Ultraviolet B irradiation of skin induces mast cell degranulation and release of tumour necrosis factor‐α

Walsh, Laurence J.

doi:10.1038/icb.1995.37

Cited by 85 publications

(81 citation statements)

References 35 publications

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“…Cord blood-derived mast cells used in this study show a phenotype that closely resembles human skin mast cells that are known to degranulate and release preformed mediators such as TNF-a in response to UVB irradiation in vivo [1,38]. However, in vitro irradiation of cord blood-derived mast cells with various doses of UVB did not induce significant degranulation.…”

Section: Discussionmentioning

confidence: 74%

“…Ultraviolet B (UVB) (280-320 nm) exposure is a major cause of sunburn characterized by an acute inflammatory response whereby erythema, changes in vascular permeability [1], dilatation of dermal blood vessels and epithelial hyperplasia are hallmark features. The acute inflammatory changes in skin following short-term irradiation by excessive UVB are well established.…”

Section: Introductionmentioning

confidence: 99%

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Ultraviolet B irradiation selectively increases the production of interleukin-8 in human cord blood-derived mast cells

Endoh

Girolamo

Hampartzoumian

et al. 2007

Clinical and Experimental Immunology

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SummaryUVB irradiation modulates immune responses in the skin and is a major cause of sunburn, during which neutrophils accumulate in the skin. Because of their abundance in skin and ability to produce a variety of proinflammatory mediators, we propose that mast cells may play a key role in ultraviolet B (UVB)-induced skin inflammation. Cord blood-derived human mast cells were treated in vitro with varying doses of UVB and production of multiple cytokines was measured in culture supernatants. UVB exposure significantly increased the release of interleukin (IL)-8 and modestly increased IL-1a production, but cytokines such as IL-2, IL-4, IL-6, IL-10, IL-12, IL-13, tumour necrosis factor (TNF)-a and interferon (IFN)-g were unaffected. Cycloheximide reduced the UVB-mediated induction of IL-8 by 30-40%, suggesting that new protein synthesis contributed to IL-8 production. In line with this, UVB treatment of mast cells significantly increased IL-8 mRNA. In contrast to its effect on IL-8 production, optimal doses of UVB did not provoke histamine or tryptase release, indicating little effect on degranulation. Our data suggest that mast cells may play a major role during UVB-induced acute inflammation by selectively inducing cytokines involved in neutrophil recruitment.

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Section: Discussionmentioning

confidence: 74%

Section: Introductionmentioning

confidence: 99%

Ultraviolet B irradiation selectively increases the production of interleukin-8 in human cord blood-derived mast cells

Endoh

Girolamo

Hampartzoumian

et al. 2007

Clinical and Experimental Immunology

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“…This notion is supported by earlier reports demonstrating that the sunburn response following skin exposure to UVB irradiation is accompanied by a rapid degranulation of cutaneous MCs. 22,23 In addition, MC products, such as tumor necrosis factor-␣ and prostaglandins, have been implicated to contribute to the inflammatory events following UVB irradiation. 23,24 Most importantly, UVB irradiation has been demonstrated to result in reduced swelling responses of MC-deficient mouse skin.…”

Section: Et-1 Exerts Its Effects In Uvb-induced Inflammation Via Et Amentioning

confidence: 99%

Inflammatory Murine Skin Responses to UV-B Light Are Partially Dependent on Endothelin-1 and Mast Cells

