SKIN MICROBIOME 17


comparing target expression in treated keratinocytes with negative control were statistically upregulated compared to untreated (data not shown). This positive modulation has also been confirmed by indirect modulation of the sensitive skin cosmetic ingredient on extracellular matrix (ECM) remodeling by activated fibroblast exosome-mediated. The exosomes from keratinocytes treated with the sensitive skin cosmetic ingredient deliver to fibroblasts a final message of ECM restructuration through the synthesis of its main components (data not shown). Moreover, exosome-mediated


communication has underlined the positive role of the sensitive skin cosmetic ingredient and the link between microbiota-skin interaction and epidermis cross talk. It has also highlighted its key role in the repression of the aging process and senescence in fibroblast via downstream signalizations pathways. Altogether, these results highlight the ability of the sensitive skin cosmetic ingredient to restore and maintain skin homeostasis.


In vivo objectivation The beneficial effects of the sensitive skin cosmetic ingredient on barrier function have been evaluated in vivo. An open intra-individual placebo-controlled study was performed on 18 volunteers with dry, atopic tendency and prone to rosacea skin. Redness, clarity, TEWL, corneocyte cohesion and hydration were evaluated after 14 days of twice daily application of standard W/O emulsion. The sensitive skin cosmetic ingredient


improves skin radiance by reducing significantly redness vs placebo by 129% as fast as 14 days while significantly improving skin clarity with lighter skin (by 200% vs placebo). TEWL significantly reduced by 36% vs


placebo as fast as 14 days. The sensitive skin cosmetic ingredient improves cutaneous barrier and regulates water exchange mechanism back to its normal balance. Thanks to cutaneous barrier strengthening, it offers skin protective effect while providing an optimal moisture level. Compared to placebo, the sensitive skin cosmetic ingredient significantly increases cutaneous hydration rate by 33% as fast as 14 days. By increasing cutaneous hydration, it presents a moisturizing effect on epidermis superficial layers. The sensitive skin cosmetic ingredient


improves cellular cohesion and reduces stratum corneum exfoliation by significantly decreasing surface occupied and by squamae and the desquamation index (-67%) versus placebo. In summary, the sensitive skin cosmetic ingredient visibly reduces skin redness,


October 2020 25 n Placebo n Kalmethic® 0.5%


20


15


10


-50% *


-67% *


5


0 Surface occupied by squamae Desquamation index


Figure 8: Evaluation of positive effect on the cellular cohesion of Kalmethic® statistical analysis was performed using T-test (* p-value<0.05 vs placebo).


strengthens skin barrier function and reduces skin dryness. Moreover, all the volunteers reported a noticeable decrease in cutaneous discomforts.


Conclusion The beneficial effects of Kalmethic®


on


signaling cascade between microbiota- epidermis have been highlighted thanks to TLRs modulation inducing a positive feedback loop on transcription factor NF- kB which in turn positively activates downstream pathways on epithelization in keratinocytes. As result, skin integrity is improved, hence reducing sensitive skin prevalence. Kalmethic thanks to its ability to firstly


positively modulate skin-microbiota interaction and secondly to regulate skin aging pathways and dermal remodeling highlighted by exosome-based dermal communication, represents an interesting, original and innovative solution to restore skin homeostasis and address sensitive skin concerns. Dedicated to sensitive skin, Kalmethic


offers a natural and powerful solution, Cosmos approved and Natrue compliant, with a very safe profile to restore and protect skin barrier function exposed to external aggressions while reducing sensitive skin’s discomforts, repressing aging and senescence process for a more beautiful skin.


References: 1 Grice E, Segre J. The skin microbiome; Nat Rev Microbiol. 2011 April; 9(4): 244-253.


2 Grice E, Kong H. Topographical and temporal diversity of the human skin microbiome;


by D-Squam® Science. 2009; 234: 1190-1192.


3 Schommer N, Gallo R. Structure and function of the human skin microbiome; Trends Microbiol. 2013; 21(12):660-668.


4 Sur I, Ulvmar M, Toftgard R. The two-faced NF-kB in the skin; International Reviews of Immunology, 27:205-223, 2008.


5 Hayden M, Ghosh S. NF-kB, the first quarter- century: remarkable progress and outstanding questions; Genes & Development 2012; 26:203-204


6 Lai Y, Nardo A, Nakatsuji T, et al. Commensal bacteria regulate TLR3-dependent inflammation following skin injury; Nat Med. 2009; 15(12):1377-1382.


7 Yuki T, Yoshida H, Akazawa Y, Komiya A, Sugiyama Y, Inoue S. Activation of TLR2 enhances tight junction barrier in epidermal keratinocytes; J. Immunol 2011; 187: 3230-3237.


8 Kuo I, Carpenter-Mendini A, Yoshida T. Activation of epidermal Toll-like receptor 2 enhances tight junction function: implication for atopic dermatitis and skin barrier repair, J Invest Dermatol. 2013;133(4):988-98.


9 Zanoni I, Ostuni R, Marek L, et al. CD14 controls the LPS-induced endocytosis of Toll- like receptor 4; NIH 2011; 147(4): 868–880.


10 Olivieri F, Rippo M, Prattichizzo F. Toll-like receptor signalling in “inflamaging”: microRNA as new players; Immunity & Ageing 2013, 10:11.


PC


11 Dimitriu P, Ilker B. New insights into the intrincic and extrinsic factors that shape the human skin microbiome, American Society for Microbiology 2019; 10(4).


12 Raposo G, Stoorvogel W. Extracellular vesicles: exosomes, microvesicles, and friends, The Journal of cell biology 2013; 200(4): 373-383.


PERSONAL CARE NORTH AMERICA . The


∆% at D14


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