ArticleCNS neuroscience & therapeutics2026
Oral Lysozyme Attenuates Neuroinflammation and Brain Injury After Traumatic Brain Injury Through Gut Microbiota-Dependent Reprogramming of Tryptophan Metabolism.
Article in CNS neuroscience & therapeutics, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
aimsTraumatic brain injury (TBI) induces secondary neuroinflammation and gut dysbiosis. This study investigated whether oral lysozyme confers neuroprotection after TBI through gut microbiota-dependent metabolic reprogramming of tryptophan metabolism.
methodsIn a severe TBI mouse model, neurological function, neuroinflammation, intestinal barrier integrity, and systemic immune homeostasis were assessed following oral lysozyme administration. Fecal untargeted metabolomics, antibiotic-mediated microbiota depletion, and fecal microbiota transplantation (FMT) were used to explore microbiota involvement. Cerebrospinal fluid (CSF) from 10 matched pairs of patients with severe TBI was analyzed for tryptophan pathway metabolites by liquid chromatography-mass spectrometry.
resultsLysozyme improved neurological outcomes, attenuated neuronal apoptosis and neuroinflammation, and restored peripheral CD4
conclusionsOral lysozyme was associated with attenuated TBI-induced neuroinflammation and brain injury, potentially through gut microbiota-dependent tryptophan metabolism reprogramming. Concordance between preclinical and clinical metabolomic data supports lysozyme as a candidate microbiota-targeted therapeutic strategy. The KYNA/QA ratio warrants further validation as a prognostic indicator in larger, longitudinal cohorts.
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