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1

Scharschmidt, Tiffany C. "Skin Dysbiosis Goes “Off-Leish”." Cell Host & Microbe 22, no. 1 (July 2017): 1–3. http://dx.doi.org/10.1016/j.chom.2017.06.017.

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2

Teng, Vannia C., and Prima K. Esti. "Skin microbiome dysbiosis in leprosy cases." International Journal of Research in Dermatology 7, no. 5 (August 23, 2021): 741. http://dx.doi.org/10.18203/issn.2455-4529.intjresdermatol20213355.

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<p>The human skin possesses a microenvironment conducive to the growth of the skin microbiome, which plays in many physiological functions in cutaneous immunity homeostasis and maturation. The microbiome composition depends on many variables, such as endogenous (host condition) or exogenous (environmental) factors and topographic location. Host-skin microbes’ interaction can be mutualism or pathogenicity. Dysbiosis or alteration in skin microbiota is associated with various dermatological diseases, including leprosy. Dysbiosis is driven by the alteration of the microbial communities themselves or due to the intrinsic features of the host. Leprosy is a chronic granulomatous disease caused by <em>Mycobacterium leprae</em> targeting the nerves and skin, leading to loss of sensation on the skin, with or without dermatologic lesions, and correlated with long term consequences, such as deformities or disability. Microvascular dysfunction and significant alterations in capillary structure due to invasion of <em>M. leprae</em> lead to altered hydration levels of the skin caused by disruption of blood flow; which changes the resident microbial community structure. The skin microbiome composition differences in leprosy patient’s skin lesions were observed; skin microbial diversity in the leprosy patients was lower than in healthy individuals. The diversity reduction was observed in freshly diagnosis leprosy patients, those at various stages of MDT, and post-MDT; indicated that both the interaction between skin microbial community and<strong> </strong><em>M. leprae</em> or the ongoing therapeutic regimen impacted the skin microbiome variation. </p><p> </p>
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3

Marson, Justin, Stefano Berto, Paul Mouser, and Hilary Baldwin. "Association between Rosacea, Environmental Factors, and Facial Cutaneous Dysbiosis." SKIN The Journal of Cutaneous Medicine 5, no. 5 (September 13, 2021): 487–95. http://dx.doi.org/10.25251/skin.5.5.6.

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Background: To investigate the microbiome composition in individuals with and without rosacea and correlate findings to individual factors that may affect facial cutaneous and enteric microbiome composition. Methods: Participants with and without rosacea (as determined by a board-certified dermatologist) were surveyed regarding factors that may affect the facial cutaneous/enteric microbiome. Microbiome samples were collected, analyzed for 16S sequences, and mapped to an optimized version of existing databases. R was used to perform Mann-Whitney/Kruskal-Wallis test for categorical comparisons. Correlation between two continuous variables was determined with linear regression models. Primary Component Analysis (PCoA) plots employed Monte Carlo permutation test to estimate p-values. All p-values are adjusted for multiple comparisons with the false discovery rate (FDR algorithm) using Benjamini-Hochberg. Results: 84 individuals with rosacea and 44 controls were evaluated. Individuals with rosacea were more likely to currently own pets (p = 0.029) and consume more alcohol (p = 0.006). Absolute bacteria abundance were similar in facial cutaneous (p = 0.36) and enteral microbiome (p = 0.29). Facial cutaneous microbiome showed significantly decreased richness and evenness (OTU: p = 0.019; Shannon: p = 0.049) and a three to four-fold decrease in abundance of 8 distinct cutaneous bacterial genera in rosacea. Enteral microbiome analysis showed significant reduction in abundance of Ruminococcaceae (FDR = 0.002) and Blautia (FDR < 0.001) and increase in Prevotellaceae (FDR = 0.024) in rosacea. Conclusion: Environmental factors may alter relative abundances of specific microbial genera and lead to microbiome diversity. Further studies with increased sample sizes and higher severity cases may further elucidate the role of dysbiosis in rosacea.
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Muharram, Luthfia Hastiani, Fauzia Ningrum Syaputri, Wulan Pertiwi, and Rizki Fika Saputri. "Aktivitas Antibakteri Ekstrak Bawang Hitam Variasi Waktu Aging Terhadap Pencegahan Dysbiosis Kulit Penyebab Jerawat." Jurnal Sains dan Kesehatan 4, no. 2 (April 30, 2022): 181–88. http://dx.doi.org/10.25026/jsk.v4i2.1035.

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Skin diseases, including acne, can be caused by a microbial imbalance (dysbiosis). The specific bacteria involved in acne dysbiosis are Cutibacterium (Propionibacterium) acnes and Staphylococcus epidermidis. Black garlic has better potential to be alternative antibiotic and chemical to curing ance and maintaining skin health, because it has antimicrobial potential and can inhibit the decrease in collagen deposition on the skin. These potentials can be alternative of antibiotics and chemicals to treat acne and maintain healthy skin. This study aimed to determine the antibacterial activity of black garlic extract against bacteria that cause acne dysbiosis. Garlic was aging with 3 variations of time (7, 14, and 21 days) then macerated with 70% alcohol and tested for antimicrobial activity to Cutibacterium acnes and Staphylococcus epidermidis with clindamycin as positive control. Black garlic extract provided inhibitory activity against Staphylococcus epidermidis and Cutibacterium acnes. The best recommendation time for aging garlic to prevent skin dysbiosis causes acne is 7 to 14 days.
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5

Pessôa, Rodrigo, Patricia Bianca Clissa, and Sabri Saeed Sanabani. "The Interaction between the Host Genome, Epigenome, and the Gut–Skin Axis Microbiome in Atopic Dermatitis." International Journal of Molecular Sciences 24, no. 18 (September 20, 2023): 14322. http://dx.doi.org/10.3390/ijms241814322.

