Kim HJ, Kim JH, Han S, Kim W
Clin Exp Otorhinolaryngol. 2022 Jun 8. doi: 10.21053/ceo.2021.01928. Epub ahead of print. PMID: 35680131.
Allergic rhinitis (AR) is an IgE and Th2-mediated inflammatory nasal disease. It originates from a sensitized immune response to inhaled allergens, which is thought to result from an imbalance in the Th1-Th2 immune regulation, resulting in increased levels of Th2 cytokines. Nasal ephitelial cells exposed to allergens induce Th2 inflammatory responses that spread to the upper airway mucosa. A commensalism host-microbial can be the basis of the innate immune responses in the nasal mucosa, and the microbial characteristics of the nasal mucus can impact the mechanisms of the initial allergic response. The aim of this study was to evaluate changes in the microbial composition in the nasal mucus of patients with AR and to understand the relationship between dysbiosis of the nasal microbiome and allergic inflammation.
The investigators analyzed the microbiota of 104 samples (n=42 participants with AR vs. n=30 healthy participants), in a total of 364,923 high-quality bacterial 16S ribosomal RNA-encoding gene sequence reads. The nasal mucus of healthy participants had mainly Proteobacteria (Ralstonia genus) and Actinobacteria (Propionibacterium genus) phyla, whereas the Firmicutes (Staphylococcus genus) phylum was significantly abundant in the nasal mucus of participants with AR. More sequencing data from 32 participants (healthy participants: n=15, AR patients: n=17) shown a greater abundance of Staphylococcus epidermidis, Corynebacterium
accolens, and Nocardia coeliaca, in 41.55% of mapped sequences in the nasal mucus of healthy participants. Patients with AR had a more pronounced dysbiosis of nasal microbiome and Staphylococcus aureus exhibited the greatest abundance (37.69%).
In conclusion, this study demonstrated that the nasal mucus of patients with AR have S. aureus–dominant dysbiosis, which suggests a role of host–microbial commensalism in allergic inflammation.