08/23/2026
Nasal Microbiome is Different from Gut Microbiome
Richard Downs, DDS
Nefense.com
For years, when we talked about the human microbiome, most of the attention went to the gut. That made sense. The intestinal tract contains an extraordinarily large and diverse population of microorganisms that influence digestion, metabolism, immune function, and human health.
There is another microbiome that deserves more attention, and we encounter it with every breath we take. It is the nasal microbiome.
The nose is not simply a passageway that carries air to the lungs. It is a sophisticated filtration and defense system. Every day the nasal passages encounter bacteria, viruses, allergens, dust, pollution and other environmental material. Mucus, cilia, the epithelial barrier, the immune system and the microorganisms living on these surfaces all play a role in what happens.
The nasal microbiome is not a smaller version of the gut microbiome. It is a lower-biomass, more restricted microbial ecosystem with its own distinct community patterns. Common organisms include members of the genera Corynebacterium, Dolosigranulum, Staphylococcus and Cutibacterium. A large 2026 study involving more than 1,600 adults identified nine distinct nasal microbial community-state types, demonstrating that there is not one single “normal” nasal microbiome.[1]
The objective of nasal health should not simply be to kill bacteria. The objective is to maintain a healthy nasal environment.
Microorganisms living in the nose interact and compete with one another for space and nutrients. Some normal residents may actually make it more difficult for potentially pathogenic organisms to establish themselves. Research involving organisms such as Dolosigranulum and Corynebacterium demonstrates that bacterial competition is an important part of upper-airway ecology.[1-3]
Finding Staphylococcus in the nose does not necessarily mean disease. Staphylococcus epidermidis, for example, is commonly found on healthy skin and nasal surfaces. Even potentially pathogenic organisms can sometimes be carried without causing disease. The more important question may be what has happened to the environment in which those organisms are living.
Inflammation, antibiotic exposure, impaired mucociliary clearance, changes in mucus, disruption of the epithelial barrier, environmental exposures and competition among microorganisms can influence which organisms survive and which become more prominent. Studies of chronic rhinosinusitis have repeatedly found alterations in the nasal microbial community, although the exact pattern is not the same in every patient or every study.[4-7] This disruption of the normal microbial ecosystem is generally referred to as dysbiosis.
There is still a question that has not been completely answered. Does dysbiosis help produce chronic inflammation, or does an inflamed and damaged nasal environment produce dysbiosis? It’s a “chicken or egg” type question.
Bacteria do not always live as individual organisms floating freely in nasal mucus. Some attach to surfaces and organize themselves into communities surrounded by an extracellular matrix. These communities are called biofilms. Bacteria living within biofilms can behave very differently from free-floating bacteria. Their metabolism and gene expression can change, and their susceptibility to antimicrobial agents and immune defenses can decrease. Biofilms have therefore become an important area of investigation in chronic rhinosinusitis.[8]
This brings us to MARCoNS. MARCoNS stands for Multiple Antibiotic Resistant Coagulase-Negative Staphylococci. Coagulase-negative staphylococci include organisms such as Staphylococcus epidermidis that normally inhabit human skin and mucosal surfaces. Therefore, simply finding a coagulase-negative Staphylococcus in the nose does not establish disease.
Some strains can acquire resistance to multiple antibiotics and can participate in biofilm formation. This has generated considerable interest in MARCoNS, particularly among practitioners treating patients with chronic inflammatory illnesses. There is interesting biology, but the science does not establish MARCoNS as an independent cause of the many systemic symptoms sometimes attributed to it. Colonization is not the same thing as infection, and association does not prove causation.
There may also be an important connection between the nasal environment and sleep. Chronic nasal inflammation, congestion and increased nasal resistance can make nasal breathing more difficult and encourage mouth breathing during sleep. Nasal obstruction does not by itself establish the cause of obstructive sleep apnea, and studies have not consistently shown that reducing nasal resistance lowers the apnea-hypopnea index. However, nasal obstruction may contribute to sleep fragmentation, subjective sleep problems and difficulty using positive airway pressure therapy.[20] Computational fluid dynamics research in patients with obstructive sleep apnea has also demonstrated that oral breathing produces airflow and pressure characteristics more favorable to pharyngeal airway collapse than nasal breathing with the mouth closed.[21]
This does not mean that MARCoNS causes sleep apnea. It does mean that if chronic inflammation or a disturbed nasal environment interferes with nasal breathing, the consequences may extend beyond the nose.
