title: Mechanistic analysis of experimental food allergen-induced cutaneous reactions.
abstract: Individuals with food allergy often present with uritcaria and atopic dermatitis. Indeed, susceptibility to food allergy may predispose to the development of these cutaneous allergic disorders. Recently, we developed a model of food allergy, whereby oral consumption of food [pea Pisum sativum L.; expressing alpha-amylase inhibitor-1 (alphaAI) from the common bean Phaseolus vulgaris L. cv Tendergreen (pea-alphaAI)] promotes a T helper cell type 2 (Th2) inflammatory response and predisposes to cutaneous allergic reactions following subsequent food allergen (alphaAI) exposure. To delineate the kinetics of food allergen-induced cutaneous reactions and examine the inflammatory mechanisms involved in this allergic reaction, we used interleukin (IL)-13-, IL-4 receptor alpha-, and eotaxin-1-deficient mice and performed serum transfer and CD4+ T cell depletion studies. We demonstrate that consumption of pea-alphaAI promotes an alphaAI-specific immunoglobulin G1 (IgG1) and IgE antibody response. Furthermore, we show that subsequent food allergen (alphaAI) challenge in the skin induced an early (3 h)- and late-phase (24 h) cutaneous allergic reaction. The early-phase response was associated with mast cell degranulation and the presence of Ig, whereas the late-phase response was characterized by a lymphoid and eosinophilic infiltrate, which was critically regulated by CD4+ T cells, IL-13, and eotaxin-1. Collectively, these studies demonstrate that food allergy can predispose to cutaneous inflammatory reactions, and these processes are critically regulated by Th2 immune factors.
authors.affiliation: Allergy and Inflammation Research Group, Division of Molecular Bioscience, The John Curtin School of Medical Research, Australian National University, Canberra, Australia.
authors.forename: Vanessa E
authors.initials: VE
authors.lastname: Prescott
authors.forename: Elizabeth
authors.initials: E
authors.lastname: Forbes
authors.forename: Paul S
authors.initials: PS
authors.lastname: Foster
authors.forename: Klaus
authors.initials: K
authors.lastname: Matthaei
authors.forename: Simon P
authors.initials: SP
authors.lastname: Hogan
mesh_terms: D000485:Allergens / Q000276:immunology*; D000818:Animals; D015550:Cell Degranulation; D002478:Cells, Cultured; D016207:Cytokines / Q000502:physiology; D003876:Dermatitis, Atopic / Q000276:immunology*; D004804:Eosinophils / Q000276:immunology / Q000648:ultrastructure; D005512:Food Hypersensitivity / Q000276:immunology*; D007073:Immunoglobulin E / Q000097:blood; D007074:Immunoglobulin G / Q000097:blood; D008407:Mast Cells / Q000276:immunology; D051379:Mice; D008807:Mice, Inbred BALB C; D018345:Mice, Knockout; D018532:Pisum sativum / Q000009:adverse effects* / Q000737:chemistry; D018418:Th2 Cells / Q000502:physiology; D013997:Time Factors; D000516:alpha-Amylases / Q000009:adverse effects / Q000037:antagonists & inhibitors* / Q000276:immunology*
chemical_list: D000485:Allergens; D016207:Cytokines; D007074:Immunoglobulin G; D007073:Immunoglobulin E; D000516:alpha-Amylases