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Atopic dermatitis (AD) is a chronic inflammatory skin disease that occurs in genetically predisposed individuals. It involves complex interactions among the host immune system, environmental factors (such as skin barrier dysfunction), and microbial dysbiosis. Genome-wide association studies (GWAS) have identified AD risk alleles; however, the associated environmental factors remain largely unknown. Recent evidence suggests that altered microbiota composition (dysbiosis) in the skin and gut may contribute to the pathogenesis of AD. Examples of environmental factors that contribute to skin barrier dysfunction and microbial dysbiosis in AD include allergens, irritants, pollution, and microbial exposure. Studies have reported alterations in the gut microbiome structure in patients with AD compared to control subjects, characterized by increased abundance of Clostridium difficile and decreased abundance of short-chain fatty acid (SCFA)-producing bacteria such as Bifidobacterium. SCFAs play a critical role in maintaining host health, and reduced SCFA production may lead to intestinal inflammation in AD patients. The specific mechanisms through which dysbiotic bacteria and their metabolites interact with the host genome and epigenome to cause autoimmunity in AD are still unknown. By understanding the combination of environmental factors, such as gut microbiota, the genetic and epigenetic determinants that are associated with the development of autoantibodies may help unravel the pathophysiology of the disease. This review aims to elucidate the interactions between the immune system, susceptibility genes, epigenetic factors, and the gut microbiome in the development of AD.
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6

De Pessemier, Britta, Lynda Grine, Melanie Debaere, Aglaya Maes, Bernhard Paetzold, and Chris Callewaert. "Gut–Skin Axis: Current Knowledge of the Interrelationship between Microbial Dysbiosis and Skin Conditions." Microorganisms 9, no. 2 (February 11, 2021): 353. http://dx.doi.org/10.3390/microorganisms9020353.

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The microbiome plays an important role in a wide variety of skin disorders. Not only is the skin microbiome altered, but also surprisingly many skin diseases are accompanied by an altered gut microbiome. The microbiome is a key regulator for the immune system, as it aims to maintain homeostasis by communicating with tissues and organs in a bidirectional manner. Hence, dysbiosis in the skin and/or gut microbiome is associated with an altered immune response, promoting the development of skin diseases, such as atopic dermatitis, psoriasis, acne vulgaris, dandruff, and even skin cancer. Here, we focus on the associations between the microbiome, diet, metabolites, and immune responses in skin pathologies. This review describes an exhaustive list of common skin conditions with associated dysbiosis in the skin microbiome as well as the current body of evidence on gut microbiome dysbiosis, dietary links, and their interplay with skin conditions. An enhanced understanding of the local skin and gut microbiome including the underlying mechanisms is necessary to shed light on the microbial involvement in human skin diseases and to develop new therapeutic approaches.
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7

Tao, Rong, Ruoyu Li, and Ruojun Wang. "Dysbiosis of skin mycobiome in atopic dermatitis." Mycoses 65, no. 3 (December 3, 2021): 285–93. http://dx.doi.org/10.1111/myc.13402.

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8

Ito, T., R. Aoyama, S. Nakagawa, Y. Yamazaki, N. Inohara, Y. Ichikawa, N. Shimojo, Y. Matsuoka-Nakamura, and M. Fujimoto. "955 Skin care improves newborn skin dysbiosis associated with atopic dermatitis." Journal of Investigative Dermatology 143, no. 5 (May 2023): S164. http://dx.doi.org/10.1016/j.jid.2023.03.966.

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9

Magnifico, Irene, Angelica Perna, Marco Alfio Cutuli, Alessando Medoro, Laura Pietrangelo, Antonio Guarnieri, Emanuele Foderà, et al. "A Wall Fragment of Cutibacterium acnes Preserves Junctional Integrity Altered by Staphylococcus aureus in an Ex Vivo Porcine Skin Model." Pharmaceutics 15, no. 4 (April 12, 2023): 1224. http://dx.doi.org/10.3390/pharmaceutics15041224.

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(1) Background alteration of the skin microbiota, dysbiosis, causes skin barrier impairment resulting in disease development. Staphylococcus aureus, the main pathogen associated with dysbiosis, secretes several virulence factors, including α-toxin that damages tight junctions and compromises the integrity of the skin barrier. The use of members of the resident microbiota to restore the skin barrier, bacteriotherapy, represents a safe treatment for skin conditions among innovative options. The aim of this study is the evaluation of a wall fragment derived from a patented strain of Cutibacterium acnes DSM28251 (c40) alone and conjugated to a mucopolysaccharide carrier (HAc40) in counteracting S. aureus pathogenic action on two tight junction proteins (Claudin-1 and ZO-1) in an ex vivo porcine skin infection model. Methods: skin biopsies were infected with live S. aureus strains ATCC29213 and DSM20491. Tissue was pre-incubated or co-incubated with c40 and HAc40. (3) Results: c40 and HAc40 prevent and counteract Claudin-1 and Zo-1 damage (4) Conclusions: c40 and the functional ingredient HAc40 represent a potential non-pharmacological treatment of skin diseases associated with cutaneous dysbiosis of S. aureus. These findings offer numerous avenues for new research.
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Blicharz, Leszek, Lidia Rudnicka, Joanna Czuwara, Anna Waśkiel-Burnat, Mohamad Goldust, Małgorzata Olszewska, and Zbigniew Samochocki. "The Influence of Microbiome Dysbiosis and Bacterial Biofilms on Epidermal Barrier Function in Atopic Dermatitis—An Update." International Journal of Molecular Sciences 22, no. 16 (August 5, 2021): 8403. http://dx.doi.org/10.3390/ijms22168403.

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Atopic dermatitis (AD) is a common inflammatory dermatosis affecting up to 30% of children and 10% of adults worldwide. AD is primarily driven by an epidermal barrier defect which triggers immune dysregulation within the skin. According to recent research such phenomena are closely related to the microbial dysbiosis of the skin. There is growing evidence that cutaneous microbiota and bacterial biofilms negatively affect skin barrier function, contributing to the onset and exacerbation of AD. This review summarizes the latest data on the mechanisms leading to microbiome dysbiosis and biofilm formation in AD, and the influence of these phenomena on skin barrier function.
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11

Smythe, Paisleigh, and Holly N. Wilkinson. "The Skin Microbiome: Current Landscape and Future Opportunities." International Journal of Molecular Sciences 24, no. 4 (February 16, 2023): 3950. http://dx.doi.org/10.3390/ijms24043950.

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Our skin is the largest organ of the body, serving as an important barrier against the harsh extrinsic environment. Alongside preventing desiccation, chemical damage and hypothermia, this barrier protects the body from invading pathogens through a sophisticated innate immune response and co-adapted consortium of commensal microorganisms, collectively termed the microbiota. These microorganisms inhabit distinct biogeographical regions dictated by skin physiology. Thus, it follows that perturbations to normal skin homeostasis, as occurs with ageing, diabetes and skin disease, can cause microbial dysbiosis and increase infection risk. In this review, we discuss emerging concepts in skin microbiome research, highlighting pertinent links between skin ageing, the microbiome and cutaneous repair. Moreover, we address gaps in current knowledge and highlight key areas requiring further exploration. Future advances in this field could revolutionise the way we treat microbial dysbiosis associated with skin ageing and other pathologies.
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12

Cannon, Alice, Holly Wilkinson, Michelle Rudden, and Mat Hardman. "P18 Investigating the role of the microbiome in chronic wound skin barrier reformation." British Journal of Dermatology 190, no. 6 (May 17, 2024): e87-e87. http://dx.doi.org/10.1093/bjd/ljae105.040.

