A new pentapeptide improves skin surface damages on face induced by Cutibacterium acnes activity.
Podium 23
Presented by: Richard Leroux
Introduction:
The human body and its microbiota, form a complex supra-organism called holobiont whose disruptions are now thought to be the cause of pathologies. 90% of teens undergo overproduction of sebum and proliferation of Cutibacterium acnes (CA). Consecutive clogging of pilosebaceous ducts often causes local irritation leading to the denaturation of neighboring tissues, creating skin blemishes, comedones, skin redness, and significant psychological damage. While cosmetic products cannot treat inflammatory acne lesions, it is possible to significantly minimise the negative aspects due to these lesions, by acting either upstream or downstream of the problem. Peptides are widely and safely used by the cosmetic industry since pioneering works of Lintner. A new peptide palmitoyl-Lysyl-Threonyl-Seryl-Lysyl-Serine (pKTSKS) controls growth, quorum, adhesion and biofilm of CA, all features involved in formation of acne lesions. pKTSKS does not act on Staphylococcus epidermidis (SE), and parallel reinforces epidermal barrier functions essential for a healthy skin while improving extracellular matrix protein synthesis such as collagens. Most of significantly impactful aspects of acne lesions were evaluated: pimples, scars, redness, brownish. In addition, microbiote sampled on skin, was analyzed.
Methods:
Various CA ribotypes (RT1-4-5) were used. Briefly, cells were in contact with pKTSKS (6-12ppm) in anaerobic conditions; all growths were measured using turbidimetry methods on samples. Biofilm studies were performed on plastic surface for 72h, planktonic cells were estimated as mentioned before while adherent cells were quantified with crystal violet. SE growths were estimated using a Bioscreen C equipment. Both human sebocytes, keratinocytes and THP1 macrophages were stressed for 24-48h with living CA at various ratio depending on the assays. IL6, TNFa, collagen-I, -IV, hyaluronate dosages were performed on cell culture medium with ELISA methods. pKTSKS was applied topically on equivalent skins for 2 days, then skins were sectioned (7µm) and stratum corneum thickness was evaluated under a microscope. Clinical evaluations were performed on Caucasian volunteers [18-58 years old; N=48]. Creams containing 12ppm of peptide or its vehicle (control) were applied for 2months on face twice a day. Impactful aspects: pimples, scars, redness, brownish were evaluated using comparative photos, images analyses equipment, multispectral camera, clinical evaluations by a dermatologist. In addition, microbiote was sampled on skin using swabs and analyzed using qRTPCR and 16S technologies.
Results:
From a preliminary screening we identified peptide pKTSKS, which reduces CA quorum by 93%*. Neither palmitic acid nor KTSKS had any effects on cells growth at the same concentrations. Peptide doesn’t have any remanence effect once cells are rinsed; their growths were identical to control, meaning that pKTSKS is not toxic to CA. It delays RT1-4-5 growth, reduces CA adhesion and biofilm formation by >70%* and 98%*. pKTSKS reduces overproduction of IL6 from human sebocytes and keratinocytes in contact with CA cells by 48%* and 89%* respectively while it triggers IL1ra synthesis in keratinocytes (28%*). pKTSKS reduces IL6 and TNFa secreted by THP1 macrophages when co-cultured with CA by 92%* and 73%* respectively. Peptide improves stratum corneum thickness by 150%* and triggers more mature keratinocytes and hyaluronate synthesis by 62%*. In contact of dermal fibroblasts, it induces collagen-I and -IV synthesis by 184%* and 98%* respectively. SE population was not significantly modified neither by the peptide nor the placebo while the CA population was reduced on skin. Cutaneous skin imperfections were significantly reduced after 1-2months by the peptide compared to placebo. Volume of lesions, of scars, and roughness were all reduced by 34%*, 19%* and 6.5%* respectively vs placebo. Volunteers noticed after 1month less scars with peptide versus placebo (92%* vs 38%) which appeared less visible (92%* vs 62%), in addition they noticed less imperfections (83%* vs 50%). Moreover redness, inflammatory lesions and residual marks were reduced significantly versus placebo by 7%*, 22%* and 17%* respectively. * p<0.05 or 0.01
Conclusion:
From a preliminary screening of micropeptides performed on CA cells, we identified the pKTSKS peptide which acts on cell growth, adherence, quorum and biofilm without killing cells. This peptide acts too on pre-inflammatory mediators of skin cells, reducing their damaging effects on neighboring tissues and avoiding consecutive irritations. This peptide reduces skin surface blemishes, redness and brownish on skin. This new peptide increases the role of the cosmetic peptides for skin in minimizing the negative aspects of rough skin.
