Substance P Enhances the Production of Interferon-induced Protein of 10 kDa by Human Keratinocytes in Synergy with Interferon-γ
Journal of Investigative Dermatology, ISSN: 0022-202X, Vol: 119, Issue: 6, Page: 1290-1297
2002
- 26Citations
- 11Captures
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Metrics Details
- Citations26
- Citation Indexes26
- 26
- CrossRef20
- Captures11
- Readers11
- 11
Article Description
A neuropeptide substance P is related to skin inflammation. Interferon-induced protein of 10 kDa (IP-10) chemoattracts T helper 1 cells, and interferon-induced protein of 10 kDa production by keratinocytes is enhanced in inflammatory skin diseases such as psoriasis. We examined the in vitro effects of substance P on interferon-induced protein of 10 kDa production by human keratinocytes. Though substance P alone did not induce interferon-induced protein of 10 kDa production, it enhanced interferon-induced protein of 10 kDa secretion, mRNA expression, and promoter activity induced by suboptimal concentrations of interferon-γ. Interferon-stimulated response element and two nuclear factor-κB sites on interferon-induced protein of 10 kDa promoter were responsible for the enhancement by substance P. Substance P alone enhanced transcriptional activity and transcription factor binding through the two nuclear factor-κB sites, whereas it did not alter interferon-γ-induced transcriptional activity and transcription factor binding through interferon-stimulated response element. The effects of substance P on interferon-induced protein of 10 kDa production and nuclear factor-κB activation were inhibited by neurokinin-1 receptor antagonist, phospholipase C inhibitor, intracellular Ca 2+ chelator, and anti-oxidant. These results suggest that substance P may induce nuclear factor-κB activation and interferon-induced protein of 10 kDa production in synergy with interferon-γ via neurokinin-1 receptor on keratinocytes. These effects of substance P may be mediated via phospholipase C activation, intra-cellular Ca 2+ signal, and reactive oxygen intermediates.
Bibliographic Details
http://www.sciencedirect.com/science/article/pii/S0022202X1530097X; http://dx.doi.org/10.1046/j.1523-1747.2002.19626.x; http://www.scopus.com/inward/record.url?partnerID=HzOxMe3b&scp=0036915653&origin=inward; http://www.ncbi.nlm.nih.gov/pubmed/12485430; https://linkinghub.elsevier.com/retrieve/pii/S0022202X1530097X
Elsevier BV
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