Journal
INFLAMMATION
Volume 45, Issue 3, Pages 949-964Publisher
SPRINGER/PLENUM PUBLISHERS
DOI: 10.1007/s10753-021-01615-8
Keywords
nitric oxide; dermatitis; inflammation
Categories
Funding
- National Institute of Arthritis and Musculoskeletal and Skin Disease of the National Institutes of Health [R01 AR061106]
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Nitric oxide plays a regulatory role in cutaneous inflammation by affecting multiple mechanisms, leading to different effects.
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 cyclooxy-genase/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.
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