A better understanding of infantile asthma through the lung microbiota
Knowledge of the specific impact of the lung microbiota on childhood asthma–an expanding field of research–is still limited. To find out more, Korean researchers conducted a very detailed genetic analysis.
Their initial hypothesis was that the differences between the study groups could play a role in inflammation, the occurrence of respiratory tract lesions and the bronchial hyperresponsiveness associated with allergic asthma.
Their comparative study was based on the examination of nasopharyngeal samples from asthmatic children, children in remission from asthma (symptom-free and untreated for a year) and healthy children. Bacteria generally associated with infantile asthma (Firmicutes, including Streptococci and Staphylococci) were especially monitored. Result: each group had a different microbiota. The abundance of Streptococci in the asthma group was confirmed, while being present in greater numbers in the remission group. Staphylococci were relatively more numerous in the asthma group than in the other two groups. Enough to demonstrate a relationship between asthma severity and bronchial hyperresponsiveness, and to correlate the presence of specific bacteria in asthmatic children with disrupted maturation of their immune system. These are new findings which could partly explain the differences in the course of the disorder observed in children. More extensive studies will be needed to supplement these results.
A genetic approach to be pursued
In comparing these three groups at a very detailed genetic level, the researchers proved that the bacterial genes of their microbiotas interacted differently with the organism. One of the main results noted was the absence of a specific anti-inflammatory agent in the respiratory microbiota of asthmatic children. Prostaglandin E synthase–by its scientific name–is known for its protective role against bronchoconstriction (contraction of the bronchi which impedes the passage of air), one of the most important manifestations of asthma. Its absence could explain the persistence of asthma in the child. These specific genetic analyses need to be extended to better describe the link between pulmonary dysbiosis and the development of infantile asthma. The stakes are high since this could help identify prognostic methods to act against the development of infantile asthma, and eventually facilitate the development of new treatments.
Kim B. S., Lee E., Lee M.-J et al. Different functional genes of upper airway microbiome associated with natural course of childhood asthma. Allergy. 2018;73:644–652