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Abstract Introduction and aims The integrity of the skin barrier plays a pivotal role in dermatological health, particularly in elderly and individuals with diabetes who are more susceptible to injury. Our skin barrier is also in direct contact with the microbiota, a diverse community of microorganisms that play wide-ranging roles in cutaneous function. Although microbial dysbiosis has been observed in elderly and diabetic skin, few studies have investigated the mechanistic links between skin barrier perturbations and the microbiome. The aim of this study was to compare barrier reformation in healthy and pathological (chronic wound) skin and determine the role of microbial dysbiosis in skin barrier perturbations. Methods Here, we developed a novel human ex vivo skin barrier model to simulate skin barrier disruption in healthy and pathological skin. Following tape stripping (n = 6 per donor type), skin barrier disruption was confirmed by measuring transepidermal water loss (TEWL). Skin barrier reformation was assessed following culture using haematoxylin and eosin staining, Nile red (lipid expression and distribution), and immunohistochemistry for skin barrier proteins (e.g. claudins, keratins). Secreted products from mixed bacterial communities were also applied to healthy tape-stripped skin to assess the influence of a healthy vs. pathological microbiome on skin barrier reformation. Results Pathological skin showed higher TEWL following barrier disruption, in addition to delayed barrier reformation and altered skin barrier protein expression. Moreover, secreted products from a pathological microbiome, with high proportions of Staphylococcus aureus, significantly delayed skin barrier reformation. Conclusions Collectively, our data provide a novel skin barrier reformation model to assess the effect of cutaneous pathology and microbial dysbiosis on skin barrier repair. Further understanding of the role of the microbiome in skin barrier function is integral to reducing infections and barrier perturbation.
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Rozas, Miquel, Astrid Hart de Ruijter, Maria Jose Fabrega, Amine Zorgani, Marc Guell, Bernhard Paetzold, and Francois Brillet. "From Dysbiosis to Healthy Skin: Major Contributions of Cutibacterium acnes to Skin Homeostasis." Microorganisms 9, no. 3 (March 18, 2021): 628. http://dx.doi.org/10.3390/microorganisms9030628.

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Cutibacterium acnes is the most abundant bacterium living in human, healthy and sebum-rich skin sites, such as the face and the back. This bacterium is adapted to this specific environment and therefore could have a major role in local skin homeostasis. To assess the role of this bacterium in healthy skin, this review focused on (i) the abundance of C. acnes in the skin microbiome of healthy skin and skin disorders, (ii) its major contributions to human skin health, and (iii) skin commensals used as probiotics to alleviate skin disorders. The loss of C. acnes relative abundance and/or clonal diversity is frequently associated with skin disorders such as acne, atopic dermatitis, rosacea, and psoriasis. C. acnes, and the diversity of its clonal population, contributes actively to the normal biophysiological skin functions through, for example, lipid modulation, niche competition and oxidative stress mitigation. Compared to gut probiotics, limited dermatological studies have investigated skin probiotics with skin commensal strains, highlighting their unexplored potential.
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14

Fournière, Mathilde, Thomas Latire, Djouhar Souak, Marc G. J. Feuilloley, and Gilles Bedoux. "Staphylococcus epidermidis and Cutibacterium acnes: Two Major Sentinels of Skin Microbiota and the Influence of Cosmetics." Microorganisms 8, no. 11 (November 7, 2020): 1752. http://dx.doi.org/10.3390/microorganisms8111752.

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Dermatological and cosmetics fields have recently started to focus on the human skin microbiome and microbiota, since the skin microbiota is involved in the health and dysbiosis of the skin ecosystem. Amongst the skin microorganisms, Staphylococcus epidermidis and Cutibacterium acnes, both commensal bacteria, appear as skin microbiota sentinels. These sentinels have a key role in the skin ecosystem since they protect and prevent microbiota disequilibrium by fighting pathogens and participate in skin homeostasis through the production of beneficial bacterial metabolites. These bacteria adapt to changing skin microenvironments and can shift to being opportunistic pathogens, forming biofilms, and thus are involved in common skin dysbiosis, such as acne or atopic dermatitis. The current evaluation methods for cosmetic active ingredient development are discussed targeting these two sentinels with their assets and limits. After identification of these objectives, research of the active cosmetic ingredients and products that maintain and promote these commensal metabolisms, or reduce their pathogenic forms, are now the new challenges of the skincare industry in correlation with the constant development of adapted evaluation methods.
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15

Williams, Michael R., and Richard L. Gallo. "Evidence that Human Skin Microbiome Dysbiosis Promotes Atopic Dermatitis." Journal of Investigative Dermatology 137, no. 12 (December 2017): 2460–61. http://dx.doi.org/10.1016/j.jid.2017.09.010.

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16

Bonzano, Laura, Francesco Borgia, Rossella Casella, Andrea Miniello, Eustachio Nettis, and Sebastiano Gangemi. "Microbiota and IL-33/31 Axis Linkage: Implications and Therapeutic Perspectives in Atopic Dermatitis and Psoriasis." Biomolecules 13, no. 7 (July 10, 2023): 1100. http://dx.doi.org/10.3390/biom13071100.

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Microbiome dysbiosis and cytokine alternations are key features of atopic dermatitis (AD) and psoriasis (PsO), two of the most prevalent and burdensome pruritic skin conditions worldwide. Interleukin (IL)-33 and IL-31 have been recognized to be major players who act synergistically in the pathogenesis and maintenance of different chronic inflammatory conditions and pruritic skin disorders, including AD and PsO, and their potential role as therapeutic targets is being thoroughly investigated. The bidirectional interplay between dysbiosis and immunological changes has been extensively studied, but there is still debate regarding which of these two factors is the actual causative culprit behind the aetiopathological process that ultimately leads to AD and PsO. We conducted a literature review on the Pubmed database assessing articles of immunology, dermatology, microbiology and allergology with the aim to strengthen the hypothesis that dysbiosis is at the origin of the IL-33/IL-31 dysregulation that contributes to the pathogenesis of AD and PsO. Finally, we discussed the therapeutic options currently in development for the treatment of these skin conditions targeting IL-31, IL-33 and/or the microbiome.
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Meason-Smith, Courtney, Thierry Olivry, Sara D. Lawhon, and Aline Rodrigues Hoffmann. "Malassezia species dysbiosis in natural and allergen-induced atopic dermatitis in dogs." Medical Mycology 58, no. 6 (November 29, 2019): 756–65. http://dx.doi.org/10.1093/mmy/myz118.

