Lower airway microbiome and metabolomic profiles of recurrent wheezing in infants: a case-control study

Main Article Content

Jiebin Chen
Sainan Chen
Huiquan Sun
Yuqing Wang

Keywords

Recurrent wheezing, Microbiome, Metabolomics, Lower airway

Abstract

Objectives: To characterize the microbiome shifts and subsequent metabolite alterations associated with recurrent wheezing (RW) in infants.


Methods: A total of 33 subjects were enrolled in this study, including 18 infants diagnosed with RW, and 15 normal infants as controls. Bronchoalveolar lavage (BAL) fluid was collected from all the subjects. Bacterial DNA was then isolated and analyzed by 16S ribosomal RNA sequencing. In addition, the metabolomic profile of BAL fluid samples was analyzed with mass spectrometry using complementary chromatographic methods. Spearman’s rank correlation analysis was conducted to explore associations between microbial taxa and metabolites.


Results: The study had 21 (63.6%) boys and 12 (36.4%) girls. The mean age was 26.8 ± 4.9 months. Haemophilus (P = 0.003) and Porphyromonas (P = 0.007) genera showed significant difference between the two groups. The metabolites of “starch and sucrose metabolism pathway” and “pentose phosphate pathway” showed significant correlations with the two bacterial genera. For starch and sucrose metabolism pathway, glucose-6-phosphate showed significant positive correlations with Haemophilus (r = 0.44 and P = 0.009) and Porphyromonas (r = 0.45 and P = 0.008). For pentose phosphate pathway, Sedoheptulose 7-phosphate, an intermediate in the pentose phosphate pathway, showed significantly positive correlations with Haemophilus (r = 0.42 and P = 0.02) and Porphyromonas (r = 0.43 and P = 0.01).


Conclusions: Our study provided new evidence that alteration in respiratory tract microbiome could be associated with RW in infants. By elucidating the microbiome and metabolite profile, we identified novel biomarkers potentially useful for personalized management of RW in infants. The future studies should validate the underlying mechanisms in longitudinal cohorts and explore interventions targeting metabolic–microbial crosstalk.

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