Premium
The lipid interaction capacity of Sin a 2 and Ara h 1, major mustard and peanut allergens of the cupin superfamily, endorses allergenicity
Author(s) -
Angelina A.,
Sirvent S.,
Palladino C.,
Vereda A.,
CuestaHerranz J.,
Eiwegger T.,
Rodríguez R.,
Breiteneder H.,
Villalba M.,
Palomares O.
Publication year - 2016
Publication title -
allergy
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 3.363
H-Index - 173
eISSN - 1398-9995
pISSN - 0105-4538
DOI - 10.1111/all.12887
Subject(s) - chemistry , phosphatidylcholine , proinflammatory cytokine , biochemistry , lipid vesicle , phospholipid , vesicle , biology , immunology , inflammation , membrane
Background Sin a 2 (11S globulin) and Ara h 1 (7S globulin) are major allergens from yellow mustard seeds and peanut, respectively. The ability of these two allergens to interact with lipid components remains unknown. Objective To study the capacity of Sin a 2 and Ara h 1 to interact with lipid components and the potential effects of such interaction in their allergenic capacity. Methods Spectroscopic and SDS ‐ PAGE binding assays of Sin a 2 and Ara h 1 with different phospholipid vesicles and gastrointestinal and endolysosomal digestions in the presence or absence of lipids were performed. The capacity of human monocyte‐derived dendritic cells (hmo DC s) to capture food allergens in the presence or absence of lipids, the induced cytokine signature, and the effect of allergens and lipids to regulate TLR 2‐L‐induced NF ‐ kB / AP ‐1 activation in THP 1 cells were analyzed. Results Sin a 2 and Ara h 1 bind phosphatidylglycerol ( PG ) acid but not phosphatidylcholine ( PC ) vesicles in a pH ‐dependent manner. The interaction of these two allergens with lipid components confers resistance to gastrointestinal digestion, reduces their uptake by hmo DC s, and enhances their stability to microsomal degradation. Mustard and peanut lipids favor a proinflammatory environment by increasing the IL ‐4/ IL ‐10 ratio and IL ‐1β production by hmo DC s. The presence of mustard lipids and PG vesicles inhibits TLR 2‐L‐induced NF ‐ kB / AP ‐1 activation in THP 1 cells. Conclusion Sin a 2 and Ara h 1 interact with lipid components, which might well contribute to explain the potent allergenic capacity of these two clinically relevant allergens belonging to the cupin superfamily.