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Abstract Malassezia dermatitis and otitis are recurrent features of canine atopic dermatitis, increasing the cost of care, and contributing to a reduced quality of life for the pet. The exact pathogenesis of secondary yeast infections in allergic dogs remains unclear, but some have proposed an overgrowth of M. pachydermatis to be one of the flare factors. The distribution of Malassezia populations on healthy and allergic canine skin has not been previously investigated using culture-independent methods. Skin swabs were collected from healthy, naturally affected allergic, and experimentally sensitized atopic dogs. From the extracted DNA, fungal next-generations sequencing (NGS) targeting the ITS region with phylogenetic analysis of sequences for species level classification, and Malassezia species-specific quantitative real-time polymerase chain reaction (qPCR) were performed. M. globosa was significantly more abundant on healthy canine skin by both methods (NGS P &lt; .0001, qPCR P &lt; .0001). M. restricta was significantly more abundant on healthy skin by NGS (P = .0023), and M. pachydermatis was significantly more abundant on naturally-affected allergic skin by NGS (P &lt; .0001) and on allergen-induced atopic skin lesions by qPCR (P = .0015). Shifts in Malassezia populations were not observed in correlation with the development of allergen-induced skin lesions. Differences in the lipid dependency of predominant Malassezia commensals between groups suggests a role of the skin lipid content in driving community composition and raises questions of whether targeting skin lipids with therapeutics could promote healthy Malassezia populations on canine skin.
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18

Wallen-Russell, Christopher, Nancy Pearlman, Samuel Wallen-Russell, Dragos Cretoiu, Dana Claudia Thompson, and Silviu Cristian Voinea. "A Catastrophic Biodiversity Loss in the Environment Is Being Replicated on the Skin Microbiome: Is This a Major Contributor to the Chronic Disease Epidemic?" Microorganisms 11, no. 11 (November 16, 2023): 2784. http://dx.doi.org/10.3390/microorganisms11112784.

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There has been a catastrophic loss of biodiversity in ecosystems across the world. A similar crisis has been observed in the human gut microbiome, which has been linked to “all human diseases affecting westernized countries”. This is of great importance because chronic diseases are the leading cause of death worldwide and make up 90% of America’s healthcare costs. Disease development is complex and multifactorial, but there is one part of the body’s interlinked ecosystem that is often overlooked in discussions about whole-body health, and that is the skin microbiome. This is despite it being a crucial part of the immune, endocrine, and nervous systems and being continuously exposed to environmental stressors. Here we show that a parallel biodiversity loss of 30–84% has occurred on the skin of people in the developed world compared to our ancestors. Research has shown that dysbiosis of the skin microbiome has been linked to many common skin diseases and, more recently, that it could even play an active role in the development of a growing number of whole-body health problems, such as food allergies, asthma, cardiovascular diseases, and Parkinson’s, traditionally thought unrelated to the skin. Damaged skin is now known to induce systemic inflammation, which is involved in many chronic diseases. We highlight that biodiversity loss is not only a common finding in dysbiotic ecosystems but also a type of dysbiosis. As a result, we make the case that biodiversity loss in the skin microbiome is a major contributor to the chronic disease epidemic. The link between biodiversity loss and dysbiosis forms the basis of this paper’s focus on the subject. The key to understanding why biodiversity loss creates an unhealthy system could be highlighted by complex physics. We introduce entropy to help understand why biodiversity has been linked with ecosystem health and stability. Meanwhile, we also introduce ecosystems as being governed by “non-linear physics” principles—including chaos theory—which suggests that every individual part of any system is intrinsically linked and implies any disruption to a small part of the system (skin) could have a significant and unknown effect on overall system health (whole-body health). Recognizing the link between ecosystem health and human health allows us to understand how crucial it could be to maintain biodiversity across systems everywhere, from the macro-environment we inhabit right down to our body’s microbiome. Further, in-depth research is needed so we can aid in the treatment of chronic diseases and potentially change how we think about our health. With millions of people currently suffering, research to help mitigate the crisis is of vital importance.
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Bobyr, V. V., V. A. Poniatovskyi, A. P. Chobotar, L. O. Stechenko, О. І. Kryvosheyeva, O. A. Nazarchuk, and О. О. Кovalenko. "Features of structural-morphological changes in cases of experimental intestinal antibiotic-induced dysbiosis." Reports of Morphology 24, no. 3 (September 27, 2018): 26–31. http://dx.doi.org/10.31393/morphology-journal-2018-24(3)-04.

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Nowadays, scientists often define dysbiosis as a condition of a microbial ecological system, in which there is a simultaneous abnormality of the functions and interaction mechanisms of its key components: macroorganism and indigenous microbiota associated with the mucous membranes of cavities and skin. At the same time, obviously, the basis of all these processes is changes of structural intestinal components that are caused by qualitative and quantitative changes in the normal microflora. Purpose: to study the ultrastructural organization of the mucous membrane of the small intestine of mice after the formation of dysbiosis of the intestine. Outbred white mice in the number of 40 units (20 - experimental and 20 control) was served as an experimental model. Antibacterial drugs (ampicillin, metronidazole and gentamicin) are used to form dysbiosis. The conducted experiments are allowed to establish that the using of antibacterial drugs in the above-mentioned doses contributes to shortening the length of the microvillus and their reduction (disappearance) in some places, destruction with subsequent disintegration. According to the results of electronograms analysis, the assumption was made about stimulating the secretory function of the small intestine enterocytes by powerful doses of antibacterial drugs. In addition, it was found that the formation of dysbiotic disorders is accompanied by a defect of the connection between epithelial cells due to the expansion of the intercellular space and the disappearance of the dense plate. Research results also indicate that antibiotics that were used in the experiment can cause development of apoptosis. In addition, it has been shown that, on the background of the dysbiotic disorders formation, the activation of immune processes is taking place, as evidenced by the appearance of a significant number of Paneth cells, plasma cells with enlarged tubules, apparently due to their filling with immunoglobulins, as well as the growth of numbers of luminalis eosinophils and basophils. The ability of antibiotics to form dysbiotic states with pronounced cytodestructive disorders in the epithelium of the small intestine with the development of apoptosis was substantiated; the argument about the immune stimulating effect of antibiotic induced dysbiosis is argued.
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Sá, Sara, Ruben Fernandes, Álvaro Gestoso, José Mário Macedo, Daniela Martins-Mendes, Ana Cláudia Pereira, and Pilar Baylina. "Cutibacterium acnes Dysbiosis: Alternative Therapeutics for Clinical Application." Applied Sciences 13, no. 21 (November 6, 2023): 12086. http://dx.doi.org/10.3390/app132112086.

