C. Pontaza

TL;DR: In this paper , the role of eosinophils in atopic dermatitis was investigated using an in-vivo S. aureus epicutaneous mouse model in which a S. Aureus-soaked gauze pad was applied to the back skin for 7 days in wildtype (WT) and eosINophil-deficient mice, and performed image, histologic, flow cytometric, and RNAseq analyses.

TL;DR: In this paper , the IL-36R signaling in skin and lung epithelia is shown to be a critical mechanism for the progression of the atopic march in mice, which is the concept whereby having early-in-life AD and a dysfunctional skin barrier during initial allergen sensitization increases the predisposition of allergic diseases at distant epithelial sites (e.g., asthma).

TL;DR: In this article , the authors used an in vivo mouse model of S. aureus skin infection whereby TNF, TNFR1, or TNFR2 deficient mice and wildtype (wt) mice were intradermally injected with bioluminescent S. anaphora and monitored for 14 days.

TL;DR: Evaluation of skin and lung inflammation by image, histologic and flow cytometric analyses revealed that both keratinocyte- and lung epithelial-intrinsic IL-36R signaling were required for the development of lung inflammation, weight loss, and neutrophil lung infiltration despite no differences in circulating neutrophils.