950 Epicutaneous staphylococcus aureus exposure triggers lung inflammation via epithelia-intrinsic IL-36R signaling

Allergic diseases have been increasing recently and affect nearly 20% of the human population, including 200 million people with atopic dermatitis (AD), 250 food allergies, 600 allergic rhinitis or asthma. The march is concept whereby having early-in-life AD a dysfunctional skin barrier during initial allergen sensitization increases predisposition at distant epithelial sites (e.g., asthma). We previously shown that IL-36R signaling was required to exacerbate progression from AD-like inflammation subsequent lung in mice. However, whether acts directly on and/or epithelia trigger towards not entirely clear. To address this gap knowledge, we performed our model WT, IL-36R-/-, keratinocyte-specific deficient (K14-cre×IL-36Rfl/fl), epithelial-specific (Nkx2-1-cre×IL-36Rfl/fl) mice, first epicutaneous Staphylococcus aureus cockroach antigen (CrA) exposure initiates inflammation, which followed by intratracheal CrA inflammation. Evaluation image, histologic flow cytometric analyses revealed both keratinocyte- epithelial-intrinsic were for development weight loss, neutrophil infiltration despite no differences circulating neutrophils. Collectively, findings suggest critical mechanism march.