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Cutibacterium acnes (C. acnes) is a Gram-positive anaerobic facultative bacterium that is part of the human skin commensal microbiome. It colonizes various regions of the body, including the face, back, and chest. While typically a harmless commensal, under certain conditions, C. acnes can become pathogenic, leading to or promoting conditions such as acne vulgaris (AV), post-surgical infections, prostate cancer, and sarcoidosis. Current treatments for C. acnes infections often involve antibiotics, but the rise of antibiotic resistance has raised concerns. This review presents the virulence factors, clinical relevance, and current treatments of C. acnes, highlighting its association with AV, post-surgical infections, and other diseases. It also explores alternative innovative therapies such as phage therapy in development/research that are gaining prominence, with a growing focus on personalized medical approaches. To enhance C. acnes treatment while minimizing side effects and antibiotic prescription concerns, numerous clinical studies have been undertaken. These investigations span various pathological profiles and employ diverse strategies, such as utilizing bacterial extracts and compounds to restore healthy skin flora. The limitations and challenges of current and innovative treatments are also addressed, emphasizing the need for multidisciplinary strategies to combat C. acnes infections effectively.
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Huang, Amy, and Sharon Glick. "Integrating Metagenomics into Personalized Medicine in Dermatology." SKIN The Journal of Cutaneous Medicine 4, no. 6 (October 27, 2020): 623–25. http://dx.doi.org/10.25251/skin.4.6.25.

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There has been a recent focus on the association between human microbiomes and disease development, disease resistance, and therapy response. Fecal transplants for inflammatory bowel disease and resistant Clostridium difficile infection have demonstrated that manipulating the gut microbiome can be beneficial in treating disease. Microbiomes are important in dermatology, where response to immune checkpoint inhibitors for melanoma therapy can be affected by differences in gut microbial composition. Bleach baths, which alter the skin microbiome, are known to be beneficial in atopic dermatitis. Gut dysbiosis, or disturbance in the gut microbiome in early life, can influence the development of systemic sclerosis and atopic dermatitis. Metagenomic sequencing can therefore be a useful addition to personalized medicine to identify therapy responders versus non-responders, patients at risk of serious side-effects from biologics and immune checkpoint inhibitors, and prebiotic supplements that aid in improving therapy response.
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Małolepsza, Aleksandra, and Tomasz Dembowski. "Probiotics and gut-skin axis - new look on factors affecting skin condition." Journal of Education, Health and Sport 31, no. 1 (May 17, 2023): 55–60. http://dx.doi.org/10.12775/jehs.2023.31.01.005.

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Introduction and purpose The human gut microbiota consists of trillions of microscopic organisms, mostly bacterias. They play a significant role in nutrient metabolism, maintenance of structural integrity of the gut mucosal barrier, immunomodulation and protection against pathogens. Many factors can influence the composition of the intestinal microbiota, for example antibiotics, diet or stress. These factors may lead to dysbiosis which causes activation of neurotransmitters. It can results in the entry of metabolites to the blood stream, systemic immune dysregulation and alteration of skin microbiota. The aim of the study was to review the literature and determine the effects of intestinal microbiota and probiotics in selected skin diseases and what is new - skin aging process. State of knowledge We analyzed numerous studies which indicate that disturbed gut microbiota can be related to some chronic diseases, including skin disorders such as atopic dermatitis, acne vulgaris, psoriasis and rosacea. Additionally, it has been proven that bacterial dysbiosis can intensify the skin aging proces. In order to reproduce normal gut microbiota probiotics are used. Despite the fact that there are only a few studies showing the unequivocal effect of probiotics on skin diseases, their results seem to be encouraging. Conclusions Proper composition of the intestinal microbiome determines the homeostasis of the human body. Disturbance of the gut microbiome play a significant role not only in development and aggravation of many skin diseases, but also have an impact on the skin aging. Despite quite a lot number of studies assessing the impact of microbiota on certain skin disorders, there is still a need to evaluate impact of probiotics. Researches indicate that they can be used as a helpful therapeutic tool. Taking this into account, it is worth considering it in the treatment process.
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Choy, Chi Tung, Un Kei Chan, Pui Ling Kella Siu, Junwei Zhou, Chi Ho Wong, Yuk Wai Lee, Ho Wang Chan, Joseph Chi Ching Tsui, Steven King Fan Loo, and Stephen Kwok Wing Tsui. "A Novel E3 Probiotics Formula Restored Gut Dysbiosis and Remodelled Gut Microbial Network and Microbiome Dysbiosis Index (MDI) in Southern Chinese Adult Psoriasis Patients." International Journal of Molecular Sciences 24, no. 7 (March 31, 2023): 6571. http://dx.doi.org/10.3390/ijms24076571.

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Psoriasis is a common chronic immune-mediated inflammatory skin disease with the association of various comorbidities. Despite the introduction of highly effective biologic therapies over the past few decades, the exact trigger for an immune reaction in psoriasis is unclear. With the majority of immune cells residing in the gut, the effect of gut microbiome dysbiosis goes beyond the gastrointestinal site and may exacerbate inflammation and regulate the immune system elsewhere, including but not limited to the skin via the gut-skin axis. In order to delineate the role of the gut microbiome in Southern Chinese psoriasis patients, we performed targeted 16S rRNA sequencing and comprehensive bioinformatic analysis to compare the gut microbiome profile of 58 psoriasis patients against 49 healthy local subjects presumably with similar lifestyles. Blautia wexlerae and Parabacteroides distasonis were found to be enriched in psoriasis patients and in some of the healthy subjects, respectively. Metabolic functional pathways were predicted to be differentially abundant, with a clear shift toward SCFA synthesis in healthy subjects. The alteration of the co-occurrence network was also evident in the psoriasis group. In addition, we also profiled the gut microbiome in 52 of the 58 recruited psoriasis patients after taking 8 weeks of an orally administrated novel E3 probiotics formula (with prebiotics, probiotics and postbiotics). The Dermatological Life Quality Index (p = 0.009) and Psoriasis Area and Severity Index (p < 0.001) were significantly improved after taking 8 weeks of probiotics with no adverse effect observed. We showed that probiotics could at least partly restore gut dysbiosis via the modulation of the gut microbiome. Here, we also report the potential application of a machine learning-derived gut dysbiosis index based on a quantitative PCR panel (AUC = 0.88) to monitor gut dysbiosis in psoriasis patients. To sum up, our study suggests the gut microbial landscape differed in psoriasis patients at the genera, species, functional and network levels. Additionally, the dysbiosis index could be a cost-effective and rapid tool to monitor probiotics use in psoriasis patients.
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Hrestak, Dora, Mario Matijašić, Hana Čipčić Paljetak, Daniela Ledić Drvar, Suzana Ljubojević Hadžavdić, and Mihaela Perić. "Skin Microbiota in Atopic Dermatitis." International Journal of Molecular Sciences 23, no. 7 (March 23, 2022): 3503. http://dx.doi.org/10.3390/ijms23073503.

