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Abstract / Description of output
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-γ
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-γ, but not IL-4, was detected in Ze–NO-treated skin (mean control 0.1±0.07pgmg−1 protein, mean IFN-γ 0.6±0.4pgmg−1 protein). We suggest that the potent inflammation induced by acidified NO2− is secondary to the release of additional mediators.
Original language | English |
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Pages (from-to) | 352–360 |
Number of pages | 1 |
Journal | Journal of Investigative Dermatology |
Volume | 128 |
Issue number | 2 |
DOIs | |
Publication status | Published - Feb 2008 |
Keywords / Materials (for Non-textual outputs)
- iNOS, inducible NOS
- NOS, NO synthases
- NO, nitric oxide
- NO2−, nitrite
- Ze, zeolite
- Ze–NO, zeolite–nitric oxide
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- 1 Finished
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Induction of neutrophil apoptosis and treatment of severe lung inflammation
1/09/07 → 29/02/12
Project: Research