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Fluconazole worsened lung inflammation, partly through lung microbiome dysbiosis in mice with ovalbumin-induced asthma

Summary

Fluconazole is an antifungal medication that works well for treating asthma caused by fungal infections, but may actually worsen asthma from other causes. In mice with allergic asthma, fluconazole killed beneficial bacteria and promoted the growth of harmful bacteria that increased inflammation. This study suggests that fluconazole should only be used for fungal-related asthma and careful monitoring is needed if used in patients with regular asthma.

Background

Asthma is a chronic inflammatory airway disease with innate immunity influenced by lung microbiota alterations. Fluconazole is commonly used as an antifungal agent, but its effects on asthma remain inconclusive, as it may reduce fungal burdens in some cases while altering bacterial populations in others.

Objective

This study investigates the effects of fluconazole treatment on lung inflammation and microbiome composition in ovalbumin-induced asthma in C57BL/6 mice, and examines the role of bacterial and fungal components in pulmonary cell inflammation.

Results

Fluconazole-treated asthma mice showed higher serum and lung cytokine levels (TNF-α and IL-6), increased pathological scores, and elevated mononuclear cells compared to untreated asthma mice. Fluconazole induced dysbiosis with reduced Firmicutes and increased Bacteroidota, and increased LPS-producing Gram-negative bacteria. In vitro studies demonstrated synergistic pro-inflammatory effects of lipopolysaccharide and beta-glucan on pulmonary cells.

Conclusion

Fluconazole exacerbated lung inflammation in ovalbumin-induced asthma partly through lung microbiome dysbiosis and the synergistic effects of bacterial lipopolysaccharide and fungal beta-glucan. Fluconazole should be reserved for treating fungal-related asthma rather than asthma from other etiologies, and its use in regular asthma patients requires careful monitoring.
  • Published in:PeerJ,
  • Study Type:Experimental Animal Study with In Vitro Analysis,
  • Source: PMID: 39484217, DOI: 10.7717/peerj.18421
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