News
Article
Author(s):
These findings indicate that asthma and allergic rhinitis may be commonly linked, emphasizing the need to identify underlying causes.
A recent study published in Frontiers in Microbiology provides data that help further understand the relationships between the nasal mycobiota and allergy-related conditions, such as allergic rhinitis with or without asthma. The findings show that the nasal mycobiota varies during health and allergic rhinitis with or without comorbid asthma, of which certain pathways and fungal interactions may relate to chronic airway disease.1
According to the investigators, nearly a quarter of Portuguese adults—where the study was conducted—report experiencing allergies that cause a runny nose. This respiratory disease, called allergic rhinitis, is frequently associated with asthma. Allergic rhinitis and asthma are believed to be different aspects of the same airway inflammatory disease, making the identification of links between the conditions crucial in understanding underlying causes.1,2
For this study, the investigators used an internal transcriber spacer 1 and 2 as well as next-generation sequencing to characterize the nasal mycobiomes of both pediatric and adult patients with allergic rhinitis (with and without asthma), asthma, and healthy controls. The authors describe the fungal taxonomic and functional profiles across the enrolled groups, comparing their composition, structure, metabolism, and network interactions. The enrolled 339 patients were also part of the ASMAPORT Project, which was a cross-sectional study of Portuguese patients—both adults and children—designed to investigate host-microbe during asthma and rhinitis.1
Patients were enrolled and categorized into the following 4 clinical groups: allergic rhinitis (n = 47); allergic rhinitis with asthma (n = 155); asthma (n = 12); and healthy controls (n = 125). The investigators collected nasal swabs from the participants for their analysis. Additionally, patients had a median age of about 12.5 ± 5.0 years and most (53.7%) were female.1
According to the findings, 7 to 10 of the 14 most abundant fungal genera (eg, Malassezia, Alternaria, Cladosporium, Penicillium, among others) differed significantly between the 4 groups. Despite this finding, none of the same genera varied significantly between the 3 respiratory disease groups. The nasal mycobiomes of those with allergic rhinitis and allergic rhinitis with asthma demonstrated the highest intra-group diversity, whereas the healthy controls showed the lowest. Additionally, alpha-diversity indices of microbial evenness only varied significantly (p ≤ .024) between those with allergic rhinitis or allergic rhinitis with asthma and the healthy controls, while all disease groups showed significant differences (p ≤ .0004) in microbial structure (eg, beta-diversity indices) when compared to the controls.2
“We showed that allergic rhinitis samples displayed a significantly higher fungal diversity and a different fungal community structure compared to those of healthy controls,” said study author Dr Luís Delgado of the University of Porto, Portugal, in a news release. “This may suggest that allergic rhinitis increases the diversity and changes the composition of the upper airway’s microbiome.”2
Further, the samples also showed that patients who had respiratory diseases had more diverse and richer mycobiomes. The fungi samples from patients who had allergic rhinitis and asthma also demonstrated more evidence of connections between the 2 conditions than the fungi in healthy controls and patients who only had allergic rhinitis. This finding signaled to the authors that the fungi may be contributing to the patient’s nasal immune environment.1,2
“Among these dominant genera we detected common fungi that have been recognized in humans as allergenic or opportunistic pathogenic fungi. This suggests that the nasal cavity is a major reservoir for fungi that could be involved in allergic rhinitis and asthma,” said Delgado in the news release. “However, we could not control all patient-specific variables, such as disease severity and related treatment levels, and patients were sampled at a single time. Addressing some of these clinical variables would be interesting follow-ups of our study, if we could get the appropriate funding.”2
REFERENCES