Everything you need to know about the cutaneous microbiome.

Often mistaken for one another, the skin microbiota and the skin microbiome are however subtly distinct. The microbiota refers to the collection of micro-organisms – bacteria, yeasts, fungi, viruses or archaea – that colonise a specific area of our body, such as the skin, the gut or the mouth. The microbiome, on the other hand, refers to the micro-organisms along with all the genetic material they contain: it therefore encompasses everything that these micro-organisms can do collectively (molecule synthesis, lipid transformation, defence against pathogens…).

The microbiome therefore describes a reality broader than the microbiota.

After the gut, the skin is the organ most densely populated with microorganisms, with an estimated concentration between 104 and 106 bacteria per square centimetre and over 200 genera identified. This ecosystem harbours around 18 phyla, of which four are dominant. These microorganisms coexist in a delicate dynamic equilibrium and contribute to skin health.

It should be noted that the cutaneous microbiota is not evenly distributed across the skin: it varies according to the characteristics of different skin regions.

• The sebaceous areas (front, back, torso), rich in sebaceous glands, are densely colonised by Cutibacterium, capable of degrading sebum triglycerides into short-chain fatty acids, such as propionic acid, which help maintain a protective acidic pH.

• The moist areas (armpits, skin folds, groin) primarily harbour Staphylococcus and Corynebacterium, which are tolerant of salt and heat.

• The dry areas (forearms, legs) are characterised by greater bacterial diversity but lower stability over time.

This microbial biogeography reflects the adaptation of species to very different local conditions: variations in pH, temperature, humidity, sebum levels or UV exposure.

The cutaneous microbiome is essential for maintaining skin health and balance. Far from being a mere community of microorganisms thriving on the skin, it forms a dynamic, living ecosystem, in constant dialogue with the cells of the skin barrier and the immune system. These interactions are vital to preserve barrier function, modulate inflammation and prevent colonisation by opportunistic pathogens.

One of the primary roles of the skin microbiome is protection against harmful microorganisms. Commensal bacteria, such as Staphylococcus epidermidis, produce antimicrobial peptides and organic acids capable of inhibiting the growth of pathogenic bacteria, such as Staphylococcus aureus. This phenomenon of ecological competition limits the proliferation of undesirable species and maintains a balance conducive to skin health. Meanwhile, the skin’s naturally acidic pH, sustained by the metabolism of lipids and fatty acids derived from sebum, helps to reinforce this antimicrobial barrier.

Furthermore, the skin microbiome also contributes to the maturation of the local immune system. From birth, the skin comes into contact with a multitude of micro-organisms that “educate” immune cells. Studies have shown that certain commensal bacteria induce immune tolerance by modulating the production of anti-inflammatory cytokines. This intervention by the microbiota helps the skin distinguish harmless agents from those that must be eliminated. A balanced microbiota prevents some of the excessive immune reactions observed in conditions such as atopic dermatitis.

The cutaneous microbiome also plays a role in healing of wounds, by modulating the interactions between the epidermis and the local immune system. Skin commensal organisms are indeed in constant communication with immune cells, notably T lymphocytes and keratinocytes, in order to maintain a balance between inflammation and tissue repair. Some research highlights the beneficial effect of Staphylococcus epidermidis, capable of stimulating alternative repair mechanisms through the recruitment of regulatory CD8+ T lymphocytes. This particular immunological dialogue, unique to commensal bacteria, appears to favour balanced healing and limit excessive inflammatory responses.

Finally, the skin microbiome plays a still underappreciated metabolic role. The microorganisms present on the skin surface contribute to the breakdown of sebum and dead skin cells, to the production of short-chain fatty acids and even to the synthesis of certain vitamins and amino acids essential to the cohesion of the skin barrier. These metabolites act directly on keratinocyte differentiation and on the quality of the hydrolipidic film.

The skin microbiome is a living ecosystem undergoing continuous evolution.

Its composition is not fixed: it evolves over the course of life, through hormonal shifts and changes in our environment or lifestyle, reflecting the constant adaptation of microorganisms. At birth, a newborn’s skin is like a blank slate that the first microbes begin to colonise. The mode of delivery influences this initial colonisation: infants born vaginally acquire a microbiota similar to their mother’s vaginal flora, rich in Lactobacillus and Prevotella, whereas those delivered by caesarean section initially harbour a flora resembling their mother’s skin, dominated by Staphylococcus and Corynebacterium. These differences tend to diminish within the first few weeks, under the influence of skin contact, nutrition and the environment.

During childhood, the skin microbiome remains relatively uniform from one body site to another. As the skin thickens and sweat and sebaceous glands mature, microbial diversity increases. During adolescence, the surge in sex hormones radically transforms the skin environment. The rise in sebum production promotes the growth of lipophilic bacteria such as Cutibacterium acnes and yeasts of the genus Malassezia. These changes explain why certain conditions, such as acne emerge during this period: some strains of C. acnes produce pro-inflammatory porphyrins that stimulate cytokine production and disrupt the local flora.

