The management of acquired reactive perforating collagenosis (ARPC) is challenging. Here, we shared two cases of ARPC combined with elderly atopic dermatitis (AD) that did not respond well to conventional treatment but responded well to the monotherapy of dupilumab, which suggests that dupilumab may be an alternative option for the treatment.

Sporothrix schenckii (S. schenckii) induces sporotrichosis, which has gained attention in recent years due to its worldwide prevalence. The dimorphic switching process is essential for the pathogenesis of S. schenckii. Previously, overexpression of several signal transduction genes, including SsDRK1 and SsSte20, was observed during the mycelium‑to‑yeast transition; these were necessary for asexual development, yeast‑phase cell formation, cell wall integrity and melanin synthesis. However, the mechanisms of the signaling pathways during dimorphic switching of S. schenckii remain unclear. In the present study, transcriptome sequencing of the 48‑h induced yeast forms and mycelium of S. schenckii was performed. In total, 24,904,510 high‑quality clean reads were obtained from mycelium samples and 22,814,406 from 48‑h induced yeast form samples. Following assembly, 31,779 unigene sequences were obtained with 52.98% GC content (The proportion of guanine G and cytosine C to all bases in nucleic acid). The results demonstrated that 12,217 genes, including genes involved in signal transduction and chitin synthesis, were expressed differentially between the two stages. According to these results, a map of the signaling pathways, including two‑component and heterotrimeric G‑protein signaling systems, Ras and MAPK cascades associated with the dimorphic switch, was drawn. Taken together, the transcriptome data and analysis performed in the present study lay the foundation for further research into the molecular mechanisms controlling the dimorphic switch of S. schenckii and support the development of anti‑S. schenckii strategies targeting genes associated with signaling pathways.

Introduction: Sporotrichosis is a fungal disease caused by a complex of Sporothrix schenckii, leading to chronic infections of the epidermis and subcutaneous tissue in both humans and animals.Methods: Through virtual screening targeting the key gene abaA to screen out the small-molecule drugs to treat Sporotrichosis. To further validate the antifungal activity of small-molecule drugs, growth curves, minimum bactericidal concentration (MBC), and minimum inhibitory concentration (MIC) for Sporothrix globosa (S. globosa) and Sporothrix schenckii (S. schenckii) were measured. In addition, we have done animal experiments to explore the function of the drugs. At the same time, qRT-PCR and transcriptome were used to verify the important role of abaA gene in Sporothrix.Results: Azelastine and Mefloquine effectively inhibit S. globosa and S. schenckii. MBC, and MIC for S. globosa and S. schenckii confirmed that both Azelastine and Mefloquine inhibited the growth of S. globosa and S. schenckii. Additionally, animal experiments demonstrated that Azelastine and Mefloquine reduced skin lesions in mice; post-treatment observations revealed improvements in inflammatory infiltration and granuloma formation. Through transcriptome analysis and qRT-PCR for validation, our findings demonstrate that the abaA gene plays a crucial role in regulating the attachment of the Sporothrix cell wall to the host matrix and in melanin regulation. Notably, when the abaA gene was inhibited, there was a marked increase in the expression of repair genes. These results emphasize the significance of the abaA gene in the biology of Sporothrix.Discussion: Two small-molecule drugs exhibit the ability to inhibit Sporothrix and treat sporotrichosis both in vitro and in murine models, suggesting their potential for development as therapeutic agents for sporotrichosis. And qRT-PCR and transcriptome results underscore the significance of the abaA gene in Sporothrix. Our results lay the foundation for the search for new treatments for other mycosis.