Loading
Life sciences · Journal article
Gut Microbes · October 15, 2026
No summary has been generated for this record yet. What follows is drawn from its source metadata only.
Journal article.
No findings were extractable from the material analysed.
Safety was not reported in the material analysed. Check the source before drawing any conclusion about harm.
The source did not state who this applies to in practice.
Graded across the dimensions that decide whether you should act, each from what the source actually supports. There is no single score, and where a dimension was not assessed it says so.
This record has not been graded across any dimension yet. Treat the label above as provisional and read the source.
What is missing. This record has no bottom line, key findings, reported figures, evidence dimensions. That is a gap in the analysis, not a judgement about the study.
Persistent infection by helminths requires limiting inflammatory damage despite incomplete pathogen clearance, yet how helminths mobilize resident microbiota to establish this state remains unclear. Here we identify a cross-kingdom metabolic relay through which Trichinella spiralis promotes systemic disease tolerance. Infection selectively expanded Ligilactobacillus murinus and redirected microbial tryptophan metabolism toward indole-3-lactic acid (ILA), a direct ligand of the aryl hydrocarbon receptor (AhR). Antibiotic perturbation abrogated ILA production, AhR activation and Treg-Th17 remodeling, whereas transfer of helminth-conditioned fecal preparations or supplementation with L. murinus or ILA restored these responses. Pharmacological inhibition or genetic deletion of AhR eliminated the protection conferred by T. spiralis, L. murinus and ILA against endotoxin-induced lung injury. In lethal SARS-CoV-2 infection, oral ILA improved survival and limited pulmonary immunopathology without reducing viral burden, thereby uncoupling host protection from pathogen control. In a human COVID-19 cohort, ILA relative abundance remained inversely associated with IFN-γ after adjustment for available clinical covariates. These findings reveal that helminths can reprogram commensal metabolism to govern systemic immune tolerance and identify microbial ILA production as a tractable postbiotic strategy for limiting inflammatory tissue damage.