Different airborne particulates trigger distinct immune pathways leading to peanut allergy in a mouse model
- PMID: 37804001
- PMCID: PMC11017991
- DOI: 10.1111/all.15908
Different airborne particulates trigger distinct immune pathways leading to peanut allergy in a mouse model
Abstract
Background: Environmental exposure to peanut through non-oral routes is a risk factor for peanut allergy. Early-life exposure to air pollutants, including particulate matter (PM), is associated with sensitization to foods through unknown mechanisms. We investigated whether PM promotes sensitization to environmental peanut and the development of peanut allergy in a mouse model.
Methods: C57BL/6J mice were co-exposed to peanut and either urban particulate matter (UPM) or diesel exhaust particles (DEP) via the airways and assessed for peanut sensitization and development of anaphylaxis following peanut challenge. Peanut-specific CD4+ T helper (Th) cell responses were characterized by flow cytometry and Th cytokine production. Mice lacking select innate immune signaling genes were used to study mechanisms of PM-induced peanut allergy.
Results: Airway co-exposure to peanut and either UPM- or DEP-induced systemic sensitization to peanut and anaphylaxis following peanut challenge. Exposure to UPM or DEP triggered activation and migration of lung dendritic cells to draining lymph nodes and induction of peanut-specific CD4+ Th cells. UPM- and DEP-induced distinct Th responses, but both stimulated expansion of T follicular helper (Tfh) cells essential for peanut allergy development. MyD88 signaling was critical for UPM- and DEP-induced peanut allergy, whereas TLR4 signaling was dispensable. DEP-induced peanut allergy and Tfh-cell differentiation depended on IL-1 but not IL-33 signaling, whereas neither cytokine alone was necessary for UPM-mediated sensitization.
Conclusion: Environmental co-exposure to peanut and PM induces peanut-specific Tfh cells and peanut allergy in mice.
Keywords: T follicular helper cells; air pollution; exposome; particulate matter; peanut allergy.
© 2023 European Academy of Allergy and Clinical Immunology and John Wiley & Sons Ltd.
Conflict of interest statement
CONFLICT OF INTEREST STATEMENT
M.D.K. receives consulting fees from UKKO. The remaining authors have no relevant conflicts of interest.
Figures






References
-
- Sampath V, Abrams EM, Adlou B, et al. Food allergy across the globe. J Allergy Clin Immunol. 2021;148(6):1347–1364. - PubMed
-
- Sicherer SH, Sampson HA. Food allergy: a review and update on epidemiology, pathogenesis, diagnosis, prevention, and management. J Allergy Clin Immunol. 2018;141(1):41–58. - PubMed
-
- Sicherer SH, Munoz-Furlong A, Godbold JH, Sampson HA. US prevalence of self-reported peanut, tree nut, and sesame allergy: 11-year follow-up. J Allergy Clin Immunol. 2010;125(6):1322–1326. - PubMed
-
- Scott LA, Jones BI, Berni TR, Berni ER, De Vries J, Currie CJ. Evaluation of the epidemiology of peanut allergy in the United Kingdom. Expert Rev Clin Immunol. 2019;15(12):1333–1339. - PubMed
Publication types
MeSH terms
Substances
Grants and funding
LinkOut - more resources
Full Text Sources
Medical
Research Materials