ArticleMicrobiome2026
Faecalibacterium prausnitzii in the gut protects against acute lung injury in influenza through butyrate educated reparative CD4
Article in Microbiome, 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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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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12 authors.
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Abstract
backgroundUncontrolled pneumonia induced by influenza virus infection results in severe lung pathology. Timely and proper tissue self-repair is critical to improve survival. This study aimed to identify probiotic strains that confer protection against acute lung injury induced by influenza virus infection and to elucidate the underlying molecular mechanisms.
resultsSignificant structural alterations in the gut microbiota were observed in influenza patients, characterized by a marked depletion in Faecalibacterium prausnitzii, whose abundance was negatively correlated with disease severity. In a murine model of influenza infection, oral administration of Faecalibacterium prausnitzii and its culture supernatant markedly alleviated lung injury. Targeted metabolomic analysis identified butyrate as the principal metabolite produced by Faecalibacterium prausnitzii that mediates lung tissue protection. Single-cell RNA sequencing further revealed that butyrate promotes the differentiation of pulmonary CD4⁺T cells into a reparative phenotype with enhanced interleukin-22 (IL-22) production. Mechanistically, butyrate facilitates IL-22 secretion through monounsaturated fatty acid biosynthesis via a histone-acetylation-dependent NR4A1-SCD1 axis. Accumulated monounsaturated fatty acids further enhance mitochondrial activities, which are essential for robust IL-22 production. Utilizing an IL-22 knockout mouse model, we confirmed the indispensable protective role of IL-22 in this gut-lung axis during influenza infection.
conclusionOur findings demonstrate that butyrate, derived from intestinal commensal Faecalibacterium prausnitzii, plays a crucial role in maintaining pulmonary tissue homeostasis during influenza infection by modulating intrinsic lipid metabolism in CD4
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