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Start Over Author "Nori U" Journal journal of investigative dermatology
3 results on '"Nori U"'

2. The Constitutive Capacity of Human Keratinocytes to Kill Staphylococcus aureus Is Dependent on β-Defensin 3

Author

Michael D. Howell, Donald Y.M. Leung, Nori U. Watson, Mark Boguniewicz, Kevin O. Kisich, and Heather R. Heizer

Subjects
Keratinocytes, Staphylococcus aureus, beta-Defensins, Biopsy, Antimicrobial peptides, Peptide binding, Human skin, Dermatology, Staphylococcal infections, medicine.disease_cause, Biochemistry, Microbiology, medicine, Humans, RNA, Messenger, Molecular Biology, Defensin, Cells, Cultured, Skin, biology, integumentary system, Glyceraldehyde-3-Phosphate Dehydrogenases, Cell Biology, Staphylococcal Infections, biology.organism_classification, medicine.disease, medicine.anatomical_structure, Gene Expression Regulation, Keratinocyte, Bacteria
Abstract

Normal skin is often exposed to bacteria, including potent pathogens such as E. coli, Staphylococcus aureus, and Streptococcus sp., but these microbes usually do not cause skin inflammation or infection in healthy individuals. Therefore, we hypothesized that there must be a constitutive mechanism for rapid destruction and elimination of small numbers of bacteria which penetrate the stratum corneum from everyday activities. This study found that exposure of keratinocytes cultured from a number of individuals to S. aureus resulted in approximately 2-3 log better killing than by HaCaT cells within 1 hour. Killing required contact between the keratinocytes and the bacteria, but was not dependent on internalization. Contact between the bacteria and the keratinocytes resulted in rapid deposition of several antimicrobial peptides onto the bacteria, but only human beta-defensin (HBD) 3 accumulated at levels sufficient to account for killing when S. aureus were exposed to human skin explants. Blocking peptide binding of HBD3 inhibited killing of the bacteria, indicating an essential role for beta-defensin 3 in the constitutive killing of bacteria by normal keratinocytes.

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3. The constitutive capacity of human keratinocytes to kill Staphylococcus aureus is dependent on beta-defensin 3.

Author

Kisich KO, Howell MD, Boguniewicz M, Heizer HR, Watson NU, and Leung DY

Subjects
Biopsy, Cells, Cultured, Gene Expression Regulation, Glyceraldehyde-3-Phosphate Dehydrogenases genetics, Glyceraldehyde-3-Phosphate Dehydrogenases metabolism, Humans, Keratinocytes pathology, RNA, Messenger genetics, RNA, Messenger metabolism, Skin metabolism, Skin microbiology, Skin pathology, Staphylococcal Infections physiopathology, Staphylococcal Infections prevention & control, Staphylococcus aureus growth & development, beta-Defensins genetics, Keratinocytes metabolism, Keratinocytes microbiology, Staphylococcus aureus pathogenicity, beta-Defensins metabolism
Abstract

Normal skin is often exposed to bacteria, including potent pathogens such as E. coli, Staphylococcus aureus, and Streptococcus sp., but these microbes usually do not cause skin inflammation or infection in healthy individuals. Therefore, we hypothesized that there must be a constitutive mechanism for rapid destruction and elimination of small numbers of bacteria which penetrate the stratum corneum from everyday activities. This study found that exposure of keratinocytes cultured from a number of individuals to S. aureus resulted in approximately 2-3 log better killing than by HaCaT cells within 1 hour. Killing required contact between the keratinocytes and the bacteria, but was not dependent on internalization. Contact between the bacteria and the keratinocytes resulted in rapid deposition of several antimicrobial peptides onto the bacteria, but only human beta-defensin (HBD) 3 accumulated at levels sufficient to account for killing when S. aureus were exposed to human skin explants. Blocking peptide binding of HBD3 inhibited killing of the bacteria, indicating an essential role for beta-defensin 3 in the constitutive killing of bacteria by normal keratinocytes.

Published
2007
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