<p>Pulmonary inflammatory response represents a predominant complication arising from influenza virus infections. This investigation elucidates the protective efficacy of <i>Lactiplantibacillus plantarum</i> GUANKE (GUANKE) supplementation against influenza A virus (IAV)-induced pulmonary damage in C57BL/6 murine models, with particular emphasis on its mechanistic underpinnings. The results showed that the use of GUANKE (5 × 10<sup>9</sup> CFU/day) or exogenous linoleic acid (a metabolite of GUANKE) supplementation (40&#xa0;mg/kg) significantly attenuated inflammatory cytokine secretion while counteracting virus-mediated downregulation of pulmonary barrier proteins. Mechanistic profiling revealed that GUANKE and GUANKE-derived linoleic acid modulates mitochondrial quality control through enhanced Parkin-dependent mitophagy coupled with restored mitochondrial oxidative phosphorylation (OXPHOS) capacity, thereby providing protection in IAV-infected mice.</p>

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Lactiplantibacillus plantarum GUANKE ameliorates influenza a virus-induced inflammation and lung barrier dysfunction through enhancing mitophagy and improving oxidative phosphorylation

  • Simin Lu,
  • Kun Yue,
  • Siqin He,
  • Jielan Mi,
  • Tao Yang,
  • Yuewen Yang,
  • Hanyu Ma,
  • Zhihong Ren,
  • Lili Ren,
  • Jianguo Xu

摘要

Pulmonary inflammatory response represents a predominant complication arising from influenza virus infections. This investigation elucidates the protective efficacy of Lactiplantibacillus plantarum GUANKE (GUANKE) supplementation against influenza A virus (IAV)-induced pulmonary damage in C57BL/6 murine models, with particular emphasis on its mechanistic underpinnings. The results showed that the use of GUANKE (5 × 109 CFU/day) or exogenous linoleic acid (a metabolite of GUANKE) supplementation (40 mg/kg) significantly attenuated inflammatory cytokine secretion while counteracting virus-mediated downregulation of pulmonary barrier proteins. Mechanistic profiling revealed that GUANKE and GUANKE-derived linoleic acid modulates mitochondrial quality control through enhanced Parkin-dependent mitophagy coupled with restored mitochondrial oxidative phosphorylation (OXPHOS) capacity, thereby providing protection in IAV-infected mice.