Defense of the skin with LL-37.

نویسندگان

  • Navid Bouzari
  • Nancy Kim
  • Robert S Kirsner
چکیده

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Skin electroporation of a plasmid encoding hCAP-18/LL-37 host defense peptide promotes wound healing.

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The human cathelicidin LL-37 host defense peptide upregulates tight junction-related proteins and increases human epidermal keratinocyte barrier function.

Both psoriasis and atopic dermatitis (AD) are not only associated with an impaired stratum corneum barrier, but also with abnormal expression of the tight junction (TJ) proteins. Because host defense peptides, including LL-37, are overexpressed in lesional psoriatic skin but are downregulated in lesional AD skin, we hypothesized that LL-37 might regulate the TJ function in keratinocytes. We dem...

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Human cathelicidin CAP18/LL-37 changes mast cell function toward innate immunity.

The antimicrobial peptide LL-37 is generated from skin keratinocytes during infection of Gram-negative bacteria and exerts a microbicidal effect. LL-37 also causes functional changes in mast cells. Mast cells in the skin are involved in the innate immune system response against microbial infections via Toll-like receptors (TLRs), such as TLR4, which that is known to recognize lipopolysaccharide...

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The antimicrobial peptide LL-37 is generated upon proteolytic cleavage of cathelicidin and limits invading pathogens by directly targeting microbial membranes as well as stimulating innate immune cell function. However, some microbes evade LL-37-mediated defense. Notably, group A Streptococcus (GAS) strains belonging to the hypervirulent M1T1 serogroup are more resistant to human LL-37 than oth...

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عنوان ژورنال:
  • The Journal of investigative dermatology

دوره 129 4  شماره 

صفحات  -

تاریخ انتشار 2009