SKIN PROTECTION
Franziska Wandrey, Daniel Schmid, Jasmin Lozza, Esther Belser, Fred Zülli – Mibelle Biochemistry, Switzerland
Modified baker’s yeast cell wall active rebalances skin
ABSTRACT
The high prevalence of allergies, for example skin eczema, in the industrialised world can be explained by an unbalanced immune system because the defence reaction against allergens involves overactivation of the T helper cell Th2 pathway. This causes immunoglobulin E antibody production and ultimately leads to histamine production and an allergic reaction, characterised in the skin by dryness, redness and itchiness. Suppression of the Th2 pathway by Th1 could alleviate allergic reactions. Treatment with a new modified cosmetic active derived from baker’s yeast cell wall, MgCM-Glucan, leads to a suppression of Th2-activated allergic response. Additionally, MgCM- Glucan improves the skin barrier, smoothness and hydration for an increased wellbeing of the skin.
In the past few decades, there has been a significant increase of allergies in the industrialised world. This does not only include the obvious allergies such as asthma and hay fever; many suffer from eczematous skin, which is characterised by chronic skin dryness, redness, itching, and inflammation. Notably, a general hypersensitivity and malfunctioning of the immune system seems to be the common cause since sufferers from eczema are prone to develop other allergic conditions.1 Although a hereditary component
definitely plays a role in developing eczema, genetics alone cannot explain the rise in eczematous skin diseases since the last century. It has been recognised that environmental factors strongly influence the number of skin eczema occurrences as well as their severity. Indeed, epidemiological research showed that people living in urban areas in smaller size families experience eczema and other allergies far more often than those in rural communities.2
Based on this, the ‘hygiene hypothesis’ was 64 PERSONAL CARE February 2016 a Pathogen Th1 response Th1 Th0 Antigen-presenting cell Th2 Th2 response IgE b
Pathogen + MgCM-Glucan
Th1 Th0 Antigen-presenting cell Th2 Th2 response B cell IgE
Figure 1: Scheme of the immune response paths activated upon pathogen encounter. a) In people suffering from allergies, the Th2 path is overactivated upon exposure to a pathogen. This leads to IgE production by B cells and ultimately atopic sensitisation. b) Treatment with MgCM-Glucan shifts the immune response following a pathogen encounter towards the Th1 path, inhibiting Th2.
postulated in 1989.3 This hypothesis
links the reduced contact with viral and bacterial pathogens during childhood to a skewed immune system development – meaning that too clean an environment can lead to hypersensitivity and allergic reactions later on.
The Th1/Th2 story The hygiene hypothesis can be best explained on a molecular level with the type 1 T helper (Th1)/type 2 T helper (Th2) immune-balance model. Upon exposure to a pathogen, antigen- presenting cells, such as dendritic cells in the skin, will activate T helper cells, which then in turn secrete cytokines to signal downstream and guide the immune response. There are two different paths this
immune response could take, depending
on which T helper cell type is activated. The first path, which involves the helper cell Th1, activates macrophages as a defence against the pathogen (Fig. 1a). Macrophages are cells of the innate immune system, which combat local inflammation by engulfing and digesting microbial intruders. In contrast, the immune response path involving Th2 stimulates B cells, which are part of the adaptive immune system (Fig. 1a). These activated B cells produce immunoglobulin E (IgE) antibodies,4 which bind to mast cells, that in turn release histamine and can subsequently lead to allergic sensitisation. Healthy individuals possess a balanced
immune response, where the appropriate path is chosen depending on the pathogen. In most cases, a Th1-mediated response involving macrophages is
Atopic sensitisation Th1 response Macrophage No pathology B cell Atopic sensitisation Macrophage No pathology
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