Better spatial tissue imaging techniques to differentiate CTCL and AD ➜ DOI: 10.1038/s41540-024-00474-x Cutaneous T-cell lymphomas (CTCLs) can be difficult to distinguish from inflammatory skin conditions like atopic dermatitis (AD). Multi-antigen imaging protein abundance maps were analyzed with spatial graphs inferred from the cells’ positions in the tissue samples. Characteristic patterns of skin tissue organization allowed a high-precision diagnosis of CTCL versus AD and psoriasis.
The gut multi-omics approach to study trajectories of atopic dermatitis ➜ DOI: 10.1016/j.jaci.2024.10.036 Latent class trajectory analysis was used to phenotype 2247 AD children who were followed from birth until 9 years of age. Multi-omics analyses (microbiome, metabolites, and gut epithelial cell transcriptome) using stool samples collected at 6 months of age were performed. Among five AD phenotypes, early-onset persistent and late-onset phenotypes showed increased risks of food allergy and wheezing treatment ever, with bronchial hyperresponsiveness only evident in the early-onset persistent phenotype. Multi-omics analyses revealed a significantly lower relative abundance of Ruminococcus gnavus and a decreased gut acetate level in the early-onset persistent phenotype, with potential associations to ACSS2, JAK-STAT signaling, and systemic Th2 inflammation. The late-onset phenotype was linked with IL-17 and barrier dysfunction.
Melatonin in AD: from sleep improvement to skin microbiota reshaping? ➜ DOI: 10.1016/j.jaci.2024.11.019 Recent studies have shown that melatonin exerted beneficial actions by remodeling intestinal microbiota composition. The authors investigated the mechanism by which melatonin treatment-induced changes in the skin microbiota composition further alleviated AD in a mouse model. They show that melatonin reshaped the skin microbiota in AD mice. The transplantation of skin microbiota from melatonin-treated mice alleviated AD symptoms in AD mice. Skin microbiota-derived propionic acid was increased in the skin of melatonin-treated AD mice, which further inhibited fatty acid-binding protein 5 (FABP5) expression to alleviate AD.
A review of the neuroimmune axis in the atopic march by neuroscientists ➜ DOI: 10.1016/j.coi.2024.102507 The immune and nervous systems have co-evolved complex mechanisms to sense environmental dangers and orchestrate a concerted response to safeguard tissue and mobilize host defenses. This review explores the neuro-immune interplay within the atopic march, emphasizing its role in host defense, inflammation resolution, and tissue repair. Nociceptors orchestrating type 2 immune responses and the progression of allergic disorders are reviewed, focusing on key regulators such as CGRP-RAMP1 and SP-MRGPRB2/A2. The authors discuss also the potential of nociceptor neuron-blocking drugs to target neuro-immunity, offering the possibility of reversing the progression of the atopic march.
Skin dryness and pruritus in AD: targeting skin kinome to fight the vicious itch-scratch cycle: ➜ DOI: 10.1016/j.jdermsci.2024.10.002 Mechanical alloknesis (MA) is itch hypersensitivity induced by normally innocuous stimuli observed in dry skin-based itch in atopic dermatitis (AD), and often triggers the vicious itch-scratch cycle. Using an acetone-ether and water (AEW) mouse model which mimics dry skin-induced MA, the authors show that all of JAK inhibitors effectively reduced MA, with abrocitinib demonstrating the most significant inhibition and that neutralizing antibodies against IL-4, IL-13, and TSLP inhibited MA in AEW mice. The authors conclude that type 2 cytokine-JAK1 signaling is involved in the development of MA in dry skin in a mouse model, but nonspecific kinome inhibition remains also possible.
