Palladino Chiara, Ellinger Isabella, Kalic Tanja, Humeniuk Piotr, Ret Davide, Mayr Vanessa, Hafner Christine, Hemmer Wolfgang, Hoffmann-Sommergruber Karin, Untersmayr Eva, Bublin Merima, Radauer Christian, Breiteneder Heimo
Institute of Pathophysiology and Allergy Research, Center for Pathophysiology, Infectiology and Immunology, Medical University of Vienna, Vienna, Austria.
Department of Dermatology, University Hospital St. Pölten, Karl Landsteiner University of Health Sciences, St. Pölten, Austria.
Front Mol Biosci. 2023 Feb 8;10:1126008. doi: 10.3389/fmolb.2023.1126008. eCollection 2023.
Peanut-allergic individuals react upon their first known ingestion of peanuts, suggesting sensitization occurs through non-oral exposure. Increasing evidence suggests that the respiratory tract is a probable site for sensitization to environmental peanuts. However, the response of the bronchial epithelium to peanut allergens has never been explored. Furthermore, food matrix-derived lipids play an important role in allergic sensitization. To contribute to a better understanding of the mechanisms of allergic sensitization to peanuts inhalation, by exploring the direct effect of the major peanut allergens Ara h 1 and Ara h 2 and peanut lipids on bronchial epithelial cells. Polarized monolayers of the bronchial epithelial cell line 16HBE14o- were stimulated apically with peanut allergens and/or peanut lipids (PNL). Barrier integrity, transport of allergens across the monolayers, and release of mediators were monitored. Ara h 1 and Ara h 2 impacted the barrier integrity of the 16HBE14o- bronchial epithelial cells and crossed the epithelial barrier. Ara h 1 also induced the release of pro-inflammatory mediators. PNL improved the barrier function of the cell monolayers, decreased paracellular permeability and reduced the amount of allergens crossing the epithelial layer. Our study provides evidence of the transport of Ara h 1 and Ara h 2 across the airway epithelium, of the induction of a pro-inflammatory milieu, and identifies an important role for PNL in controlling the amount of allergens that can cross the epithelial barrier. These, all together, contribute to a better understanding of the effects of peanuts exposure on the respiratory tract.
花生过敏个体在首次已知摄入花生时就会产生反应，这表明致敏是通过非口服暴露发生的。越来越多的证据表明，呼吸道可能是对环境中的花生致敏的部位。然而，支气管上皮对花生过敏原的反应从未被研究过。此外，食物基质衍生的脂质在过敏性致敏中起重要作用。为了更好地理解花生吸入致敏的机制，我们通过探索主要花生过敏原Ara h 1和Ara h 2以及花生脂质对支气管上皮细胞的直接作用来进行研究。用花生过敏原和/或花生脂质（PNL）对支气管上皮细胞系16HBE14o-的极化单层进行顶端刺激。监测屏障完整性、过敏原跨单层的转运以及介质的释放。Ara h 1和Ara h 2影响了16HBE14o-支气管上皮细胞的屏障完整性，并穿过上皮屏障。Ara h 1还诱导了促炎介质的释放。PNL改善了细胞单层的屏障功能，降低了细胞旁通透性，并减少了穿过上皮层的过敏原量。我们的研究提供了Ara h 1和Ara h 2跨气道上皮转运的证据，以及促炎环境诱导的证据，并确定了PNL在控制可穿过上皮屏障的过敏原量方面的重要作用。所有这些共同有助于更好地理解花生暴露对呼吸道的影响。