The human body and its microbiota, form a complex supra-organism called holobiont whose disruptions are now thought to be the cause of pathologies. 90% of teens undergo overproduction of sebum and proliferation of Cutibacterium acnes (CA). Consecutive clogging of pilosebaceous ducts often causes local irritation leading to the denaturation of neighboring tissues, creating skin blemishes, comedones, skin redness, and significant psychological damage. While cosmetic products cannot treat inflammatory acne lesions, it is possible to significantly minimise the negative aspects due to these lesions, by acting either upstream or downstream of the problem. Peptides are widely and safely used by the cosmetic industry since pioneering works of Lintner. A new peptide palmitoyl-Lysyl-Threonyl-Seryl-Lysyl-Serine (pKTSKS) controls growth, quorum, adhesion and biofilm of CA, all features involved in formation of acne lesions. pKTSKS does not act on Staphylococcus epidermidis (SE), and parallel reinforces epidermal barrier functions essential for a healthy skin while improving extracellular matrix protein synthesis such as collagens. Most of significantly impactful aspects of acne lesions were evaluated: pimples, scars, redness, brownish. In addition, microbiote sampled on skin, was analyzed.
Methods:
Various CA ribotypes (RT1-4-5) were used. Briefly, cells were in contact with pKTSKS (6-12ppm) in anaerobic conditions; all growths were measured using turbidimetry methods on samples. Biofilm studies were performed on plastic surface for 72h, planktonic cells were estimated as mentioned before while adherent cells were quantified with crystal violet. SE growths were estimated using a Bioscreen C equipment. Both human sebocytes, keratinocytes and THP1 macrophages were stressed for 24-48h with living CA at various ratio depending on the assays. IL6, TNFa, collagen-I, -IV, hyaluronate dosages were performed on cell culture medium with ELISA methods. pKTSKS was applied topically on equivalent skins for 2 days, then skins were sectioned (7µm) and stratum corneum thickness was evaluated under a microscope. Clinical evaluations were performed on Caucasian volunteers [18-58 years old; N=48]. Creams containing 12ppm of peptide or its vehicle (control) were applied for 2months on face twice a day. Impactful aspects: pimples, scars, redness, brownish were evaluated using comparative photos, images analyses equipment, multispectral camera, clinical evaluations by a dermatologist. In addition, microbiote was sampled on skin using swabs and analyzed using qRTPCR and 16S technologies.
Results:
From a preliminary screening we identified peptide pKTSKS, which reduces CA quorum by 93%*. Neither palmitic acid nor KTSKS had any effects on cells growth at the same concentrations. Peptide doesn’t have any remanence effect once cells are rinsed; their growths were identical to control, meaning that pKTSKS is not toxic to CA. It delays RT1-4-5 growth, reduces CA adhesion and biofilm formation by >70%* and 98%*. pKTSKS reduces overproduction of IL6 from human sebocytes and keratinocytes in contact with CA cells by 48%* and 89%* respectively while it triggers IL1ra synthesis in keratinocytes (28%*). pKTSKS reduces IL6 and TNFa secreted by THP1 macrophages when co-cultured with CA by 92%* and 73%* respectively. Peptide improves stratum corneum thickness by 150%* and triggers more mature keratinocytes and hyaluronate synthesis by 62%*. In contact of dermal fibroblasts, it induces collagen-I and -IV synthesis by 184%* and 98%* respectively. SE population was not significantly modified neither by the peptide nor the placebo while the CA population was reduced on skin. Cutaneous skin imperfections were significantly reduced after 1-2months by the peptide compared to placebo. Volume of lesions, of scars, and roughness were all reduced by 34%*, 19%* and 6.5%* respectively vs placebo. Volunteers noticed after 1month less scars with peptide versus placebo (92%* vs 38%) which appeared less visible (92%* vs 62%), in addition they noticed less imperfections (83%* vs 50%). Moreover redness, inflammatory lesions and residual marks were reduced significantly versus placebo by 7%*, 22%* and 17%* respectively. * p<0.05 or 0.01
Conclusion:
From a preliminary screening of micropeptides performed on CA cells, we identified the pKTSKS peptide which acts on cell growth, adherence, quorum and biofilm without killing cells. This peptide acts too on pre-inflammatory mediators of skin cells, reducing their damaging effects on neighboring tissues and avoiding consecutive irritations. This peptide reduces skin surface blemishes, redness and brownish on skin. This new peptide increases the role of the cosmetic peptides for skin in minimizing the negative aspects of rough skin.