Mycoplasma pneumoniae infection impairs asthma control in pediatric patients and exacerbates allergic airway inflammation

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OBJECTIVE: To analyze the effect of Mycoplasma pneumoniae (M. pneumoniae) infection on asthma control and its underlying characteristic mechanisms, and to provide evidence-based support for the clinical management of asthma control in children with asthma. METHODS: We enrolled children with asthma and performed a retrospective medical record review, M. pneumoniae detection and isolation from respiratory samples, in vitro antibiotic susceptibility testing, and metabolomic sequencing of bacteria. An ovalbumin-induced allergic asthma model was established using BALB/c mice, which were further divided into the M. pneumoniae-infected asthma group and the non-infected asthma group. Bronchoalveolar lavage fluid from the mice was subjected to detection of M. pneumoniae DNA and 16 S rRNA gene sequencing. Lung tissues were processed for hematoxylin-eosin staining to assess inflammatory infiltration. Periodic acid-Schiff staining was used to evaluate mucus hypersecretion. Metabolomic profiling and transcriptomic analysis were also performed. RESULTS: We included 145 children with asthma in the clinical cohort. The uncontrolled asthma rate in patients with asthma and M. pneumoniae co-infection was significantly higher than that in patients with asthma only. Among the respiratory specimens, 28 M. pneumoniae nucleic acid-positive samples were identified as genotype M4-5-7-2, and all of these strains carried an A2063G mutation in the 23 S rRNA gene. In the murine asthma model, M. pneumoniae infection significantly exacerbated allergic asthma. Specifically, M. pneumoniae infection led to aggravated allergic symptoms, increased airway hyperresponsiveness, elevated serum immunoglobulin E levels, and higher pathological scores in lung tissue as shown by hematoxylin-eosin staining and periodic acid-Schiff staining. Consistently, 16 S rRNA gene sequencing and transcriptomic and metabolomic analyses showed that M. pneumoniae infection was accompanied by changes in respiratory microbiota composition and altered the phosphatidylinositol 3-kinase/protein kinase signaling pathway, as well as variations in butanoate metabolism profiles. Notably, the changes of butanoate metabolism may be correlated with sophorose, which is a metabolite produced by M. pneumoniae. CONCLUSION: This study shows that M. pneumoniae infection reduces the level of asthma control in pediatric patients with asthma. In the murine asthma model, M. pneumoniae infection exacerbates allergic airway inflammation, which may be correlated with altered butanoate metabolism induced by the infection.

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