Peptides protect normal skin and ease sensitive skin

Sensitive skin is a widespread disorder that is normally accompanied by prickling, burning, tingling, pain, itching, erythema, dilated capillaries, hyperpigmentation and/or flush. Such disturbances can be induced and exacerbated by several factors like pollution, UV radiation, heat, adverse weather, sport practice, specific foods, stress and/or even the use of certain everyday substances like soap, cosmetics or even perfumes. As the visible consequences of sensitive skin mainly affects the facial zone, there is an increased interest in lessening them and reducing the discomfort that they cause. It is also worth mentioning that the very same factors that cause sensitive skin alterations can turn normal skin into sensitive after a certain period of exposure. This undesired change occurs as such challenging agents are able to temporarily or permanently weaken the skin’s natural protection system, which becomes sensitised and then presents the same symptoms as sensitive skin. Thus, not only reducing sensitive skin disturbances but also preventing normal skin from turning into sensitive (enhancement of the cutaneous natural defence system) becomes essential to raise skin comfort.

Changes in sensitive skin

It is agreed that sensitive skin is characterised by a hyperreactivity of the skin to external stimuli that increases redness, dehydration and transepidermal water loss (TEWL) for example, leading not only to a fragile appearance but also to premature wrinkle formation. There is also a proved relationship between the disruption of the permeability of the skin barrier system and the lipids in the stratum corneum (SC). An acute barrier disruption raises the pH of normal SC, activating serine proteases in the outer epidermis that degrade the key processing enzymes required for the homeostasis of the normal permeability of the barrier.1 Personal wellness and comfort is already affected by these alterations but they may get worse and lead to inflammatory disorders such as atopic dermatitis (AD) or acne, which share a common pattern of barrier impairment and increased vascular reactivity. In addition, the threshold for pruritic stimuli is lower in sensitive skin and inflammatory and/or pruritic chronic disorders, which may result in a peripheral itch sensation. During inflammation or hypersensitivity, a specific type of sensory neuron liberates peptides and neurotransmitters that result in the release of other products like cytokines, which reinforce inflammation. Expressed in keratinocytes, afferent neurons and inflammatory cells among others, proteinase activated receptor 2 (PAR-2) mediates neurogenic inflammation and participates in this cytokines release, especially of interleukin-6 (IL-6) and interleukin-8 (IL-8).1–3 PAR-2 is also involved in the delay of the barrier function recovery, increase of cellular excitability and response to stimuli, via receptors like the transient receptor potential vanilloid-1 (TRPV1). TRPV1 is a non-selective plasmamembrane ion-channel that mediates the responses to stimuli and participates in neurogenic inflammation, contributing to the presence of additional inflammatory elements like IL-6 and IL-8.2 When the skin is exposed to allergens for instance, PAR-2 is stimulated inducing allergic inflammation and directly affecting the structure and function of the epidermal barrier, whose disruption facilitates the further penetration of the allergens, propagating a vicious cycle.1 Besides, inflammatory disorders are linked to facial redness and telangiectasia (dilated capillaries), concentrated in the central third of the face.4 Despite its uncertain etiology, facial redness is connected to strong emotions, sport practise, UV radiation, some foods (spicy) or drinks, adverse weather and certain elements of the natural immune system response, like cathelicidins and kallikreins.4,5 Cathelicidins are potent antimicrobial compounds that promote the expression of extracellular matrix components and angiogenesis, and coordinate local vascular function.5,6 In humans, these antibiotic molecules are inactive as a pro-protein named 18kDa cationic antimicrobial protein (CAP18) until the proteolytic processing by the skin serine protease kallikrein-5 turns it biologically active as 37-amino-acid peptide (LL-37).5,6 Once activated, LL-37 generates an angiogenic effect and increase of proinflammatory metabolites (IL-6, IL-8...) that finally induce capillary dilation, papules, redness, inflammation and, sometimes, post-inflammatory hyperpigmentation.5,6 In redness skin, LL-37 expression is abnormally high as well as IL-6 and IL-8 levels, and cathelicidins.5,6 Additionally, local inflammation has negative effects on skin firmness and elasticity too as it activates matrix metalloproteinases that increase the degradation of collagen and elastin, worsening skin properties and appearance. Therefore, the reduction of the elements and events that induce sensitive skin alterations, like the exacerbated release of ILs, would ameliorate skin comfort.