ArticleFrontiers in cellular and infection microbiology2022
Gut microbiota-derived indole 3-propionic acid partially activates aryl hydrocarbon receptor to promote macrophage phagocytosis and attenuate septic injury.
Article in Frontiers in cellular and infection microbiology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 53 papers.
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Who cites it
53 citing papers in PubMed, 72 citations in OpenAlex.
- Dietary tryptophan mitigates lung ischemia-reperfusion injury in association with increased indole-3-propionate and aryl hydrocarbon receptor signaling.Gut microbes · 2026Article
- Short-Chain Fatty Acids in Sepsis: Mechanisms of Action and Therapeutic Advances.Biomedicines · 2026Review
- Higher abundance ofmSystems · 2026Article
- Gut‑brain axis in anesthesia and critical illness: Molecular crosstalk and its impact on delirium and outcome (Review).International journal of molecular medicine · 2026Review
- Aryl hydrocarbon receptor pharmacology-mechanisms, ligands, and therapeutic potential.Pharmacological reviews · 2026Review
- Aryl Hydrocarbon Receptor Signaling in Aging: A Key Modulator of Brain Homeostasis.Molecular neurobiology · 2026Review
- Article
- The Collaborative Collapse: Bile Acid Dysmetabolism as a Central Pathogenic Driver in Canine and Feline Multi-Systemic Disorders-From Mechanisms to Precision Therapeutics.Veterinary sciences · 2026Review
- Demystifying the role of postbiotics in inflammation mediated metabolic disorders: an updated review.Food science and biotechnology · 2026Review
- A systematic exploration of gut microbiota-driven blood metabolites in sepsis: an integrated bioinformatics and genetic association study.Frontiers in genetics · 2026Article
- Limosilactobacillus reuteri DSM17938 Attenuates Neuroinflammatory Responses After Spinal Cord Injury by Modulating Tryptophan Metabolism.Probiotics and antimicrobial proteins · 2026Article
- Deoxycholic acid promotes anxiety- and depression-like behaviors in mice via modulation of the gut microbial metabolite indole-3-propionic acid.Frontiers in immunology · 2026Article
- Microbial tryptophan metabolites modulate blood-brain and gut barriersNeuroscience applied · 2026Article
- Cell death in sepsis: unveiling new perspectives on organ dysfunction.Frontiers in cell and developmental biology · 2026Review
- Phenylacetylglutamine exacerbates sepsis-induced cardiac dysfunction and left ventricular remodeling via the ferroptosis and TLR4/NF-κB pathway.Frontiers in cardiovascular medicine · 2026Article
- [Indole-3-acetic acid alleviatesNan fang yi ke da xue xue bao = Journal of Southern Medical University · 2025Article
- Indole-3-propionic acid exacerbates cisplatin-induced chronic kidney disease through the AHR/NF-κB signaling pathway.iScience · 2025Article
- Chemotherapy-driven intestinal dysbiosis and indole-3-propionic acid rewire myelopoiesis to promote a metastasis-refractory state.Nature communications · 2025Article
- Article
- Effect of the gut microbiota-derived tryptophan metabolite indole-3-acetic acid in pneumonia.Nature communications · 2025Observational
Corrections and comments
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Authors and funding
10 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Sepsis is associated with a high risk of death, and the crosstalk between gut microbiota and sepsis is gradually revealed. Indole 3-propionic acid (IPA) is a gut microbiota-derived metabolite that exerts immune regulation and organ protective effects. However, the role of IPA in sepsis is not clear. In this study, the role of IPA in sepsis-related survival, clinical scores, bacterial burden, and organ injury was assessed in a murine model of cecal ligation and puncture-induced polymicrobial sepsis. Aryl hydrocarbon receptor (AhR) highly specific inhibitor (CH223191) was used to observe the role of AhR in the protection of IPA against sepsis. The effects of IPA on bacterial phagocytosis by macrophages were investigated
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.