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( Chao Hsuan Chen ),( Yan Han Wang ),( Teruaki Nakatsuji ),( Yu Tsueng Liu ),( Christos C. Zouboulis ),( Richard L. Gallo ),( Liangfang Zhang ),( Ming Fa Hsieh ),( Chun Ming Huang ) 한국미생물 · 생명공학회 2011 Journal of microbiology and biotechnology Vol.21 No.4
Free fatty acids (FFAs) are known to have bacteriocidal activity and are important components of the innateimmune system. Many FFAs are naturally present in human and animal skin, breast milk, and in the bloodstream. Here, the therapeutic potential of FFAs against methicillin-resistant Staphylococcus aureus (MRSA) is demonstrated in cultures and in mice. Among a series of FFAs, only oleic acid (OA) (C18:1, cis-9) can effectively eliminate Staphylococcus aureus (S. aureus) through cell wall disruption. Lauric acid (LA, C12:0) and palmitic acid (PA, C16:0) do not have this ability. OA can inhibit growth of a number of Gram-positive bacteria, including hospital and community-associated MRSA at a dose that did not show any toxicity to human sebocytes. The bacteriocidal activities of FFAs were also demonstrated in vivo through injection of OA into mouse skin lesions previously infected with a strain of MRSA. In conclusion, our results suggest a promising therapeutic approach against MRSA through boosting the bacteriocidal activities of native FFAs, which may have been co-evolved during the interactions between microbes and their hosts.
Collagen Synthesis Is Suppressed in Dermal Fibroblasts by the Human Antimicrobial Peptide LL-37
Park, Hyun Jeong,Cho, Dae Ho,Kim, Hee Jung,Lee, Jun Young,Cho, Baik Kee,Bang, Sa Ik,Song, Sang Yong,Yamasaki, Kenshi,Di Nardo, Anna,Gallo, Richard L The Society for Investigative Dermatology, Inc 2009 The Journal of investigative dermatology Vol.129 No.4
LL-37 is a human cathelicidin antimicrobial peptide that is released in the skin after injury and acts to defend against infection and modulate the local cellular immune response. We observed in human dermal keloids that fibrosis was inversely related to the expression of cathelicidin and sought to determine how LL-37 influenced expression of types I and III collagen genes in dermal fibroblasts. At nano-molar concentrations, LL-37 inhibited baseline and transforming growth factor-β-induced collagen expression. At these concentrations, LL-37 also induced phosphorylation of extracellular signal-regulated kinase (ERK) within 30 minutes. Activation of ERK, and the activation of a G-protein-dependent pathway, was essential for inhibition of collagen expression as pertussis toxin or an inhibitor of ERK blocked the inhibitory effects of LL-37. c-Jun N-terminal kinase and p38 mitogen-activated protein kinase inhibitors did not alter the effects of cathelicidin. Silencing of the Ets-1 reversed inhibitory effects of LL-37. Taken together, these findings show that LL-37 can directly act on dermal fibroblasts and may have antifibrotic action during the wound repair process.Journal of Investigative Dermatology (2009) 129, 843–850; doi:10.1038/jid.2008.320; published online 16 October 2008