Patients whose allergies cause the sniffles have different fungi living in their noses, compared to healthy people

(Press-News.org) Nearly a quarter of Portuguese adults have allergies that cause a runny nose. This respiratory disease, formally called allergic rhinitis and frequently associated with asthma, is a common problem around the world, and the upper airway is a key target for research into the underlying disease processes. Now a global team of researchers has discovered that patients with allergy-induced sniffles and asthma have different fungal colonies or mycobiomes in their noses, suggesting potential lines of enquiry for future treatments.  

“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 Dr Luís Delgado of the University of Porto, Portugal, one of the authors of the article in Frontiers in Microbiology. “This may suggest that allergic rhinitis increases the diversity and changes the composition of the upper airway’s microbiome.” 

A miniature mycological world 

Allergic rhinitis causes sneezing, itching, inflamed nasal mucous membranes, and a blocked and runny nose. It’s often comorbid with asthma, which also involves inflammation and obstructed airways. Allergic rhinitis and asthma may even be different aspects of the same airway inflammatory disease, which makes it critical to identify the links between them and the underlying causes.  

To study the nasal mycobiome, the researchers recruited 214 participants from among children and young adults attending an immunology and asthma clinic in Porto. 155 patients had both allergic rhinitis and asthma, while 47 were only diagnosed with allergic rhinitis and 12 with asthma. 125 healthy controls were also enrolled. 

The scientists took samples from the participants’ noses using nasal swabs and sequenced the fungal DNA they found, focusing on two specific regions to identify different fungal species and develop an overview of each participant’s mycobiome. After quality controls, they had 306 samples to work with.  

They then used network analysis to understand the relationships between different genera of fungi, and to characterize the different communities of fungi present in healthy and sick participants. They also investigated the function of different fungi, looking at the metabolic pathways they affect, to try to understand the implications of any mycobiome variation between the groups of patients.   

Coughs and sneezes 

The most common families of fungi across all samples were Ascomycota and Basidiomycota. In these two families, 14 genera dominated the mycobiomes. 

“Among these dominant genera we detected common fungi that have been recognized in humans as allergenic or opportunistic pathogenic fungi,” said Delgado. “This suggests that the nasal cavity is a major reservoir for fungi that could be involved in allergic rhinitis and asthma.” 

There was a very clear and statistically significant difference between the patients with respiratory diseases and the healthy controls – and no significant difference between the different groups of patients with respiratory diseases. The patients with respiratory diseases had more diverse and richer mycobiomes. The fungi sampled from patients with both allergic rhinitis and asthma also showed more evidence of connections between them than the fungi in the healthy participants’ noses and those who only had allergic rhinitis. This could indicate that the fungi are affecting the nose’s immune environment.  

The scientists also found that three metabolic pathways associated with the production of a building block for DNA and RNA — 5-aminoimidazole ribonucleotide or AIR — were overabundant in the mycobiome of patients with allergic rhinitis and asthma. AIR is linked to purine production, necessary for energy metabolism and DNA synthesis. If further studies confirm this link and identify the exact problem, AIR could be a future therapeutic target for treatment or diagnosis. 

“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,” Delgado cautioned, explaining that the study’s cross-sectional design gives a broad picture, but doesn’t show how the mycobiome changes over time. Longitudinal studies might give a better idea of whether fungi drive disease processes, and if so which fungi are responsible. 

“Addressing some of these clinical variables would be interesting follow-ups of our study, if we could get the appropriate funding,” said Delgado. “If we cannot go further at this stage, the key data and hypothesis are published here for others to replicate, and to finally link the laboratory bench to the clinic.” 

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