The Nasal Microbiome: An Overlooked Player in Autoimmune Disease

In recent years, the scientific community has increasingly recognized the critical role of the microbiome in regulating immune health. While much attention has been given to the gut microbiome, new research points to another important — and often overlooked — ecosystem: the nasal microbiome.

Disruptions in this delicate balance, known as nasal dysbiosis, are now being linked to the development and progression of several autoimmune diseases, including systemic lupus erythematosus (SLE) and rheumatoid arthritis.

Nasal Dysbiosis and Autoimmunity

A healthy nasal cavity is colonized by a diverse community of beneficial microbes that help regulate immune function, maintain mucosal health, and act as a frontline defense against pathogens. However, studies have shown that individuals with autoimmune diseases often exhibit a reduction in beneficial nasal bacteria and an overgrowth of pathogenic species (Manfredo Vieira et al., 2018; Perl, 2020).

One pathogen of particular concern is Staphylococcus aureus. Research has shown that S. aureus colonization is significantly more common in individuals with autoimmune conditions and may even precede disease flares (Baldan et al., 2020).

S. aureus can manipulate the immune system in several ways:

  • It produces superantigens that trigger widespread, inappropriate T-cell activation.

  • It secretes toxins that break down tissue barriers, allowing deeper colonization.

  • It stimulates the production of pro-inflammatory cytokines that contribute to systemic inflammation.

The result is a state of chronic immune activation that may accelerate or exacerbate autoimmune processes.

Staphylococcus aureus: More Than a Passenger

Colonization of the nasal cavity by Staphylococcus aureus is not merely incidental. In lupus, for example, higher rates of nasal S. aureus colonization have been linked to increased disease activity scores (Münz et al., 2015). In rheumatoid arthritis, nasal S. aureus may contribute to joint flares through systemic dissemination of inflammatory signals.

Given this connection, researchers are exploring ways to target and rebalance the nasal microbiome as a novel approach to autoimmune management.

Our Research: BioFilm Clear and Staphylococcus aureus

At BioFilm Clear, we are passionate about advancing research on nasal health and immunity. We recently conducted an in vitro agar plate study to assess the effectiveness of BioFilm Clear against Staphylococcus aureus.

In our experiment, a nasal swab positive for S. aureus was cultured on mannitol salt agar plates. One plate was treated with BioFilm Clear, while a second served as a control. After one week of incubation:

  • The untreated control plate showed visible colonies of S. aureus.

  • The BioFilm Clear-treated plate exhibited no bacterial growth, indicating complete eradication of the pathogen under the test conditions.

These preliminary findings are encouraging and support BioFilm Clear’s role as a powerful tool for individuals looking to support nasal biome balance and reduce pathogenic biofilm burden.

Moving Toward a Healthier Nasal Microbiome

While larger clinical trials are needed, the growing body of evidence suggests that addressing nasal dysbiosis may be an important strategy for individuals dealing with autoimmune issues.

At BioFilm Clear, our goal is to help you optimize your nasal environment and support a healthy immune system — naturally and effectively.

Because a healthy nose may be the first step to a healthy body.


References:

  • Baldan R, Cigana C, Testa F, Bianconi I, et al. (2020). "Harnessing the microbiome to combat Staphylococcus aureus nasal colonization." Clinical Microbiology and Infection.

  • Manfredo Vieira S, et al. (2018). "Translocation of a gut pathobiont drives autoimmunity in mice and humans." Science.

  • Münz C, Lünemann JD, Getts MT, Miller SD. (2015). "Antigen-specific tolerance strategies for the prevention and treatment of autoimmune disease." Nature Reviews Immunology.

  • Perl A. (2020). "Activation of mTOR (mechanistic target of rapamycin) in rheumatic diseases." Nature Reviews Rheumatology.v

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