Metz¹,

Lammel²,

Gibbs

et al. 2006

The American Journal of Pathology

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Endothelin (ET-1) has been shown to crucially contribute to UV-induced skin responses such as tanning.To test whether ET-1 is also involved in early cutaneous reactions to UV, we assessed ET-1 skin levels in UV-irradiated mice. In correlation with the levels of UV-induced skin inflammation, ET-1 concentrations increased substantially and continually. Moreover, blocking of ET-1 receptors (ET A ) resulted in significantly decreased cutaneous inflammation following UV irradiation. When we assessed skin responses to ET-1 injections, we observed prominent mast cell degranulation and mast cell-dependent inflammation. Since mast cells also critically contributed to UV-induced inflammation, we determined the ET-1-dependent inflammatory response to UV in the absence and presence of these cells. Interestingly, ET A blockade did not decrease UV-induced inflammation in mast cell-deficient mice, unless these mice had been adoptively transferred with mast cells before irradiation. This indicates that skin inflammation due to UV irradiation is caused in part by ET-1 acting on skin mast cells. Immediate skin responses following exposure to sunlight are largely mediated by UV-B light (UVB): low to moderate doses of UVB result in tanning, whereas intense UVB irradiation also gives rise to considerable inflammation, ie, solar dermatitis. UVB-induced tanning is widely regarded to result from the up-regulation of pigment production in epidermal melanocytes, which is induced by melanogens released from activated keratinocytes. In contrast, the cellular and molecular mechanisms involved in the induction of inflammatory skin responses to UVB are largely unknown.Recently, the vasoconstrictor peptide endothelin-1 (ET-1), one of the melanogens that contributes to UVBinduced tanning, 1,2 was found to promote inflammation in various pathological processes. For example, we and others have recently shown that ET-1 levels are up-regulated in murine septic peritonitis and that elevated ET-1 levels contribute to morbidity and mortality in this setting.3,4 Increased ET-1 production and mRNA expression have been demonstrated in lung tissue and bronchoalveolar lavage fluid in different models of airway inflammation. [5][6][7] In addition, elevated ET-1 concentrations are also present in patients with systemic lupus erythematosus, Takayasu arteritis, or Raynaud's phenomenon, where, in the latter case, the increase was shown clearly to contribute to disease severity. 8 These observations indicate that ET-1, in addition to having stimulatory effects on melanocytes, may orchestrate the induction of inflammatory responses after UVB irradiation. Two recent reports support this notion. First, the expression of ET-1 and its receptors ET A and ET B in murine skin was found to be markedly and rapidly upregulated after UVB irradiation, both in the dermis and epidermis.9 Second, intracutaneous injections of ET-1 reportedly trigger inflammatory reactions, including a pronounced flare response associated with sensations of a burning itch, a classic symptom of a ...

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“…Its level is raised in ultraviolet-exposed skin and it may act by altering Langerhans cell morphology and function. 53 Mast cells store large amounts of TNF-a, which are released on activation. 50 A murine study suggests that the degree of susceptibility to ultraviolet-Binduced local immunosuppression depends on TNF-a levels within the epidermis after ultraviolet-B irradiation.…”

Section: Mast Cells and Cutaneous Malignancies S Ch'ng Et Almentioning

confidence: 99%

Mast cells and cutaneous malignancies

Ch’ng

Wallis

Yuan³

et al. 2006

Modern Pathology

167

166

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This paper reviews the role of mast cells in the development and progression of basal cell carcinoma, squamous cell carcinoma and malignant melanoma. Mast cells accumulate around cutaneous malignancies. Current evidence suggests that mast cells contribute to the tumorigenesis of cutaneous malignancies through four mechanisms. (1) Immunosuppression: Ultraviolet-B radiation, the most important initiator of cutaneous malignancies, activates mast cells. Upon irradiation of the skin, trans-urocanic acid in the epidermis isomerizes to cis-urocanic acid, which stimulates neuropeptide release from neural c-fibers. These neuropeptides in turn trigger histamine secretion from mast cells, leading to suppression of the cellular immune system. (2) Angiogenesis: Mast cells are the major source of vascular endothelial growth factor in basal cell carcinoma and malignant melanoma. Vascular endothelial growth factor is one of the most potent angiogenic factors, which also induces leakage of other angiogenic factors across the endothelial cell wall into the matrix. Mast cell proteases reorganize the stroma to facilitate endothelial cell migration. As well, heparin, the dominant mast cell proteoglycan, assists in blood-borne metastasis. (3) Degradation of extracellular matrix: Through its own proteases, and indirectly via interaction with other cells, mast cells participate in degradation of the matrix, which is required for tumor spread. (4) Mitogenesis: Mast cell mediators including fibroblast growth factor-2 and interleukin-8 are mitogenic to melanoma cells. Current evidence supports an accessory role for mast cells in the development and progression of cutaneous malignancies. Emerging data, however, also suggest that mast cells might, in fact, have opposing roles in tumor biology, and the microenvironment could polarize mast cells to possess either promoting or inhibitory effects on tumors.

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Ultraviolet B irradiation of skin induces mast cell degranulation and release of tumour necrosis factor‐α

Cited by 85 publications

References 35 publications

Ultraviolet B irradiation selectively increases the production of interleukin-8 in human cord blood-derived mast cells

Ultraviolet B irradiation selectively increases the production of interleukin-8 in human cord blood-derived mast cells

Inflammatory Murine Skin Responses to UV-B Light Are Partially Dependent on Endothelin-1 and Mast Cells

Mast cells and cutaneous malignancies

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