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The skin microbiota represents an ecosystem composed of numerous microbial species interacting with each other, as well as with host epithelial and immune cells. The microbiota provides health benefits to the host by supporting essential functions of the skin and inhibiting colonization with pathogens. However, the disturbance of the microbial balance can result in dysbiosis and promote skin diseases, such as atopic dermatitis (AD). This review provides a current overview of the skin microbiota involvement in AD and its complex interplay with host immune response mechanisms, as well as novel therapeutic strategies for treating AD focused on restoring skin microbial homeostasis.
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Magnifico, Irene, Giulio Petronio Petronio, Noemi Venditti, Marco Alfio Cutuli, Laura Pietrangelo, Franca Vergalito, Katia Mangano, Davide Zella, and Roberto Di Marco. "Atopic Dermatitis as a Multifactorial Skin Disorder. Can the Analysis of Pathophysiological Targets Represent the Winning Therapeutic Strategy?" Pharmaceuticals 13, no. 11 (November 22, 2020): 411. http://dx.doi.org/10.3390/ph13110411.

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Atopic dermatitis (AD) is a pathological skin condition with complex aetiological mechanisms that are difficult to fully understand. Scientific evidence suggests that of all the causes, the impairment of the skin barrier and cutaneous dysbiosis together with immunological dysfunction can be considered as the two main factors involved in this pathological skin condition. The loss of the skin barrier function is often linked to dysbiosis and immunological dysfunction, with an imbalance in the ratio between the pathogen Staphylococcus aureus and/or other microorganisms residing in the skin. The bibliographic research was conducted on PubMed, using the following keywords: ‘atopic dermatitis’, ‘bacterial therapy’, ‘drug delivery system’ and ‘alternative therapy’. The main studies concerning microbial therapy, such as the use of bacteria and/or part thereof with microbiota transplantation, and drug delivery systems to recover skin barrier function have been summarized. The studies examined show great potential in the development of effective therapeutic strategies for AD and AD-like symptoms. Despite this promise, however, future investigative efforts should focus both on the replication of some of these studies on a larger scale, with clinical and demographic characteristics that reflect the general AD population, and on the process of standardisation, in order to produce reliable data.
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Skowron, Krzysztof, Justyna Bauza-Kaszewska, Zuzanna Kraszewska, Natalia Wiktorczyk-Kapischke, Katarzyna Grudlewska-Buda, Joanna Kwiecińska-Piróg, Ewa Wałecka-Zacharska, Laura Radtke, and Eugenia Gospodarek-Komkowska. "Human Skin Microbiome: Impact of Intrinsic and Extrinsic Factors on Skin Microbiota." Microorganisms 9, no. 3 (March 5, 2021): 543. http://dx.doi.org/10.3390/microorganisms9030543.

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The skin is the largest organ of the human body and it protects the body from the external environment. It has become the topic of interest of researchers from various scientific fields. Microorganisms ensure the proper functioning of the skin. Of great importance, are the mutual relations between such microorganisms and their responses to environmental impacts, as dysbiosis may contribute to serious skin diseases. Molecular methods, used for microorganism identification, allow us to gain a better understanding of the skin microbiome. The presented article contains the latest reports on the skin microbiota in health and disease. The review discusses the relationship between a properly functioning microbiome and the body’s immune system, as well as the impact of internal and external factors on the human skin microbiome.
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Park, Hee Jin, Ok-Yi Jeong, Sung Hak Chun, Yun Hong Cheon, Mingyo Kim, Suhee Kim, and Sang-Il Lee. "Butyrate Improves Skin/Lung Fibrosis and Intestinal Dysbiosis in Bleomycin-Induced Mouse Models." International Journal of Molecular Sciences 22, no. 5 (March 9, 2021): 2765. http://dx.doi.org/10.3390/ijms22052765.

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Systemic sclerosis (SSc) is an autoimmune disorder characterized by fibrosis of the skin and internal organs. Despite several studies on SSc treatments, effective treatments for SSc are still lacking. Since evidence suggests an association between intestinal microbiota and SSc, we focused on butyrate, which has beneficial effects in autoimmune diseases as a bacterial metabolite. Here, we investigated the therapeutic potential of sodium butyrate (SB) using a bleomycin-induced fibrosis mouse model of SSc and human dermal fibroblasts (HDFs). SB attenuated bleomycin-induced dermal and lung fibrosis in mice. SB influenced fecal microbiota composition (phyla Actinobacteria and Bacteroidetes, genera Bifidobacterium and Ruminococcus_g2). SB controlled macrophage differentiation in mesenteric lymph nodes, spleen, and bronchoalveolar lavage cells of mice with bleomycin-induced skin fibrosis. Profibrotic and proinflammatory gene expression was suppressed by SB administration in skin. Furthermore, SB inhibited transforming growth factor β1-responsive proinflammatory expression with increased acetylation of histone 3 in HDFs. Subcutaneous SB application had antifibrogenic effects on the skin. Butyrate ameliorated skin and lung fibrosis by improving anti-inflammatory activity in a mouse model of SSc. Butyrate may exhibit indirect and direct anti-fibrogenic action on fibroblasts by regulating macrophage differentiation and inhibition of histone deacetylase 3. These findings suggest butyrate as an SSc treatment.
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Costa, Flavia G., and Alexander R. Horswill. "Overcoming pH defenses on the skin to establish infections." PLOS Pathogens 18, no. 5 (May 26, 2022): e1010512. http://dx.doi.org/10.1371/journal.ppat.1010512.

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Skin health is influenced by the composition and integrity of the skin barrier. The healthy skin surface is an acidic, hypertonic, proteinaceous, and lipid-rich environment that microorganisms must adapt to for survival, and disruption of this environment can result in dysbiosis and increase risk for infectious diseases. This work provides a brief overview of skin barrier function and skin surface composition from the perspective of how the most common skin pathogen, Staphylococcus aureus, combats acid stress. Advancements in replicating this environment in the laboratory setting for the study of S. aureus pathogenesis on the skin, as well as future directions in this field, are also discussed.
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Kubica, Malgorzata, Falk Hildebrand, Brigitta M. Brinkman, Dirk Goossens, Jurgen Del Favero, Ken Vercammen, Pierre Cornelis, et al. "The skin microbiome of caspase-14-deficient mice shows mild dysbiosis." Experimental Dermatology 23, no. 8 (July 16, 2014): 561–67. http://dx.doi.org/10.1111/exd.12458.

