Everything you need to know about the skin microbiome.

Often confused, the skin microbiota and microbiome are nevertheless subtly different. The microbiota refers to all microorganisms – bacteria, yeasts, fungi, viruses, or archaea – that inhabit a specific area of our body, such as the skin, gut, or mouth. The microbiome, on the other hand, encompasses these microorganisms along with all their genetic material: it therefore describes everything these microbes can collectively accomplish (molecule synthesis, lipid transformation, defense against pathogens…).

The microbiome thus encompasses a broader reality than the microbiota.

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

It should be noted that the skin microbiota is not uniformly distributed across the skin: it varies depending on the characteristics of the skin regions.

• The sebaceous regions (forehead, back, chest), rich in sebaceous glands, are densely populated by Cutibacterium, which can degrade sebum triglycerides into short-chain fatty acids, such as propionic acid, that maintain a protective acidic pH.

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

• The dry areas(forearms, legs) exhibit 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, or UV exposure.

The skin microbiome is essential for maintaining skin health and balance. Far from being merely a collection of microorganisms thriving on the skin, it constitutes a living, interactive ecosystem, in constant dialogue with the cells of the skin barrier and the immune system. These exchanges are essential for preserving barrier function, modulating inflammation, and preventing colonization by opportunistic pathogens.

One of the skin microbiome’s primary roles is to defend 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 ecological competition limits the proliferation of undesirable species and maintains a balance that supports skin health. Meanwhile, the skin’s naturally acidic pH, sustained by the metabolism of lipids and fatty acids derived from the sebum, helps reinforce this barrière antimicrobienne.

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

The skin microbiome also plays a role in the healing of wounds, by modulating the interactions between the epidermis and the local immune system. The skin’s commensal organisms are in constant communication with immune cells, particularly T lymphocytes and keratinocytes, 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 unique immunological dialogue, characteristic of commensal bacteria, appears to promote balanced wound healing and limit excessive inflammatory responses.

Finally, the skin microbiome plays a still underestimated metabolic role. Microorganisms present on the skin’s surface contribute to the breakdown of sebum and dead cells, the production of short-chain fatty acids, and even the synthesis of certain vitamins and amino acids essential for 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 in perpetual evolution.

Its composition is not static: it changes over the years, with hormonal shifts and alterations in our environment or lifestyle, reflecting the constant adaptation of microorganisms. At birth, the newborn’s skin resembles a blank canvas awaiting colonization by initial microorganisms. The mode of delivery influences this first establishment: infants born vaginally inherit a microbiota similar to the maternal vaginal flora, rich in Lactobacillus and Prevotella, whereas those delivered by cesarean section exhibit an initial flora resembling the mother’s skin, dominated by Staphylococcus and Corynebacterium. These differences tend to diminish within the first weeks under the influence of skin-to-skin contact, nutrition, and the environment.

During childhood, the skin microbiome still remains relatively uniform from one body site to another. Then, as the skin thickens and the sweat and sebaceous glands develop, microbial diversity increases. During adolescence, the surge of sex hormones radically transforms the skin environment. Increased sebum production promotes the proliferation of lipophilic bacteria such as Cutibacterium acnes and yeasts of the genus Malassezia. These changes explain why certain conditions like acne appear at this stage: certain strains of C. acnes produce pro-inflammatory porphyrins that stimulate cytokine production and disrupt the local flora.

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

The composition and diversity of the skin microbiome also appear to depend on an 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 behavioral factors. The female skin is generally thinner, more acidic, better hydrated, and more pampered due to more frequent use of cosmetics by women, which promotes colonization by various bacterial species. In contrast, the male microbiome appears 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 found at the level of bacterial community structure. In men, the phylum dominant after the Actinobacteria is generally Firmicutes, whereas in women it is Proteobacteria. Some differences are even evident at the genus level: for example, Staphylococcus and Anaerococcus are more abundant in men, while Sphingomonas, Pelomonas and Streptococcus are more represented in women. These disparities reflect physiological differences between the sexes, such as higher sebum production and perspiration in men, as well as environmental factors and personal care habits.

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

The skin microbiota defends the skin through a process known as colonization resistance. This mechanism relies on commensal microorganisms’ ability to prevent the establishment and proliferation of pathogens. When this balance is disrupted, that is, in dysbiosis, the microbiota’s composition changes and certain species that were once beneficial may become harmful to the host, a shift recognized in the pathogenesis of various skin diseases.

One of the most 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 from phylogroup 1A1, are linked to acne. These strains possess virulence factors that promote bacterial adhesion and immune system activation, which triggers a local inflammatory response. Furthermore, C. acnes can form biofilms within follicles, contributing to the persistence of infection. Excessive 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 disease results from a combination of factors: epidermal barrier disruption, immune dysregulation, and microbial imbalance. During an inflammatory flare, there is a marked increase in staphylococci, particularly S. aureus and S. epidermidis, while overall microbial diversity decreases. These changes coincide with worsening symptoms, suggesting a close relationship between bacterial burden 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 highlights the link between a skin microbiota imbalance and skin inflammation. Several studies have shown a overexpression of the TLR-2 receptor in the epidermis of rosacea patients, 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 that promote vasodilation. Moreover, the chitin from the exoskeleton of the Demodex further amplifies this response via this same TLR-2 receptor.

Note : Vitiligo, psoriasis or alopecia are other dermatological conditions that can be influenced by skin dysbiosis.

Preserving the balance of the skin microbiota relies on a simple skincare routine and gentle treatments. Indeed, using harsh cleansers or exfoliating too often can disrupt the skin flora and promote dysbiosis, paving the way for inflammation and infection. Likewise, repeated exposure to aggressive environmental factors such as sun or pollution can alter microbial composition and reduce diversity, which is essential for a properly functioning microbiome. A straightforward routine including a mild cleansing, a moisturizing regimen tailored to one’s skin type and sun protection helps maintain a stable environment that supports colonization by beneficial bacteria.

Diet and lifestyle also play an indirect role. A balanced diet promotes overall health and could support the skin microbiota via thegut-skin axis. This term refers to the bidirectional communication between the gut and the skin, through which the state of the gut microbiota, inflammation, and the metabolites produced can influence skin health, and vice versa. In addition, limiting 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 skin microbiome.

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