Obesity-Related Allergic Disease Mechanisms
Summary
Obesity is increasingly recognised as a modifier of allergic disease severity and incidence through a complex interplay between adipose-derived mediators, immune cell function and environmental exposures. Excess adipose tissue secretes a range of bioactive molecules including leptin, adiponectin and inflammatory adipokines, which can skew T helper cell polarisation towards a type 2 (Th2) profile. This pro-allergic milieu promotes the activation and survival of type II innate lymphoid cells (ILC2s) and eosinophils, driving heightened airway and mucosal inflammation. Concurrent metabolic alterations such as hyperlipidaemia and insulin resistance further amplify allergic reactivity by altering dendritic cell antigen presentation and barrier integrity. Emerging evidence also implicates obesity in the modulation of immunoglobulin E (IgE) sensitisation patterns, thereby increasing the risk of rhinitis, dermatitis and asthma. Understanding these intersecting pathways is critical for developing targeted interventions to mitigate allergic morbidity in populations with high obesity prevalence.
Research from Nature Portfolio
Recent studies have demonstrated that childhood obesity exacerbates allergic rhinitis symptoms under conditions of environmental air pollution. Obese children with rhinitis display enhanced nasal mucosal inflammation and greater impairment of peak expiratory flow in response to elevated particulate matter and carbon monoxide levels, suggesting that adiposity primes the respiratory mucosa for amplified pollutant-induced immune activation. This work emphasises the synergistic effect of metabolic status and environmental exposure in driving allergic inflammation.
Obesity-Related Allergic Disease Mechanisms publication trend
The graph below shows the total number of articles in obesity-related allergic disease mechanisms across all publications each year (not limited to Nature Index journals).
Technical terms
Adipokine: A bioactive peptide secreted by adipose tissue that modulates inflammatory and metabolic processes.
Leptin: An adipokine that regulates energy balance and promotes Th2 immune responses.
ILC2 (Type II innate lymphoid cell): A lymphoid lineage cell that produces type II cytokines in response to alarmins and adipokines.
Eosinophil: A granulocyte involved in mediating tissue inflammation in allergic conditions.
Immunoglobulin E (IgE): An antibody isotype that binds allergens and triggers mast cell and basophil activation.
Hyperlipidaemia: An elevated level of lipids in the blood, associated with immune modulation and barrier dysfunction.
References
- Allergic rhinitis children with obesity are more vulnerable to air pollution: a cross sectional study. Scientific Reports (2023).
- Leptin Regulated ILC2 Cell through the PI3K/AKT Pathway in Allergic Rhinitis. Mediators of Inflammation (2020).
- Role of Leptin/Osteopontin Axis in the Function of Eosinophils in Allergic Rhinitis with Obesity. Mediators of Inflammation (2018).
- Differential Effects of Obesity, Hyperlipidaemia, Dietary Intake and Physical Inactivity on Type I versus Type IV Allergies. Nutrients (2022).
About these summaries
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