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Zhang, Meiling, Ziwei Jiang, Dongqing Li, Deming Jiang, Yelin Wu, Hongyan Ren, Hua Peng, and Yuping Lai. "Oral Antibiotic Treatment Induces Skin Microbiota Dysbiosis and Influences Wound Healing." Microbial Ecology 69, no. 2 (October 10, 2014): 415–21. http://dx.doi.org/10.1007/s00248-014-0504-4.

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31

Tran, J., A. Vaughn, W. Burney, R. Sivamani, and R. Crawford. "528 Curcumin-mediated modulation of bacterial communities in inflammatory skin dysbiosis." Journal of Investigative Dermatology 139, no. 5 (May 2019): S90. http://dx.doi.org/10.1016/j.jid.2019.03.604.

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SINGH, TEJ PRATAP, Victoria Lovins, Lucas P. Carvalho, Edgar M. Carvalho, Elizabeth Grice, and Phillip A. Scott. "Regulatory T cells control Th1 responses to sustain bacterial immunity and skin barrier function." Journal of Immunology 208, no. 1_Supplement (May 1, 2022): 58.03. http://dx.doi.org/10.4049/jimmunol.208.supp.58.03.

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Abstract Commensals actively contribute to homeostasis in the skin, but a perturbation of the skin bacteria leading to a dysbiosis often promotes increased inflammation. How regulatory mechanisms control the degree of inflammation associated with a dysbiosis is unclear. Here we used a Staphylococcus aureus isolate from Leishmania braziliensis patients to study the regulation of the host immune response in the skin and its consequence during cutaneous leishmaniasis. Topical colonization with S. aureus induced type 17 responses with minimal skin inflammation. Analysis of Foxp3+ Treg cells revealed IL-6 dependent accumulation of Blimp-1 expressing RORgt+Foxp3+ Treg cells in colonized skin, and that may play a protective regulatory role. To test this, we depleted Foxp3+ Treg cells, which resulted in significant inflammation and a higher bacterial burden on the skin. Additionally, there was some decrease in IL-17 responses, but a significant increase in the IFN-γ production from CD4+ T cells. Moreover, blockade of IFN-γ in Foxp3+ Treg depleted mice restored commensal immunity, barrier function and inflammation. In mice infected with L. braziliensis, depletion of Foxp3+ T cells had a minimal effect on lesion development. However, depletion of Foxp3+ T cells in S. aureus colonized and L. braziliensis infected mice resulted in significantly more inflammation and bacterial burden than control mice without altering the parasite burden. Taken together, we identified a role for Foxp3+ Treg cells in limiting inflammatory responses to skin bacteria by controlling production of IFN-γ by CD4+ T cells.
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Plantamura, Emilie, Amiran Dzutsev, Mathias Chamaillard, Sophia Djebali, Lyvia Moudombi, Lilia Boucinha, Morgan Grau, et al. "MAVS deficiency induces gut dysbiotic microbiota conferring a proallergic phenotype." Proceedings of the National Academy of Sciences 115, no. 41 (September 24, 2018): 10404–9. http://dx.doi.org/10.1073/pnas.1722372115.

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Prominent changes in the gut microbiota (referred to as “dysbiosis”) play a key role in the development of allergic disorders, but the underlying mechanisms remain unknown. Study of the delayed-type hypersensitivity (DTH) response in mice contributed to our knowledge of the pathophysiology of human allergic contact dermatitis. Here we report a negative regulatory role of the RIG-I–like receptor adaptor mitochondrial antiviral signaling (MAVS) on DTH by modulating gut bacterial ecology. Cohousing and fecal transplantation experiments revealed that the dysbiotic microbiota of Mavs−/− mice conferred a proallergic phenotype that is communicable to wild-type mice. DTH sensitization coincided with increased intestinal permeability and bacterial translocation within lymphoid organs that enhanced DTH severity. Collectively, we unveiled an unexpected impact of RIG-I–like signaling on the gut microbiota with consequences on allergic skin disease outcome. Primarily, these data indicate that manipulating the gut microbiota may help in the development of therapeutic strategies for the treatment of human allergic skin pathologies.
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Rodríguez María Lourdes, Rosa Alcira Cristina, Nastri María Lorena, and Jewtuchowicz Virginia Martha. "Oral dysbiosis exacerbates the virulence of Candida parapsilosis sensu stricto via up-regulation of the CPH2 biofilm master gene." World Journal of Advanced Research and Reviews 10, no. 1 (April 30, 2021): 01–011. http://dx.doi.org/10.30574/wjarr.2021.10.1.0107.

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Candida parapsilosis sensu stricto is the second to third most frequent cause of candidemia. Studies place this yeast as a frequent colonizer of niches of the oral cavity, predominantly in pathological conditions. We hypothesize that a buccal environment in dysbiosis enhances the virulence of C. parapsilosis sensu stricto. Objective: To evaluate at the phenotype and molecular level the production of biofilm in oral isolates of C. parapsilosis sensu stricto and correlate the results with the clinical origin (dysbiosis versus eubiosis). Material and methods: The biofilm-forming ability was compared in 50 oral isolates of C. parapsilosis sensu stricto obtained from patients with and without oral dysbiosis; by quantification of biofilm biomass and metabolic activity. The results were corroborated by optical and confocal fluorescence microscopy, and correlated with the transcriptional activity of CPH2, by RT-qPCR. The data were analyzed by Excel 2010, and InfoStat 2018, with a 95% confidence interval. Results: The metabolic activity in biofilm was significantly higher in oral dysbiosis relative to control (p = 0.0025). Basal expression of CPH2 increased 2.8 times more in oral dysbiosis related to the control condition and showed no significant differences with pathogenic isolates of this same yeast, derived from onychomycosis lesions. Conclusion: The oral cavity in dysbiosis increases the virulence of C. parapsilosis sensu stricto due to possible changes in epigenetic marks. This finding suggests that the oral cavity in dysbiosis may be an alternative route to the skin in the epidemiology of nosocomial candidemia.
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Prajapati, Disha P., and Tanvi R. Dodiya. "A REVIEW ON SKIN MICROBIOME: NOVEL STRATEGY IN COSMETICS." International Journal of Research in Ayurveda and Pharmacy 12, no. 3 (July 6, 2021): 99–102. http://dx.doi.org/10.7897/2277-4343.120382.

