Allergies are on the rise, however, there’s still a great deal we don’t know about what causes them. A new study published on December 17 in Frontiers on Microbiology investigates how allergic rhinitis and asthma might be affected by our nasal mycobiome—or in less technical terms, the fungi that live in our noses.
Our airways interact constantly with our environment. This makes their immune response a vital defense against disease. We’ve long been aware that the nasal cavity can function as a reservoir for bacteria, and that if pathogenic bacteria establish themselves there, they can spread to other parts of the respiratory tract and cause respiratory illnesses.
However, bacteria aren’t the only things that can take up residence in our nasal cavities. Our noses host multiple species of fungi—and as Luis Delgado, one of the study’s authors, tells Popular Science, “The role of the fungal communities residing in the upper airways in rhinitis and asthma is practically unknown.”
It’s no surprise that fungi live in our noses; every time we breathe in, we inhale startling quantities of fungal spores. How many? “Fungal spores have been calculated to represent more than 50,000 spores per cubic meter of air during specific fungal seasons,” Delgado says. However, most of these spores simply come and go; we breathe them in, and then breathe them out again. As Delgado explains, being exposed to a variety of spores might even be beneficial, as demonstrated by what he calls “the farm effect,” where people who grow up in “natural[ly] microbe-rich and microbe-diverse environments” like farms prove less susceptible to asthma and allergies.
Some of these spores do take up root in our noses, and in their study, Delgado and his team investigated whether there are any differences in the mycobiomes of people who suffer from allergic rhinitis, asthma, or both conditions, and those of people who do not have either condition. Their research found that “seven to ten of the 14 most abundant fungal genera in the nasal cavity differed significantly” between sufferers of these conditions and a control group.
It’s tempting to conclude that the fungi found in people with asthma and/or allergic rhinitis, but not in the control group, might be responsible for these conditions. However, Delgado cautions against drawing such direct conclusions: “Causal relation may not be inferred with our study design and results.” He also notes that “[while] the nasal cavity is a major reservoir for allergenic or opportunistic fungi (i.e. those that may be pathogenic in special circumstances), we should note that local/airways fungal infection and even fungal … sensitization/allergy are the exception, and not the rule, in the clinical presentation of allergic rhinitis and asthma.”
Nevertheless, the study’s results provide tantalizing hints that there is some relationship between the mycobiome and these conditions. It also raises questions about the theory of a “single airway disease,” which suggests that distinctions between allergic rhinitis, asthma, and similar conditions are largely arbitrary, and that all these conditions are manifestations of a combined airway inflammatory disease. This idea was advanced in the early 2000s and remains influential today–most notably, Delgado says, it “forms the basis of ARIA (Allergic Rhinitis and its Impact on Asthma) guidelines, currently widely used in the diagnostic and combined management of these diseases.”
However, as Delgado explains, several recent papers have challenged this idea, “suggest[ing] that rhinitis alone and rhinitis with comorbid asthma may represent two distinct diseases with different allergen sensitization.” There are several distinct differences between the two conditions and their responses to various treatments—and as it turns out, there are also distinct differences in the mycobiomes of participants suffering from only allergic rhinitis, those with asthma alone, and those with both conditions.
There also appear to be differences in the way the various species of fungi interact in each case. Delgado explains, “Interestingly, it was the group with rhinitis and comorbid asthma that showed a higher and more diverse mycobiome network with multiple positive and negative (competition) interactions among fungal taxa; healthy controls and rhinitis patients showed fewer significant interactions, all of which were positive (the connected microorganisms may benefit from the presence of the each other).”
This hints at an area for future research, especially because, as Delgado points out, “Previous research has shown that changes of the patterns of co-abundance and exclusion can be indicative of underlying disease processes that may be disrupting the ‘healthy’ fungal connectivity and structure networks.” In other words, the differing nature of mycobiomes might be—to some extent, at least—a symptom of these conditions, rather than a cause.
There’s also the question of how the various bacteria and fungi in our nasal cavities might interact: “We did not address bacterial/fungal (micro/mycobiome) interactions in this study,” says Delgado. “[These] are possibly essential in a healthy respiratory microbiome network—or, on the other hand, may have specific positive or negative interactions facilitating airways inflammation and disease expression. Deciphering candidate fungal–bacterial interactions would be an interesting follow-up of our study.”
In truth, the intimidatingly complex interactions of the various denizens of our nasal passages will most likely take years of research to untangle. Nevertheless, this research suggests that to understand exactly why some of us are cursed with noses more susceptible to allergic conditions than others, we’ll have to get familiar with our nasal fungi.
