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The murine lung microbiome is dysbalanced by the human pathogenic fungus Aspergillus fumigatus resulting in enrichment of anaerobic bacteria

ABSTRACT: Here, we report significant changes in the composition of the lung microbiome and metabolome of mice under immune suppression, infection of immunosuppressed mice with virulent and avirulent strains of the clinically important human-pathogenic fungus Aspergillus fumigatus, and treatment with the clinically used antifungal drug voriconazole. Our data also indicate the important role of the gut microbiome for the lung homeostasis mediated by the plasma metabolome. In the lung microbiome, infection by A. fumigatus led to a significant increase of anaerobic bacteria, most prominently of Ligilactobacillus murinus. We also isolated live bacteria including L. murinus from the murine lower respiratory tract. In vitro, L. murinus is tolerated and even internalized by alveolar epithelial cells. Co-cultivation of L. murinus and A. fumigatus led to a reduction in oxygen concentration accompanied by an increase of L. murinus cells suggesting that A. fumigatus establishes a microaerophilic niche, thereby promoting growth of anaerobic bacteria.

INSTRUMENT(S): Liquid Chromatography MS - alternating - reverse phase

PROVIDER: MTBLS12262 | MetaboLights | 2025-07-04

REPOSITORIES: MetaboLights

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			Action	DRS
	220801-LC1-NEG-1-003-Blank_001.mzML	Mzml
	220801-LC1-NEG-1-004-RP-SST.mzML	Mzml
	220801-LC1-NEG-1-005-Blank_002.mzML	Mzml
	220801-LC1-NEG-1-006-QC_001.mzML	Mzml
	220801-LC1-NEG-1-009-QC_002.mzML	Mzml

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Project description:Background: The microbiome is increasingly being linked to cancer risk. Little is known about the lung and oral cavity microbiomes in healthy smokers (SM), and even less for electronic cigarette (EC) users, compared healthy never-smokers (NS). Methods: In a cross-sectional pilot study of SM (N=8), EC users (N=10) and NS (N=10) saliva and bronchoscopy-collected bronchoalveolar lavage samples were collected. Bacteria species were identified through metatranscriptome profiling by RNA-sequencing to study associations with the lung and oral microbiome. Pairwise comparisons and linear modeling was assessed with false discovery rates <0.1. Results: Total bacterial load was similar for the SM, EC users and NS, and there was no differences in the bacterial diversity across groups. In the lung, there were 44 bacterial species that were statistically significantly different for SM/NS, 80% of which were decreased in the SM. There were 12 bacterial species that were different for SM/EC users, all of which were decreased, 10 of which were also identified in the SM/NS comparison. The 2 bacterial species unique to SM/EC comparison were Neisseria sp. KEM232 and Curvibacter sp. AEP1-3. From the top 5 decreased species in SM/EC, 3 were also identified in the SM/NS comparison (Neisseria elongata, Neisseria sicca, and Haemophilus parainfluenzae) and 2 of these were unique to the SM/EC comparison (Neisseria zoodegmatis and Ottowia sp. oral taxon 894). There were 8 species increased in SM compared to NS, none of which are known to be clinically significant. In the oral microbiome, 152 bacteria species were differentially abundant for the SM/NS analysis, and only 17 for the EC/NS comparison, all which were also present in SM/NS comparisons. There were 21 bacteria that were differentially abundant in both the lung and oral cavity for SM and NS, 95% also were decreased in the SM. Conclusion: Smoking and EC use do not appear to materially affect the lung microbiome, although differences are noted of unclear clinical significance. Most differentially abundant bacteria decreased, which may be due to a toxic effect of cigarette smoke, including a change in humidity or heating. Given the low number of overlapping oral and lung microbes, the oral microbiome does not appear to be a good surrogate for smoking-related effects in the lung.

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The murine lung microbiome is dysbalanced by the human pathogenic fungus Aspergillus fumigatus resulting in enrichment of anaerobic bacteria

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