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Nitric oxide (NO) plays an important role in the cutaneous response to UV radiation and in cutaneous inflammation. The presence of inducible NO synthase protein in a number of inflammatory dermatoses, coupled with the induction of an intense cutaneous inflammatory infiltrate following topical application of the NO donor-acidified nitrite (NO2-), has set the paradigm of NO being an inflammatory mediator in human skin. Using zeolite NO (Ze-NO), a chemically inert, pure NO donor, we have shown that NO per se produces little inflammation. Biologically, relevant doses of Ze-NO induce a dermal CD4-positive T-cell infiltrate and IFN-gamma secretion. In contrast acidified nitrite, releasing equal quantities of NO (measured by dermal microdialysis and cutaneous erythema), induces an intense epidermal infiltrate of macrophages with a similar dermal infiltrate of CD3-, CD4-, CD8-, and CD68-positive cells and neutrophils. Suction blisters were created in Ze-NO-treated and control skin. IFN-gamma, but not IL-4, was detected in Ze-NO-treated skin (mean control 0.1 +/- 0.07 pg mg(-1) protein, mean IFN-g 0.670.4 pgmg(-1) protein). We suggest that the potent inflammation induced by acidified NO2- is secondary to the release of additional mediators.
FingerprintDive into the research topics of 'Topically applied nitric oxide induces T-Lymphocyte infiltration in human skin, but minimal inflammation'. Together they form a unique fingerprint.
- 1 Finished
GR/T09705/01: Designing Porous Metal-Organic Frameworks to Store and Deliver Large Amounts of Nitric Oxide
Morris, R. E. & Butler, A. R.
1/12/04 → 31/01/08