Objectives. Host–microbial commensalism can shape the innate immune responses in the nasal mucosa, and the microbial characteristics of the nasal mucus directly impact the mechanisms of initial allergic responses in the nasal epithelium. We sought to determine alterations of the microbial composition in the nasal mucus of patients with allergic rhinitis (AR) and to elucidate the interplay between dysbiosis of the nasal microbiome and allergic inflammation.Methods. A total of 364,923 high-quality bacterial 16S ribosomal RNA–encoding gene sequence reads from 104 samples from the middle turbinate mucosa of healthy participants and patients with AR was obtained and analyzed using the Quantitative Insights into Microbial Ecology pipeline.Results. We analyzed the microbiota in samples of nasal mucus from patients with AR (n = 42) and clinically healthy participants (n = 30). Proteobacteria (Ralstonia genus) and Actinobacteria (Propionibacterium genus) phyla were predominant in the nasal mucus of healthy subjects, whereas the Firmicutes (Staphylococcus genus) phylum was significantly abundant in the nasal mucus of patients with AR. Especially, Ralstonia genus were significantly dominant in the clinically healthy subjects. Additional pyrosequencing data from 32 subjects (healthy participants: N=15, AR patients: N=17) revealed a greater abundance of Staphylococcus epidermidis, Corynebacterium accolens, and Nocardia coeliaca, accounting for 41.55% of mapped sequences in the nasal mucus of healthy participants. The dysbiosis of nasal microbiome was more pronounced and Staphylococcus aureus exhibited the greatest abundance (37.69%) in the presence of microbial distribution in the nasal mucus of patients with AR depending on the positive response to house dust mites and patient age and height. Conclusions. This study revealed alterations in the nasal microbiome that occur in the nasal mucus of patients with AR at the levels of microbial genera and species. S. aureus–dominant dysbiosis was distinctive in the nasal mucus of patients with AR, suggesting a role of host–microbial commensalism in allergic inflammation.