Interleukin‐10 inhibits IgE‐mediated nitric oxide synthase induction and cytokine synthesis in normal human keratinocytes

Becherel, Pierre-André; Goff, Liliane Le; Ktorza, Sandra; Ouaaz, F; Mencia‐Huerta, Jean‐Michel; Dugas, Bernard; Debré, Patrice; Mossalayi, M. Djavad; Arock, Michel

doi:10.1002/eji.1830251042

Cited by 61 publications

(34 citation statements)

References 25 publications

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“…Primary cultures of human keratinocytes have also been reported to respond to LPS/INF␥ or TNF␣ by producing NO, suggesting the expression of an inducible type of NOS in response to inflammatory stimuli (24,25,47). In addition, UV radiation stimulates the release of proinflammatory cytokines (TNF␣, IL-1) by keratinocytes.…”

Section: Discussionmentioning

confidence: 99%

“…For amplification of the cDNA, the following gene-specific primers were used: the cNOS primer set corresponded to nucleotide 4327-4344 (5 Ј -ACCCTGCAGGCCAAGAA-3 Ј ) and (5 Ј -GGAGCT-GAAAACCTCAT-3 Ј ), which is complementary to nucleotides 4712-4729 of human brain NOS cDNA (46). The iNOS synthase primer set were sense (5 Ј -ATGCCAGATGGCAGCATCAGA-3 Ј ) and antisense (5 Ј -ACTTCCTCCAGGATGTTGTA-3 Ј ) (47). GAPDH primer set were from Clontech (Ozyme, France).…”

Section: Reverse Transcription-pcr Analysismentioning

confidence: 99%

“…Interestingly, nitric oxide (NO) that is a diffusible free radical, displaying pleiotropic bioregulatory effects in diverse cells and tissues (21,22) has been reported to be produced by melanocytes (23) and keratinocytes in response to proinflammatory cytokines (24,25). Moreover, NO contributes to erythema, in response to UVB light, by increasing blood flow in human skin microcirculation (26).…”

Section: Introductionmentioning

confidence: 99%

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Nitric oxide produced by ultraviolet-irradiated keratinocytes stimulates melanogenesis.

Romero-Graillet

Aberdam²,

Clement³

et al. 1997

J. Clin. Invest.

268

204

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Ultraviolet (UV) radiation is the main physiological stimulus for human skin pigmentation. Within the epidermalmelanin unit, melanocytes synthesize and transfer melanin to the surrounding keratinocytes. Keratinocytes produce paracrine factors that affect melanocyte proliferation, dendricity, and melanin synthesis. In this report, we show that normal human keratinocytes secrete nitric oxide (NO) in response to UVA and UVB radiation, and we demonstrate that the constitutive isoform of keratinocyte NO synthase is involved in this process. Next, we investigate the melanogenic effect of NO produced by keratinocytes in response to UV radiation using melanocyte and keratinocyte cocultures. Conditioned media from UV-exposed keratinocytes stimulate tyrosinase activity of melanocytes. This effect is reversed by NO scavengers, suggesting an important role for NO in UVinduced melanogenesis. Moreover, melanocytes respond to NO-donors by decreased growth, enhanced dendricity, and melanogenesis. The rise in melanogenesis induced by NOgenerating compounds is associated with an increased amount of both tyrosinase and tyrosinase-related protein 1.These observations suggest that NO plays an important role in the paracrine mediation of UV-induced melanogenesis. ( J. Clin. Invest. 1997. 99:635-642.)

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Section: Discussionmentioning

confidence: 99%

Section: Reverse Transcription-pcr Analysismentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Nitric oxide produced by ultraviolet-irradiated keratinocytes stimulates melanogenesis.

Romero-Graillet

Aberdam²,

Clement³

et al. 1997

J. Clin. Invest.

268

204

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“…This effect of IL-10 appears to be mediated by TNF-␣ (37), because IL-10 down-regulates TNF-␣ production by keratinocytes (31), and prolonged treatment with anti-IL-10 mAb results in increased TNF-␣ production (38). Furthermore, IL-10 is a key mediator that induces tolerance by low-dose UV exposure, because i.p.…”

Section: Discussionmentioning

confidence: 99%

“…Keratinocytes are one of the major sources of TNF-␣, and IL-10 down-regulates TNF-␣ production by keratinocytes (10,28,31). IL-10 is involved in mediating tolerance induced by low-dose UV (32).…”

Section: Anti-il-10 Mab Treatment At the Elicitation Site Abrogated Umentioning

confidence: 99%

Ultraviolet Light Exposure Suppresses Contact Hypersensitivity by Abrogating Endothelial Intercellular Adhesion Molecule-1 Up-Regulation at the Elicitation Site

Komura

Hasegawa

Hamaguchi

et al. 2003

The Journal of Immunology

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Hapten sensitization through UV-exposed skin induces systemic immune suppression, which is experimentally demonstrated by inhibition of contact hypersensitivity (CHS). Although this UV-induced effect has been shown to be mediated by inhibition of the afferent phase of the CHS, the UV effects on the efferent (elicitation) phase remain unknown. In this study, UV effects on endothelial ICAM-1 expression at elicitation sites were first examined. Mice were sensitized by hapten application onto UV-exposed back skin, and ears were challenged 5 days later. ICAM-1 up-regulation at nonirradiated elicitation sites following hapten challenge was eliminated by UV exposure on sensitization sites distant from elicitation sites. To assess whether loss of the ICAM-1 up-regulation at elicitation sites contributed to UV-induced immunosuppression, we examined CHS responses in UV-exposed ICAM-1-deficient (ICAM-1−/−) mice that genetically lacked the ICAM-1 up-regulation. ICAM-1−/− mice exhibited reduced CHS responses without UV exposure, but UV exposure did not further reduce CHS responses in ICAM-1−/− mice. Furthermore, ICAM-1 deficiency did not affect the afferent limb, because ICAM-1−/− mice had normal generation of hapten-specific suppressor and effector T cells. This UV-induced immunosuppression was associated with a lack of TNF-α production after Ag challenge at elicitation sites. Local TNF-α injection before elicitation abrogated the UV-induced CHS inhibition with increased endothelial ICAM-1 expression. TNF-α production at elicitation sites was down-regulated by IL-10, a possible mediator produced by hapten-specific suppressor T cells that are generated by UV exposure. These results indicate that UV exposure inhibits CHS by abrogating up-regulation of endothelial ICAM-1 expression after Ag challenge at elicitation sites.

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Interleukin 10 Treatment of Psoriasis

Asadullah

Döcke²,

Ebeling³

et al. 1999

Arch Dermatol

141

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Interleukin‐10 inhibits IgE‐mediated nitric oxide synthase induction and cytokine synthesis in normal human keratinocytes

Cited by 61 publications

References 25 publications

Nitric oxide produced by ultraviolet-irradiated keratinocytes stimulates melanogenesis.

Nitric oxide produced by ultraviolet-irradiated keratinocytes stimulates melanogenesis.

Ultraviolet Light Exposure Suppresses Contact Hypersensitivity by Abrogating Endothelial Intercellular Adhesion Molecule-1 Up-Regulation at the Elicitation Site

Interleukin 10 Treatment of Psoriasis

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