Relationship of Microbial Profile With Airway Immune Response in Eosinophilic or Neutrophilic Inflammation of Asthmatics.

PURPOSE

Different characteristics of airway microbiome in asthmatics may lead to differential immune responses, which in turn cause eosinophilic or neutrophilic airway inflammation. However, the relationships among these factors have yet to be fully elucidated.

METHODS

Microbes in induced sputum samples were subjected to sequence analysis of 16S rRNA. Airway inflammatory phenotypes were defined as neutrophils (>60%) and eosinophils (>3%), and inflammation endotypes were defined by levels of T helper (Th) 1 (interferon-γ), Th2 (interleukin [IL]-5 and IL-13), Th-17 (IL-17), and innate Th2 (IL-25, IL-33, and thymic stromal lymphopoietin) cytokines, inflammasomes (IL-1β), epithelial activation markers (granulocyte-macrophage colony-stimulating factor and IL-8), and Inflammation (IL-6 and tumor necrosis factor-α) cytokines in sputum supernatants was assessed by enzyme-linked immunosorbent assay.

RESULTS

The numbers of operational taxonomic units were significantly higher in the mixed (n = 21) and neutrophilic (n = 23) inflammation groups than in the paucigranulocytic inflammation group (n = 19; < 0.05). At the species level, , , , , , and levels were significantly higher in the eosinophilic inflammation group (n = 20), whereas levels were significantly higher in the neutrophilic inflammation group compared to the other subtypes ( < 0.05). Additionally, IL-5 and IL-13 concentrations were correlated with the percentage of eosinophils ( < 0.05) and IL-13 levels were positively correlated with the read counts of and ( < 0.05). IL-1β concentrations were correlated with the percentage of neutrophils ( < 0.05). had a tendency to be positively correlated with the read count of ( = 0.095), and was negatively correlated with that of ( < 0.05).

CONCLUSIONS

Difference of microbial patterns in airways may induce distinctive endotypes of asthma, which is responsible for the neutrophilic or eosinophilic inflammation in asthma.