Cytokine-Mediated Inflammation in Allergic Asthma

Allergic asthma is a chronic respiratory disorder marked by airway hyper-responsiveness, reversible obstruction and inflammation driven by an aberrant immune response to innocuous environmental allergens. Central to its pathogenesis is a network of cytokines—small protein mediators—that orchestrate the recruitment and activation of inflammatory cells such as eosinophils, mast cells and type 2 helper T (Th2) lymphocytes. On allergen exposure, airway epithelial cells release alarmins (for example interleukin-33 and thymic stromal lymphopoietin) that prime innate lymphoid cells and dendritic cells, skewing adaptive immunity towards a Th2-dominant profile. Th2 cells in turn secrete interleukin-4, interleukin-5 and interleukin-13, which drive IgE class switching in B cells, eosinophil survival and goblet cell hyperplasia. This cytokine milieu promotes airway remodelling—characterised by subepithelial fibrosis, smooth muscle hypertrophy and mucus overproduction—and underpins the episodic wheeze, dyspnoea and cough that afflict millions worldwide. Therapeutic strategies have evolved from broad anti-inflammatory corticosteroids and bronchodilators to targeted biological agents that neutralise key cytokines or their receptors, reflecting the global imperative to refine personalised treatment and reduce disease burden.

Research from Nature Portfolio

Polydatin, a natural stilbene glycoside, has been shown to attenuate mast cell-mediated allergic inflammation by direct inhibition of the Src-family kinases Lyn and Syk. In vitro studies demonstrated that polydatin suppresses degranulation and reduces expression of tumour necrosis factor-α, interleukin-4 and interleukin-1β. In murine models of passive cutaneous and systemic anaphylaxis, treatment with polydatin diminished vascular permeability and histamine release. Mechanistic analysis revealed down-regulation of downstream signalling pathways including MAPK, PI3K/Akt and NF-κB, alongside activation of the cytoprotective Nrf2/HO-1 axis. These findings position polydatin as a promising candidate for modulating cytokine-mediated events in allergic airway disease.

Cytokine-Mediated Inflammation in Allergic Asthma publication trend

The graph below shows the total number of articles in cytokine-mediated inflammation in allergic asthma across all publications each year (not limited to Nature Index journals).

Technical terms

Cytokine: A soluble protein released by immune or structural cells that regulates inflammation, cell recruitment and effector functions in the airway.

Th2 cell: A subset of CD4+ T lymphocytes that secretes interleukin-4, interleukin-5 and interleukin-13 to promote allergic inflammation and IgE production.

Eosinophil: A granulocyte that is recruited to the airway in response to cytokines and releases cytotoxic mediators contributing to tissue damage.

Mast cell: A resident immune cell in the airway mucosa that degranulates upon IgE-mediated activation, releasing histamine and pro-inflammatory cytokines.

Airway hyper-responsiveness: An exaggerated bronchoconstrictive response to stimuli, driven by inflammation and remodelling of the airway wall.

IgE: Immunoglobulin E, an antibody isotype that binds to mast cells and basophils, triggering degranulation upon allergen cross-linking.

References

1. Baicalin Inhibits Airway Smooth Muscle Cells Proliferation through the RAS Signaling Pathway in Murine Asthmatic Airway Remodeling Model. Oxidative Medicine and Cellular Longevity (2023).
2. Formononetin inhibits IgE by huPlasma/PBMCs and mast cells/basophil activation via JAK/STAT/PI3-Akt pathways. Frontiers in Immunology (2024).
3. Polydatin inhibits mast cell-mediated allergic inflammation by targeting PI3K/Akt, MAPK, NF-κB and Nrf2/HO-1 pathways. Scientific Reports (2017).
4. Type 2 immunity in asthma. World Allergy Organization Journal (2018).
5. Treatment of allergic asthma: Modulation of Th2 cells and their responses. Respiratory Research (2011).