What question did this study set out to answer?

To investigate the protective effects of Lactiplantibacillus plantarum GUANKE against influenza A virus-induced lung damage and inflammation.

February 13, 2026Open Access

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

Key Points

To investigate the protective effects of Lactiplantibacillus plantarum GUANKE against influenza A virus-induced lung damage and inflammation.
Conducted experiments using C57BL/6 murine models infected with influenza A virus.
Administered GUANKE supplementation at 5 × 10^9 CFU/day and linoleic acid at 40 mg/kg.
Measured inflammatory cytokine levels and pulmonary barrier protein expression.
Analyzed mitochondrial function, specifically mitophagy and oxidative phosphorylation.
GUANKE supplementation significantly reduced inflammatory cytokine secretion.
GUANKE counteracted the downregulation of pulmonary barrier proteins caused by the virus.
Enhanced Parkin-dependent mitophagy was observed with GUANKE and linoleic acid supplementation.
Restored oxidative phosphorylation capacity was confirmed in IAV-infected mice.

Abstract

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.

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Cite This Study

Lu et al. (Tue,) studied this question.

synapsesocial.com/papers/698ebeb185a1ff6a930160cf https://doi.org/https://doi.org/10.1007/s00018-026-06081-9

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