In adulthood, the cutaneous microbiome reaches a state of relative equilibrium. The composition of microbial communities varies primarily by body site, as described above. Nevertheless, the microbiome remains sensitive to many factors, such as stress, diet, exposure to sunlight, pollution, or even the use of cosmetics. Furthermore, during ageing, with decreased sebum secretion and increased skin pH, certain bacteria proliferate at the expense of others. Studies show a decrease in populations of Cutibacterium and Lactobacillus, associated with a relative increase in Corynebacterium and Streptococcus. These imbalances contribute to low-grade chronic inflammation and the increased fragility of mature skin.

The composition and diversity of the skin microbiota also appear to depend on the individual's gender. Recent studies focusing on facial flora have shown that, overall, women exhibit a higher bacterial diversity than men. This difference can be explained by several physiological and behavioural factors. The female skin is generally thinner, more acidic, better hydrated and more pampered through the more frequent use of cosmetics by women, which promotes colonisation by different bacterial species. In contrast, the male microbiota appears to be dominated by a smaller number of bacteria, notably anaerobes such as Cutibacterium spp., which thrive in sebum-rich, oxygen-poor environments.

These variations are also observed in the structure of the bacterial community. In men, the phylum dominant after the Actinobacteria is generally Firmicutes, whereas in women it is Proteobacteria. Some differences even extend to the genus level: for example, Staphylococcus and Anaerococcus are more abundant in men, whereas Sphingomonas, Pelomonas and Streptococcus are more prevalent in women. These disparities reflect physiological differences between the sexes, such as sebum production and perspiration, more pronounced in men, but also environmental factors and personal care habits.

Note : Ethnicity also seems to influence the skin microbiome. For example, certain species of Corynebacterium and of Proteobacteria are more abundant in East Asian and African populations, while others are specific to Hispanic or European groups. However, with globalisation and migration, the boundaries between ethnic microbial profiles are becoming less distinct.

The skin microbiota defends the skin through a process known as colonisation resistance. This relies on the ability of commensal micro-organisms to prevent the establishment and proliferation of pathogenic agents. When this balance is disrupted, that is, in the case of dysbiosis, the composition of the microbiota changes and certain species that were previously beneficial may become detrimental to the host, a shift recognised in the pathogenesis of various skin diseases.

One of the most extensively studied examples is acne, an inflammatory skin disease associated with the bacterium Cutibacterium acnes. Although this species is naturally present on the skin, certain strains, notably those of phylogroup 1A1, are linked to acne. These strains possess virulence factors that favour bacterial adhesion and immune system activation, thereby triggering local inflammation. Moreover, C. acnes can form biofilms within follicles, contributing to the persistence of the infection. Excess sebum production, common during adolescence, is one of the causes of proliferation of C. acnes, as this bacterium feeds on the triglycerides in sebum.

Another model illustrating cutaneous dysbiosis is atopic dermatitis. This chronic, relapsing condition arises from a combination of factors: impairment of the epidermal barrier, immune dysregulation and microbial imbalance. During an inflammatory flare-up, one observes a marked increase in staphylococci, particularly S. aureus and S. epidermidis, while overall microbial diversity decreases. These changes coincide with a worsening of symptoms, suggesting a close relationship between bacterial load and clinical severity. Moreover, it has been shown that S. aureus can trigger mast cell degranulation via its δ-toxin, thereby activating Th2-type inflammatory pathways and compromising the skin barrier.

The rosacea also emphasises the link between an imbalance of the skin microbiota and cutaneous inflammation. Several studies have shown an overexpression of the TLR-2 receptor in the epidermis of patients with rosacea, notably activated by an increased presence of mites Demodex folliculorum. This excessive stimulation triggers an inflammatory cascade with the production of pro-inflammatory cytokines, such as IL-1β and IL-8, as well as prostaglandins promoting vasodilation. Moreover, the chitin from the exoskeleton of Demodex further amplifies this response via the same TLR-2 receptor.

Note : The vitiligo, the psoriasis or even alopecia are other dermatological conditions that skin dysbiosis can influence.

Maintaining the balance of skin microbiota relies on a simple skin-care routine and gentle treatments. Indeed, the use of harsh cleansers or overly frequent exfoliation can disrupt the skin’s microbial flora and promote dysbiosis, opening the door to inflammation and infection. Similarly, repeated exposure to aggressive environmental factors such as sunlight or pollution can alter the microbial composition and reduce diversity, which is nonetheless essential to the proper functioning of the microbiome. A simple routine including a gentle cleansing, hydration suited to one’s skin type and sun protection helps to maintain a stable environment conducive to colonisation by beneficial bacteria.

Diet and lifestyle also play an indirect role. A balanced diet supports overall health and may help maintain the skin microbiota via the gut-skin axis. This term refers to the bidirectional communication between the gut and the skin, whereby the state of the gut microbiota, inflammation and the metabolites produced can influence skin health, and vice versa. Furthermore, reducing stress, getting enough sleep and avoiding unnecessary antibiotic use help prevent dysbiosis. Finally, the market for pre-, pro- and postbiotics is currently expanding rapidly and could offer a solution to support the cutaneous microbiome.

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