{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,5,28]],"date-time":"2026-05-28T16:02:00Z","timestamp":1779984120976,"version":"3.53.1"},"reference-count":66,"publisher":"Frontiers Media SA","license":[{"start":{"date-parts":[[2026,5,28]],"date-time":"2026-05-28T00:00:00Z","timestamp":1779926400000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"content-domain":{"domain":["frontiersin.org"],"crossmark-restriction":true},"short-container-title":["Front. Microbiol."],"abstract":"<jats:sec>\n                    <jats:title>Introduction<\/jats:title>\n                    <jats:p>\n                      Sepsis-induced acute lung injury (S-ALI) is a life-threatening condition in intensive care units. The gut-lung axis has recently emerged as an important regulator of pulmonary inflammation. However, the role of\n                      <jats:italic>Faecalibacterium prausnitzii<\/jats:italic>\n                      (\n                      <jats:italic>F. prausnitzii<\/jats:italic>\n                      ) in S-ALI remains unclear.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>\n                      In this study, 16S rRNA high-throughput sequencing revealed significant gut microbiota dysbiosis in S-ALI patients, characterized by a markedly reduced relative abundance of\n                      <jats:italic>F. prausnitzii<\/jats:italic>\n                      . Moreover, the depletion of this probiotic was associated with increased clinical inflammatory indices and disease severity. Subsequently, the effects of\n                      <jats:italic>F. prausnitzii<\/jats:italic>\n                      strain intervention on S-ALI were investigated in two S-ALI murine models, including cecal ligation puncture (CLP) and lipopolysaccharide (LPS)-induced models.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>\n                      We found that\n                      <jats:italic>F. prausnitzii<\/jats:italic>\n                      intervention significantly attenuated acute lung injury in sepsis by reducing inflammation and oxidative stress. Importantly,\n                      <jats:italic>F. prausnitzii<\/jats:italic>\n                      treatment restored gut microbial homeostasis by enhancing intestinal barrier integrity and increasing the production of short-chain fatty acids (SCFAs), particularly butyrate. Mechanistically, non-targeted metabolomics analysis revealed that the protective effects of\n                      <jats:italic>F. prausnitzii<\/jats:italic>\n                      may be associated with the modulation of arachidonic acid (AA) metabolism, accompanied by increased levels of the anti-inflammatory mediator lipoxin A4 (LXA4). In addition, the expression of Nrf2 and HO-1 was upregulated in the intervention group, suggesting a potential involvement of the LXA4-Nrf2-HO-1 signaling pathway. Correlation analysis further indicated complex interactions among gut microbiota, SCFAs, metabolomic profiles, and inflammatory and oxidative stress-related factors following\n                      <jats:italic>F. prausnitzii<\/jats:italic>\n                      intervention.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Discussion<\/jats:title>\n                    <jats:p>\n                      Collectively,\n                      <jats:italic>F. prausnitzii<\/jats:italic>\n                      ameliorates the progression of S-ALI by restoring gut microecology and may be associated with AA metabolism and oxidative stress-related pathways, which may contribute to a potential therapeutic strategy targeting the gut-lung axis and AA metabolic pathways.\n                    <\/jats:p>\n                  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