Dermatology Service Veterans Affairs Medical Center, Department of Dermatology, University of California, San Francisco, CA, USA.
Dermatology Hospital of Southern Medical University, Guangzhou, 510091, China.
Inflammation. 2022 Jun;45(3):949-964. doi: 10.1007/s10753-021-01615-8. Epub 2022 Jan 30.
Nitric oxide (NO), a signaling molecule, regulates biological functions in multiple organs/tissues, including the epidermis, where it impacts permeability barrier homeostasis, wound healing, and antimicrobial defense. In addition, NO participates in cutaneous inflammation, where it exhibits pro-inflammatory properties via the cyclooxygenase/prostaglandin pathway, migration of inflammatory cells, and cytokine production. Yet, NO can also inhibit cutaneous inflammation through inhibition of T cell proliferation and leukocyte migration/infiltration, enhancement of T cell apoptosis, as well as through down-regulation of cytokine production. Topical applications of NO-releasing products can alleviate atopic dermatitis in humans and in murine disease models. The underlying mechanisms of these discrepant effects of NO on cutaneous inflammation remain unknown. In this review, we briefly review the regulatory role of NO in cutaneous inflammation and its potential, underlying mechanisms.
一氧化氮(NO)作为一种信号分子,调节包括表皮在内的多个器官/组织的生物学功能,其影响表皮的渗透性屏障稳态、伤口愈合和抗菌防御。此外,NO 参与皮肤炎症,通过环氧化酶/前列腺素途径、炎症细胞的迁移和细胞因子的产生表现出促炎特性。然而,NO 也可以通过抑制 T 细胞增殖和白细胞迁移/浸润、增强 T 细胞凋亡以及下调细胞因子产生来抑制皮肤炎症。NO 释放产品的局部应用可以减轻人类和小鼠疾病模型中的特应性皮炎。NO 对皮肤炎症的这些不同作用的潜在机制尚不清楚。在这篇综述中,我们简要回顾了 NO 在皮肤炎症中的调节作用及其潜在机制。