The skin produces antimicrobial peptides such as cathelicidins, which control the proliferation of skin microbes. Cathelicidins not only directly reduce the number of microbes, but also cause cytokine secretion, which induces inflammation, angiogenesis and reepithelialization. Conditions such as atopic dermatitis have been linked to suppressing cathelicidin production. [28] In rosacea, abnormal treatment with cathelicidin causes inflammation. Psoriasis has been linked to the autoDNA of cathelicidin peptides that cause autoinflammation. An important factor that controls cathelicidin is vitamin D3. [29] In the past, vitamin B12 supplementation has been associated with acne in a subset of individuals.79,80,81,82,83 Recently, this has been linked to supplemental vitamin B12, which promotes the biosynthesis of vitamin B12 in P. acne, which subsequently increases the production of porphyrins, which can induce skin inflammation and the development of acne72. Interestingly, P. associated with acne.
ACNES strains have been found to produce significantly higher levels of porphyrin84. Gribbon, E. M., Cunliffe, W. J. & Holland, K. T. Interaction of Propionibacterium acnes with skin lipids in vitro. J. General microbiol.
139, 1745-1751 (1993). In summary, this review offers an analysis of the skin microbiome in health and disease in a previously unexplored resolution. Analysis at this level was possible thanks to technical advances in DNA extraction techniques and methods for preparing sequence libraries optimized for the diverse but low biomass of skin samples. In addition, the development of new software pipelines that leverage the depth of information available in shotgun metagenomic sequencing data has improved our understanding of the human skin microbiome. However, many questions remain about the function of the skin microbiota: what role do skin microorganisms play in maintaining health or promoting disease states? Bacteria in the normal endogenous skin flora are almost as resistant to heat damage as skin cells. Bacteria on the surface are killed by heat, as are tissue cells on the surface, and initial cultures are usually sterile. Bacteria in hair follicles and sebaceous glands can survive (depending on the extent of the burn), and the quantitative number of biopsied samples may have the same number of bacteria per gram (103) as in the tissue before burning.4,5,6 The average cell generation time under optimal conditions is about 20 minutes. As a result, the number of a single bacterial cell can reach more than 10 billion in 24 hours.7 As the number of these bacteria increases after thermal injury, reaching levels of >105 bacteria per gram of tissue, they exit the hair follicles and sebaceous glands and begin to migrate through the wound and colonize the dermal subcutaneous border. If the burn is not treated, perivascular growth is accompanied by thrombosis of the vessels and necrosis of all remaining dermal elements, potentially turning partial burns into full-thickness burns.
As bacterial growth increases, the frequency of viable tissue invasion and sepsis also increases.8,9 Histologically, invasive bacterial infection in unburned tissue is observed. Other signs of invasion may include bleeding in unburned tissue, thrombosis in small vessels with ischemic necrosis of unburned tissue, and dense bacterial growth in the subescharre space. The usual course of bacterial colonization over the days is from Gram positive to Gram negative. By day 21 after cremation, 57% of open burns will be colonized with extended-spectrum pseudomonas β-lactamases. Natural progression with the multiplication of bacteria and deepening of the burned wound is systematically avoided with modern burn care. With a combination of cleaning, antimicrobial topical medications, antibiotic dressings, adherent dressings, and early surgery, the progression and infection of burns is prevented in most burn patients. But even in the presence of modern care, early exposure to a virulent pathogen after injury can quickly lead to invasive burn infection and necrotizing soft tissue infection. Knowledge of the circumstances of the burn and the natural development of a healing or surgically treated burn are crucial to patient safety. Journal of the European Academy of Dermatology and Venereology: „Microbiome in healthy skin, update for dermatologists.” The initial colonization of a newborn`s skin usually occurs during vaginal delivery through the birth canal. The baby`s skin is initially sterile during birth by caesarean section. Meisel, J. S.
et al. Studies on the skin microbiome are strongly influenced by experimental design. J. Invest. Dermatol. 136, 947-956 (2016). This article describes how skin microbiome studies can be influenced by methodology. Jo, J. H., Kennedy, E. A. & Kong, H. H.
Topographic and physiological differences of the cutaneous mycobiome in health and disease. Virulenz 8, 324-333 (2016). Composition of the skin microbiota. In sequencing studies in healthy adults20,21,22,23, it has been found that the composition of microbial communities depends primarily on skin site physiology, with changes in the relative abundance of bacterial taxa associated with wet, dry, and sebum-like microenvironments. Sebous sites were dominated by lipophilic species of Propionibacterium, while bacteria that thrive in humid environments, such as Staphylococcus and Corynebacterium species, were preferentially abundant in wetlands, including bends of elbows and feet (Fig. 2; Table 1). Unlike bacterial communities, the composition of the fungal community was similar at all central sites of the body, regardless of physiology.23,24 Malassezia fungi dominated the body and arms, while foot sites were colonized by a more diverse combination of Malassezia spp., Aspergillus spp., Cryptococcus spp., Rhodotorula spp., Epicoccum spp. and others24 (Fig. 2).
Bacteria were the most abundant kingdom at all sites, and fungi were the least common25 (Fig. 2); However, there are many more bacterial reference genomes than fungal reference genomes, which may contribute in part to this observed difference. Interestingly, fungal abundance was low overall, even on the feet, where fungal diversity was high. International Journal of Cosmetic Science: „Revealing the secret life of the skin – you never walk alone with the microbiome.” Seborrheic dermatitis is a hyperproliferative skin condition that itches and usually affects the scalp. A fungal component is thought to participate in the pathogenesis of the disease, since a wide range of fungicides effectively fights seborrheic dermatitis. The presumed target of these fungicides is Malassezia spp., the dominant fungi that are grown from the skin and are particularly found in areas of sebum such as the scalp. Improvement in seborrheic dermatitis is associated with reduced levels of Malassezia spp. on the scalp.77 However, no improvement is observed when the scalp is treated with antibacterial agents78.
The proposed enhancement mechanism involves Malassezia lipase genes that process sebum to release free fatty acid metabolites (oleic acid). These metabolites then penetrate the upper layers of the skin and promote hyperproliferation and inflammation.79 From Malassezia spp. are present on healthy skin and are not sufficient on their own to cause seborrheic dermatitis, other factors likely contribute to their pathogenicity and ability to cause disease. Kong, H. H. et al. Temporal shifts in the skin microbiome associated with disease flare-ups and treatment in children with atopic dermatitis. 22, 850-859 (2012).
This is the first study in which the skin of people with longitudinal atopic dermatitis has been taken and sequenced. Many common skin conditions are attributed an underlying microbial contribution, as clinical improvement is observed through antimicrobial treatments. However, a causal microbial component that fully satisfies Koch`s postulates has rarely been identified in these skin diseases.