune responses to enteric bacterial pathogens in mice.Brain, behavior, and immunity · 2025Article
- Gut sensory neurons as regulators of neuro-immune-microbial interactions: from molecular mechanisms to precision therapy for IBD/IBS.Journal of neuroinflammation · 2025Review
- Substance P receptor signaling contributes to host maladaptive responses during enteric bacterial infection.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Advance on establishment of pathological model of ulcerative colitis.Frontiers in veterinary science · 2025Review
- Recent Developments in On-Demand Voiding Therapies.The Journal of pharmacology and experimental therapeutics · 2024Review
- Substance P receptor signaling contributes to host maladaptive responses during enteric bacterial infection.bioRxiv : the preprint server for biology · 2024Article
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7 authors at 1 institution in 1 country.
Funding
Abstract
Mucosal immunity is critical to host protection from enteric pathogens and must be carefully controlled to prevent immunopathology. Regulation of immune responses can occur through a diverse range of mechanisms including bi-directional communication with neurons. Among which include specialized sensory neurons that detect noxious stimuli due to the expression of transient receptor potential vanilloid receptor 1 (TRPV1) ion channel and have a significant role in the coordination of host-protective responses to enteric bacterial pathogens. Here we have used the mouse-adapted attaching and effacing pathogen Citrobacter rodentium to assess the specific role of TRPV1 in coordinating the host response. TRPV1 knockout (TRPV1-/-) mice had a significantly higher C. rodentium burden in the distal colon and fecal pellets compared to wild-type (WT) mice. Increased bacterial burden was correlated with significantly increased colonic crypt hyperplasia and proliferating intestinal epithelial cells in TRPV1-/- mice compared to WT. Despite the increased C. rodentium burden and histopathology, the recruitment of colonic T cells producing IFNγ, IL-17, or IL-22 was similar between TRPV1-/- and WT mice. In evaluating the innate immune response, we identified that colonic neutrophil recruitment in C. rodentium infected TRPV1-/- mice was significantly reduced compared to WT mice; however, this was independent of neutrophil development and maturation within the bone marrow compartment. TRPV1-/- mice were found to have significantly decreased expression of the neutrophil-specific chemokine Cxcl6 and the adhesion molecules Icam1 in the distal colon compared to WT mice. Corroborating these findings, a significant reduction in ICAM-1 and VCAM-1, but not MAdCAM-1 protein on the surface of colonic blood endothelial cells from C. rodentium infected TRPV1-/- mice compared to WT was observed. These findings demonstrate the critical role of TRPV1 in regulating the host protective responses to enteric bacterial pathogens, and mucosal immune responses.
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