It’s been known that asthmatic lungs are different from healthy
lungs in many aspects, including housing different strains of bacteria. So far, studies haven’t been able to tell
whether these differences are due to asthma, associated allergies (atopy), or
treatment with different drugs. They
also haven’t been able to determine how these differences affect the way asthma
manifests itself and how asthma can be treated.
In this month’s issue of JACI, Durack and colleagues aim to answer these
pressing questions (J Allergy Clin Immunol 2017; 140(1): 63-75).
Durack and other investigators looked at the bacterial
communities in 84 individuals, split into three groups: (1) 42 atopic asthmatic
subjects, (2) 21 atopic non-asthmatic subjects, and (3) 21 non-atopic
non-asthmatic, otherwise healthy, subjects.
They also looked at inflammatory markers and changes in bronchial
hyperresponsiveness after 6 weeks of treatment with fluticasone, an inhaled
steroid commonly used for asthma treatment.
What they found is that the types of bacteria in each of the
three groups were significantly different. This included the group with atopy
without asthma, suggesting that atopy itself is associated with different
patterns of bacterial colonization of the bronchi, but these patterns also
differed from those in the subjects with atopic asthma. The bacteria seen in the asthmatic patients expressed
genes for different metabolic pathways that result in products previously
linked to risks for asthma development.
And subjects with high levels of allergy/atopy-related inflammation
markers in their bronchial epithelium (“T2-high asthma”) had overall lower
amounts of bacteria. Differences were
also found in the asthmatic subjects who responded to fluticasone, in that
their bronchial bacteria were less different from those in healthy subjects
than were the bronchial bacteria in the non-responsive asthmatics.
Overall these findings suggest that bacterial composition in
the lungs is associated with various immunologic and clinical features of the
disease. It also suggests that targeting
these bacteria may be a way to help prevent, or even treat, asthma in the
future.