Mycobacterial Influence on Allergic Airway Inflammation

Allergic airway inflammation, exemplified by asthma, arises from an exaggerated type 2 immune response characterised by eosinophil infiltration, elevated immunoglobulin E (IgE) levels and airway hyperresponsiveness. Mycobacteria and mycobacterial components can modulate this pathology by skewing the immune balance towards type 1 responses, enhancing regulatory pathways and promoting tissue repair. Exposure to whole bacilli or purified antigens such as Ag85B, Rv3619c and cell wall fractions induces dendritic cell maturation, stimulates interferon-γ production and expands regulatory T cells, which in turn suppress Th2 cytokines (IL-4, IL-5, IL-13) and reduce eosinophilic inflammation. Nebulised preparations of inactivated mycobacteria have demonstrated prophylactic and therapeutic effects in animal models, attenuating airway hyperreactivity and mucus metaplasia via modulation of pathways including IL-33/ST2, TGF-β/Smad and Notch/Jagged1. Collectively, these findings highlight the potential of mycobacteria-based interventions to reprogramme aberrant allergic responses, offering a complementary strategy to conventional corticosteroid therapy and providing insight into the inverse epidemiological association observed between tuberculosis exposure and atopic disease.

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Mycobacterial Influence on Allergic Airway Inflammation publication trend

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Technical terms

Th1 and Th2 cells: Subsets of CD4+ T helper cells that drive cellular and humoral immunity respectively, with Th1 cells producing interferon-γ and Th2 cells producing IL-4, IL-5 and IL-13.

Regulatory T cells (Treg): A specialised lymphocyte population expressing Foxp3 that suppresses overactive immune responses and maintains tolerance.

Cytokines: Soluble proteins, such as IL-10, IL-17, IL-33 and TGF-β, that mediate communication between immune cells and orchestrate inflammatory or regulatory processes.

Airway hyperresponsiveness (AHR): Exaggerated bronchoconstriction in response to stimuli, a hallmark of asthma measured in preclinical models.

Bronchoalveolar lavage fluid (BALF): Liquid collected from the lung airway for analysis of cellular and molecular markers of inflammation.

References

1. Effects of Mycobacteria Major Secretion Protein, Ag85B, on Allergic Inflammation in the Lung. PLOS ONE (2014).
2. Inhalation of nebulized Mycobacterium vaccae can protect against allergic bronchial asthma in mice by regulating the TGF-β/Smad signal transduction pathway. Allergy, Asthma & Clinical Immunology (2020).
3. Mycobacterium tuberculosis–Specific Antigen Rv3619c Effectively Alleviates Allergic Asthma in Mice. Frontiers in Pharmacology (2020).
4. Decrease of IL-5 Production by Naive T Cells Cocultured with IL-18-Producing BCG-Pulsed Dendritic Cells from Patients Allergic to House Dust Mite. Vaccines (2021).
5. Inverse relation between atopic status and tuberculin response in adult asthmatics.. Tuberkuloz ve Toraks (2012).