619 Pentapeptide to Control Acne
DMSO nor pKTSKS (Figure 5) affected S. epidermidis growth. These results can be compared
with those displayed in Figure 2 to highlight the role of pKTSKS on bacterial growth.
Furthermore, S. epidermidis abundance in the microbiota of volunteers was also measured
during the clinical trial described above. S. epidermidis population was not modified by
pKTSKS in vivo: +15.4% (p =0.36). These data confirm that pKTSKS inhibits C. acnes
without modulating S. epidermidis growth.
EFFECT OF PKTSKS ON EPIDERMIS
Skin barrier functions. The epidermal barrier is one of the keystones of our body’s protection.
A good barrier preserves skin hydration and provides a healthy substrate for resident
microbiota. It requires an epidermis whose keratinocytes are fully differentiated. Incomplete
keratinocytes differentiation can lead to thinning of the stratum corneum and to a greater
penetration of bacterial allergens favoring proinflammatory mechanisms. Figure 6 and
Table I show the positive effect of pentapeptide pKTSKS on epidermal differentiation.
Whereas epidermis thickness is moderately modified (−6%), stratum corneum thickness
increases by 186% (p 0.01 versus control gel).
1.3
1.35
1.4
1.45
1.5
1.55
1.6
30h 20h
Time (h)
Effect of pKTSKS on S. epidermidis growth
Solvent control pKTSKS 6ppm pKTSKS 9ppm pKTSKS 12ppm
Figure 5. Effect of pKTSKS on S. epidermidis growth kinetic over time (n =7). Turbidity measurements
(OD600nm) on S. epidermidis, to evaluate effect of pKTSKS on S. epidermidis growth after 20 h and 30 h of
treatment with pKTSKS.
Figure 6. Effect of pKTSKS (9 ppm) on Stratum Corneum Thickness in LSE. The thickness of the stratum
corneum was measured in H&E-stained sections, as indicated by white bars (n =4). LSE were topically treated
with pKTSKS or control for 48 h, embedded in freezing media, and sectioned into 5–7 µm slices for analysis.
OD
600nm

620 JOURNAL OF COSMETIC SCIENCE
Hyaluronic acid production by human keratinocytes. Hyaluronic acid is a natural skin moisturizer
existing both in the dermis and around keratinocytes. It allows the transfer of nutrients,
vitamins, salts, and of immune cells into the epidermis. Human keratinocytes were
placed in contact with various concentrations of pKTSKS to assess its ability to induce the
production of hyaluronic acid. Hyaluronic acid production by keratinocytes thus increased
significantly in a dose-dependent manner by 33%–62% (Figure 7).
EFFECT OF PKTSKS ON DERMIS
Dermal matrix restructuring through protein synthesis. Pentapeptide pKTSKS was demonstrated
to trigger the production of dermal extracellular matrix proteins by fibroblasts. Thus,
collagen-I production is increased under conditions described above by 184%, collagen-IV
by 98% and fibronectin by 67% (Table II).
EFFECT OF PKTSKS ON INFLAMMATORY RESPONSE
In acne condition, proinflammatory cytokines are upregulated due to bacterial proliferation
and pore clogging. Although this inflammatory process is transitory, prolonged cytokines
production results in scarring.27 This led us to study the effect of pKTSKS on inflammatory
cytokines.
IL-6 production by human sebocytes and keratinocytes in presence of C. acnes. C. acnes can disturb
skin homeostasis and trigger proinflammatory mediators release from skin cells, such as
IL-6. Human sebocytes and keratinocytes were first treated with pKTSKS for 24 hours.
Table I
Effect of pKTSKS (9 ppm) Applied Onto the Surface of LSE Thickness of Stratum Corneum (n =4)
Stratum corneum thickness (µm) Variation (%)
Control 16 ± 5 Reference.
pKTSKS 9 ppm 45 ± 11 +186% p 0.01
0
1000
2000
3000
4000
5000
6000
7000
8000
Solvent control pKTSKS 6ppm pKTSKS 9ppm pKTSKS 12ppm
Kerag415nocyte treatment
Effect of pKTSKS on hyaluronic acid producg415on
Figure 7. Variation in hyaluronic acid production by human keratinocytes effect of pKTSKS (n =5).
Secretion (ng/106 keratinocytes) of hyaluronic acid in supernatants of keratinocytes treated with pKTSKS
(6 ppm, 9 ppm, 12 ppm).
ng/10^6cell