A recent study published within the Science Advances Journal evaluated the role of Cutibacterium acnes in improving the skin’s barrier function with regard to antimicrobial activity, transepidermal water loss, and paracellular diffusion.
Study: Commensal Cutibacterium acnes induce epidermal lipid synthesis essential for skin barrier function. Image Credit: Kateryna Kon/Shutterstock.com
Background
The epithelial surface comprises a number of cell layers stacked over a skinny membrane. It’s widespread throughout the body and forms a barrier between the external environment and the host.
Epithelial surfaces (e.g., skin) have many functions, resembling regulating body temperature and controlling the lack of electrolytes and water from the host.
The skin also harbors many useful microbes which protect the host from pathogenic invasion. For these complex functions, keratinocytes synthesize lipids within the skin, accumulating within the stratum corneum, the outermost layer of the epidermis.
The important thing component of stratum corneum is corneocytes, that are surrounded by a matrix composed of cholesterol, ceramides, and free fatty acids.
Alterations within the composition or arrangement of epidermal lipids cause various skin diseases, resembling psoriasis, atopic dermatitis, and lamellar ichthyosis. Skin lipid composition can be related to antimicrobial activity.
Nevertheless, it shouldn’t be clear whether the skin microbiome stimulates the epidermal lipid barrier or whether the synthesis of those lipids in response to microbial signals influences the dynamic barrier function of the skin.
Cutibacterium acnes is one of the vital common commensal bacterial species on the skin barrier. This bacterium is related to the event of pimples vulgaris, a typical skin disorder.
Several studies have indicated that C. acnes induces proinflammatory cytokine, triggers chemokine expression, and influences sebocyte differentiation and viability.
As well as, it also contributes to barrier homeostasis by decreasing the surface pH via the metabolization of free fatty acids from sebum.
This acidic environment inhibits pathogenic bacteria (e.g., Staphylococcus aureus) without compromising healthy commensal bacteria. Despite these observations, the precise role of C. acnes in skin health shouldn’t be well understood.
In regards to the study
The present study hypothesized that skin commensal bacteria influence lipid synthesis by keratinocytes, an integral part of the skin barrier.
To check this hypothesis, the conventional neonatal human epidermal keratinocytes (NHEKs) were treated with conditioned media (CM) from bacterial species commonly found on human skin. Total lipid accumulation was quantified using the Oil Red O (ORO) staining technique.
It was observed that the metabolites synthesized by C. acnes induce keratinocytes to extend lipid synthesis. The in vitro and in vivo experimental findings highlighted that C. acnes mediates lipid synthesis by producing propionic acid, which subsequently triggers keratinocyte PPARα. The lipid accumulation impacted the permeability properties of the skin, which influenced the antimicrobial activity of the epidermis.
This study provided evidence of the useful function of C. acnes regarding enhanced barrier function and preventive bacterial proliferation. Notably, the role of the skin microbiome on epidermal homeostasis is highlighted on this study.
TAGs, minor components of lamellar bodies present in the stratum corneum, are most abundantly induced by C. acnes. Nevertheless, the precise role of TAGs in epidermal homeostasis is poorly understood.
A previous study has shown that individuals with atopic dermatitis have reduced TAG (TAG46, TAG48, and TAG50) levels, related to decreased abundance of C. acnes.
A breakdown of TAG provides fatty acids required for synthesizing ceramide, a vital lipid linked to permeability barrier function. Linoleic acid is one other fatty acid required for acylceramide synthesis, which is crucial for corneocyte lipid envelope formation.
The present study revealed that C. acnes exposure increased triglycerides containing linolenic acid and total ceramide in NHEKs.
These findings indicate the potential of linoleic acid being hydrolyzed from TAG, which subsequently contributes to acylceramide synthesis to assist in skin barrier function.
Within the presence of pimples, there may be a possibility of reduced host response to C. acnes, which decreases linoleic acid levels and weakens the barrier. This impaired barrier results in pathogenic invasion on the follicle and triggers acute inflammation linked to the disease.
The full lipid extracted from NHEKs after exposure to C. acnes CM or propionic acid was linked to increased antimicrobial efficacy against C. acnes. The rise in antimicrobial activity may very well be as a result of lipids extracted from NHEKs.
It has also been observed that C. acnes metabolizes TAGs into small-chain fatty acid (SCFA) under anaerobic conditions, which ultimately causes a lipid-rich environment.
Taken together, C. acnes or its SCFA metabolites was chargeable for increased lipids within the epidermis, essential for barrier formation and antimicrobial activity.
Conclusions
C. acnes is related to a posh skin system via induction of lipid synthesis, SCFA production, and assisting the metabolism of potential lipids by other microbes.
In the long run, more research is required to know the connection between the host and commensal microbes for managing the ultimate composition of health-associated skin microbiota.