Phosphodiesterase 4 (PDE4) is highly expressed in keratinocytes and immune cells and promotes pro-inflammatory responses upon activation. The activity of PDE4 has been attributed to various inflammatory conditions, leading to the development and approval of PDE4 inhibitors as host-directed therapeutics in humans. For example, the topical PDE4 inhibitor, crisaborole, is approved for the treatment of mild-to-moderate atopic dermatitis and has shown efficacy in patients with psoriasis. However, the role of crisaborole in regulating the immunopathogenesis of inflammatory skin diseases and infection is not entirely known. Therefore, we evaluated the effects of crisaborole in multiple mouse models, including psoriasis-like dermatitis, AD-like skin inflammation with and without filaggrin mutations, and Staphylococcus aureus skin infection. We discovered that crisaborole dampens myeloid cells and itch in the skin during psoriasis-like dermatitis. Furthermore, crisaborole was effective in reducing skin inflammation in the context of filaggrin deficiency. Importantly, crisaborole reduced S. aureus skin colonization during AD-like skin inflammation. However, crisaborole was not efficacious in treating S. aureus skin infections, even as adjunctive therapy to antibiotics. Taken together, we found that crisaborole reduced itch during psoriasis-like dermatitis and decreased S. aureus skin colonization upon AD-like skin inflammation, which act as additional mechanisms by which crisaborole dampens the immunopathogenesis in mouse models of inflammatory skin diseases. Further examination is warranted to translate these preclinical findings to human disease.
Macrophages are versatile myeloid leukocytes with flexible cellular states to perform diverse tissue functions beyond immunity. This plasticity is however often hijacked by diseases to promote pathology. Scanning kinetics of macrophage states by single-cell transcriptomics and flow cytometry, we observed atopic dermatitis drastically exhausted a resident subtype S1.
Background And Aims: Seborrheic dermatitis (SD) is a chronic inflammatory skin condition that affects patients' quality of life. Emerging evidence suggests that vitamin and mineral deficiencies may contribute to its progression, although the exact etiology remains unclear.
Objective: This case-control study assessed the serum levels of vitamin D and zinc in SD patients compared to a healthy control group, with a focus on how these deficiencies relate to disease severity.
The connection between the immune response and the composition of gut microbiota has been associated with an increased prevalence of atopic dermatitis in the first year of life. The study aimed to investigate gut microbiota characteristics in infants with atopic dermatitis compared to healthy infants to better understand the link between early-life microbiota composition and the development of atopic dermatitis. The study analyzed the intestinal microbiota of 121 infants with clinical signs of atopic dermatitis, divided into Group I (infants with atopic dermatitis) and Group II (healthy controls).
Background: Sensitive skin causes discomfort from irritants, impacting quality of life. While hypoallergenic moisturizers help prevent moisture loss, some ingredients can still cause irritation. Treatments like steroids and calcineurin inhibitors have side effects, and chemical sunscreens can cause irritation in sensitive skin.
