Research has revealed that the pathogenesis of atopic dermatitis (AD) involves complex interactions between the host’s genetic factors, immune system, and microbiome. Notably, the overgrowth of Staphylococcus aureus on the skin of patients with AD plays a significant role in worsening the disease. The bacteria’s V8 protease activates protease-activated receptor 1 on sensory nerves, triggering itch and perpetuating the cycle of skin damage and inflammation.

Current findings have highlighted the importance of studying the skin microbiome in AD and its role in itch and inflammation. The discovery that S. aureus V8 protease is a key contributor to itch in AD opens new avenues for potential treatments, including the use of protease inhibitors. Additionally, current therapies such as anti–IL-4Ra have shown rapid effects on reducing both itch and bacterial colonization, suggesting a link between microbial activity and the effectiveness of these treatments. As research advances, there is growing recognition of the need to explore how targeting bacterial proteases like V8 can improve the management of AD and enhance the quality of life for affected patients.

Reference: Gallo RL, Horswill AR. Staphylococcus aureus: The Bug Behind the Itch in Atopic Dermatitis. J Invest Dermatol. 2024 May;144(5):950-953. doi: 10.1016/j.jid.2024.01.001. Epub 2024 Feb 29. PMID: 38430083.