MARCoNS and α-MSH
A 2026 study added an interesting piece to this discussion. Researchers retrospectively examined 188 adults being treated within a Chronic Inflammatory Response Syndrome framework who initially had positive MARCoNS cultures. They compared patients who remained MARCoNS-positive with patients who subsequently became MARCoNS-negative.
Patients who became MARCoNS-negative demonstrated higher circulating alpha-melanocyte-stimulating hormone, or α-MSH, trajectories than those who remained MARCoNS positive.[19] α-MSH is often associated with pigmentation, but it also participates in immune regulation, inflammatory signaling and neuroendocrine communication.
The investigators also examined matrix metalloproteinase-9, or MMP-9, and vasoactive intestinal peptide, or VIP. MMP-9 is a zinc-dependent enzyme involved in extracellular-matrix remodeling. Neutrophils and other inflammatory cells can release MMP-9, and excessive activity can contribute to inflammatory tissue and barrier changes.
VIP is a neuropeptide called vasoactive intestinal peptide. Despite its name, it is not confined to the gastrointestinal tract. VIP participates in vascular regulation, smooth-muscle activity, glandular secretion and communication between the nervous and immune systems. Interestingly, the MARCoNS-specific relationship observed with α-MSH was not demonstrated with MMP-9 or VIP.[19]
That finding deserves further investigation, but it does not demonstrate that MARCoNS causes low α-MSH or that eliminating MARCoNS restores normal neuroendocrine function. The study was retrospective and observational, and patients were receiving other interventions.
The Nose, Immune System and Nervous System
The nasal mucosa is an immunologically active tissue. The epithelial cells lining the nose do much more than create a physical wall. They recognize microbial and environmental signals and communicate with immune cells. The nasal cavity also contains sensory nerves, blood vessels, mucus-producing cells, antimicrobial molecules and resident microorganisms.
This creates an important intersection between microbiology, immunology and neurology. We have become accustomed to hearing about the gut-brain axis. The upper respiratory tract also communicates with the nervous and immune systems. That does not mean bacteria living in the nose are routinely entering or “infecting” the brain. The more appropriate concept is communication among the nasal mucosa, nervous system and immune system.
What Does This Mean for Nasal Hygiene?
For decades, nasal hygiene largely meant saline. Saline, particularly normal saline, remains useful. Nasal irrigation can mechanically remove mucus, allergens, particulate matter and accumulated secretions and is well established as an adjunct in the management of chronic sinonasal symptoms.[9]
Compounds other than saline can provide additional benefits. Two compounds that have received increasing attention are hypochlorous acid and xylitol.
Hypochlorous Acid and Innate Immunity
Hypochlorous acid, or HOCl, is interesting because our immune system already makes it. Activated neutrophils use the enzyme myeloperoxidase to generate HOCl as part of the oxidative system used to kill microorganisms. HOCl is therefore not simply an antimicrobial chemical. It is one of the molecules used by our own innate immune defenses.
Low-concentration HOCl solutions have been investigated for nasal use. In a prospective randomized placebo-controlled study of adults with chronic sinonasal symptoms that had persisted despite medical treatment, low-concentration HOCl nasal irrigation resulted in improvement in symptoms, with some outcomes favoring HOCl over saline.[10]
HOCl has also been investigated in children with chronic sinusitis. Both saline and HOCl irrigation improved symptoms, while radiographic improvement was greater in the HOCl group.[11]
Another randomized study evaluated a 0.02% HOCl nasal spray following Functional Endoscopic Sinus Surgery. HOCl improved postoperative endoscopic findings and demonstrated an overall clinical effect similar to saline irrigation.[12]
Laboratory research has also demonstrated that HOCl can kill bacteria contained within established staphylococcal biofilms.[13] This particular research was performed in vitro and was not a clinical nasal study. It therefore should not be interpreted as demonstrating that an HOCl nasal product eliminates sinonasal biofilms in patients.
