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α-MSH reduces the internalization ofStaphylococcus aureusand down-regulates HSP 70, integrins and cytokine expression in human keratinocyte cell lines.
- Source :
- Experimental Dermatology; Dec2004, Vol. 13 Issue 12, p748-754, 7p
- Publication Year :
- 2004
-
Abstract
- Donnarumma G, Paoletti I, Buommino E, Tufano MA, Baroni A.α-MSH reduces the internalization ofStaphylococcus aureusand down-regulates HSP 70, integrins and cytokine expression in human keratinocyte cell lines.α-melanocyte-stimulating hormone (α-MSH) is a neuropeptide predominantly produced by the pituitary gland, but it is also generated by many extra-pituitary cells including keratinocytes of the skin. This neuropeptide has anti-inflammatory and antimicrobial effects and probably contributes in innate immunity.Staphylococcus aureusis the aetiological agent of a wide range of infections in humans. Colonization of human skin byS.aureusis a characteristic feature of several skin diseases and is often followed by tissue invasion and severe cell damage. The aim of our study was to detect a possible role ofα-MSH during the early infection stages in the adhesion and penetration of keratinocytes before cell damage. Our data demonstrated thatα-MSH precociously down-regulates the production of integrins such asβ1 and heat shock surface protein 70, essential molecules for the entry ofS.aureus. Moreover, in our experimental model,α-MSH induces the down-regulation of the pro-inflammatory cytokine expression and of the adhesion molecules in keratinocytes activated byS.aureus. Our data suggest thatα-MSH plays a protective role in the skin by reducing infection and the inflammatory process. [ABSTRACT FROM AUTHOR]
- Subjects :
- CELLS
KERATINOCYTES
GLYCOPROTEINS
MOLECULES
PSYCHOANALYSIS
CELL culture
Subjects
Details
- Language :
- English
- ISSN :
- 09066705
- Volume :
- 13
- Issue :
- 12
- Database :
- Complementary Index
- Journal :
- Experimental Dermatology
- Publication Type :
- Academic Journal
- Accession number :
- 15123583
- Full Text :
- https://doi.org/10.1111/j.0906-6705.2004.00218.x