Journal
JOURNAL OF INVESTIGATIVE DERMATOLOGY
Volume 128, Issue 2, Pages 352-360Publisher
ELSEVIER SCIENCE INC
DOI: 10.1038/sj.jid.5701096
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Funding
- Engineering and Physical Sciences Research Council [GR/T09705/01] Funding Source: researchfish
- Medical Research Council [G0601481, G9900991B] Funding Source: researchfish
- Medical Research Council [G0601481] Funding Source: Medline
- MRC [G0601481] Funding Source: UKRI
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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.
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