There is another finding that I believe is particularly interesting when we consider the nasal microbiome. Wu and colleagues tested 0.01% HOCl against actual nasal secretions obtained from patients with chronic rhinosinusitis. After one minute of exposure, bacteria were recovered from 26 of 50 HOCl-treated specimens compared with 27 of 50 untreated specimens. After five minutes, bacteria were recovered from 14 of 32 specimens in both groups. In other words, short exposure to HOCl did not significantly reduce recoverable bacteria from these human nasal secretions.[14]
This does not prove that HOCl has no effect on the nasal microbiome. The researchers used bacterial cultures rather than microbiome sequencing, and we should not claim more than the study demonstrated. What it does show is that the antimicrobial activity demonstrated with HOCl under laboratory conditions does not necessarily translate into indiscriminate bacterial killing in the complex environment of nasal mucus. Mucus, proteins, organic material, concentration and contact time all matter.
None of these clinical studies evaluated HypoNasal. They evaluated other HOCl formulations at concentrations and under conditions specified by the individual investigators. Their findings therefore support continued interest in HOCl as a molecule for nasal use, but they cannot be used as clinical evidence that HypoNasal itself produces the same outcomes.
Xylitol and the Nasal Environment
Most dental professionals know xylitol because of its long history in oral health. Xylitol has also been investigated as a nasal irrigant.
A randomized pilot study reported improvement in chronic rhinosinusitis symptoms with xylitol irrigation.[15] Subsequent randomized studies have continued to investigate xylitol in patients with chronic rhinosinusitis and following sinus surgery.[16-18]
One finding is particularly interesting from an airway perspective. A 2017 study comparing xylitol and saline irrigation reported increased nasal nitric oxide and increased expression of inducible nitric oxide synthase following xylitol treatment.[16]
Nitric oxide is an important part of upper-airway physiology. The paranasal sinuses are an important source of nasal nitric oxide, which participates in airway physiology and innate host defense.
A 2024 randomized controlled study following Functional Endoscopic Sinus Surgery also reported a reduction in the prevalence of Staphylococcus aureus in nasal secretions following two months of xylitol irrigation.[17] Other microbial changes were also observed, so the study should not be interpreted to mean that xylitol simply eliminates undesirable bacteria while leaving every beneficial organism untouched.
The evidence for xylitol became more substantial with a 2026 systematic review and meta-analysis. Seven studies involving a total of 263 participants were evaluated. Xylitol irrigation produced significantly greater improvement in subjective sinonasal outcomes than saline. However, pooled objective measures, including endoscopic findings, olfactory function and mucociliary clearance, did not demonstrate significant overall differences.[18]
Again, these studies did not evaluate XyloClean. They investigated other xylitol formulations and methods of nasal irrigation. The findings support scientific interest in xylitol for nasal use, but they do not constitute clinical trials of XyloClean and should not be presented as though they do.
We Should Not Be Trying to Sterilize the Nose
One of the most important lessons coming from microbiome research is that bacteria are not the enemy. The healthy nose contains bacteria. The objective of nasal hygiene should therefore not be to sterilize the nasal passages. It should be to support an environment in which mucus, cilia, epithelial cells, immune defenses and the normal microbial community can function together.
This is especially important when discussing antimicrobial products. The finding that short-term exposure to HOCl did not significantly reduce recoverable bacteria from human nasal secretions is reassuring in this context, but it is not the same as demonstrating preservation of the microbiome.[14] We still need studies using modern sequencing techniques to determine what repeated HOCl exposure does to nasal microbial diversity and community composition over time.
A Different Way to Think About the Nose
There is mucus. There are cilia. There is an epithelial barrier. There are immune cells. There are antimicrobial molecules. There is nitric oxide. There are resident microorganisms interacting with one another and with us.
When this environment is healthy, these systems work together. When it becomes disturbed, simply trying to kill every microorganism we can find may not be the answer.
This is part of the thinking behind our interest in HOCl- and xylitol-based nasal products. HOCl is a molecule produced by our own innate immune system. Xylitol has been investigated in human studies for its effects on the nasal environment and chronic sinonasal symptoms.
HypoNasal and XyloClean themselves were not the products used in the studies discussed in this article. The published research helps us understand the biology of HOCl and xylitol and provides direction for further research, but it should not be used to claim clinical results for products that were not actually tested.
The science of the nasal microbiome is still developing. We do not yet know everything we need to know about how nasal hygiene products affect that ecosystem over months or years. What we do know is that the nose has its own ecology, and maintaining that environment deserves considerably more attention than it has received.
References
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