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Human skin is the largest organ composing a complex ecosystem harbouring different types of microorganisms such as bacteria, viruses, fungi and mites that are together known as the skin microbiome. These organisms play an important role in communicating and instructing the cutaneous arm of the immune system to keep the skin healthy. Diet, hormonal imbalance, lifestyle, use of medications and cosmetics have been reported to influence the composition of skin microbiome. These factors can sometimes cause an imbalance in the microbiome leading to a condition known as ‘dysbiosis’. This disruption can then lead to several skin disorders such as dandruff, acne, psoriasis, or atopic dermatitis. Hygiene products, make-up, perfume, skin cream, nail polish, soap, shampoo, shaving cream, deodorant etc. also implicated in modifying the skin microbiome. Consumers today are moving towards a simpler, cleaner and nature based products for cosmetics. Microbiome balancing skincare natural products can respond to the rising concerns of environment pollution, skin sensitivity and premature ageing. These products can enrich the skin to repair itself by boosting skins immune system and natural defence barrier. These natural products are meant to remove pathogenic but to retain the composition mutualistic organism. The skincare market has recently embraced these distinct approaches of targeting the skin microbiome through different fronts like Probiotics, Prebiotics and Postbiotics.
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Bratoiu, Ioana, Alexandra Burlui, Patricia Richter, Anca Cardoneanu, Ciprian Rezus, and Elena Rezus. "Digestive Dysbiosis in Systemic Scleroderma: a Review." Journal of Interdisciplinary Medicine 6, no. 2 (June 1, 2021): 53–59. http://dx.doi.org/10.2478/jim-2021-0018.

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Abstract Systemic sclerosis (SSc) is a rare autoimmune disease characterized by widespread microvasculopathy, inflammation, and fibrosis of the skin and internal organs. The involvement of the gastrointestinal tract is associated with a wide variety of symptoms and affects circa 90% of patients during the course of the disease. The gastrointestinal microbiota contains trillions of microbial cells and has been found to contribute to both local and systemic homeostasis. In both health and disease, a dynamic interrelationship between gut microbiome activity and the host immune system has been identified. Gastrointestinal dysbiosis has been described as having an important role in obesity, diabetes mellitus, liver disease, cardiovascular and neuropsychiatric disorders, neoplasia, as well as autoimmunity. Recent scientific data indicates a notable role of dysbiosis in the pathogenesis of SSc-related digestive involvement together with various other clinical manifestations. The present review aims to summarize the recent findings regarding digestive dysbiosis as well as the relationship between gastrointestinal microbiota and certain features of SSc.
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Jang, Jae-Hwan, Sun-Young Jang, Sora Ahn, Ju-Young Oh, Mijung Yeom, Seok-Jae Ko, Jae-Woo Park, et al. "Chronic Gut Inflammation and Dysbiosis in IBS: Unraveling Their Contribution to Atopic Dermatitis Progression." International Journal of Molecular Sciences 25, no. 5 (February 27, 2024): 2753. http://dx.doi.org/10.3390/ijms25052753.

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Emerging evidence suggests a link between atopic dermatitis (AD) and gastrointestinal disorders, particularly in relation to gut microbial dysbiosis. This study explored the potential exacerbation of AD by gut inflammation and microbial imbalances using an irritable bowel syndrome (IBS) mouse model. Chronic gut inflammation was induced in the model by intrarectal injection of 2,4,6-trinitrobenzene sulfonic acid (TNBS), followed by a 4-week development period. We noted significant upregulation of proinflammatory cytokines in the colon and evident gut microbial dysbiosis in the IBS mice. Additionally, these mice exhibited impaired gut barrier function, increased permeability, and elevated systemic inflammation markers such as IL-6 and LPS. A subsequent MC903 challenge on the right cheek lasting for 7 days revealed more severe AD symptoms in IBS mice compared to controls. Further, fecal microbial transplantation (FMT) from IBS mice resulted in aggravated AD symptoms, a result similarly observed with FMT from an IBS patient. Notably, an increased abundance of Alistipes in the feces of IBS mice correlated with heightened systemic and localized inflammation in both the gut and skin. These findings collectively indicate that chronic gut inflammation and microbial dysbiosis in IBS are critical factors exacerbating AD, highlighting the integral relationship between gut and skin health.
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Umemoto, Naoka, Maki Kakurai, Takanao Matsumoto, Kenta Mizuno, Otomi Cho, Takashi Sugita, and Toshio Demitsu. "Dupilumab Alters Both the Bacterial and Fungal Skin Microbiomes of Patients with Atopic Dermatitis." Microorganisms 12, no. 1 (January 22, 2024): 224. http://dx.doi.org/10.3390/microorganisms12010224.

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The skin microbiome at lesion sites in patients with atopic dermatitis (AD) is characterized by dysbiosis. Although the administration of dupilumab, an IL-4Rα inhibitor, improves dysbiosis in the bacterial microbiome, information regarding the fungal microbiome remains limited. This study administered dupilumab to 30 patients with moderate-to-severe AD and analyzed changes in both fungal and bacterial skin microbiomes over a 12-week period. Malassezia restricta and M. globosa dominated the fungal microbiome, whereas non-Malassezia yeast species increased in abundance, leading to greater microbial diversity. A qPCR analysis revealed a decrease in Malassezia colonization following administration, with a higher reduction rate observed where the pretreatment degree of colonization was higher. A correlation was found between the group classified by the Eczema Area and Severity Index, the group categorized by the concentration of Thymus and activation-regulated chemokine, and the degree of skin colonization by Malassezia. Furthermore, an analysis of the bacterial microbiome also confirmed a decrease in the degree of skin colonization by the exacerbating factor Staphylococcus aureus and an increase in the microbial diversity of the bacterial microbiome. Our study is the first to show that dupilumab changes the community structure of the bacterial microbiome and affects the fungal microbiome in patients with AD.
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Zhan, Mengting, Zhenyu Huang, Gaofeng Cheng, Yongyao Yu, Jianguo Su, and Zhen Xu. "Alterations of the Mucosal Immune Response and Microbial Community of the Skin upon Viral Infection in Rainbow Trout (Oncorhynchus mykiss)." International Journal of Molecular Sciences 23, no. 22 (November 14, 2022): 14037. http://dx.doi.org/10.3390/ijms232214037.

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The skin is the largest organ on the surface of vertebrates, which not only acts as the first line of defense against pathogens but also harbors diverse symbiotic microorganisms. The complex interaction between skin immunity, pathogens, and commensal bacteria has been extensively studied in mammals. However, little is known regarding the effects of viral infection on the skin immune response and microbial composition in teleost fish. In this study, we exposed rainbow trout (Oncorhynchus mykiss) to infectious hematopoietic necrosis virus (IHNV) by immersion infection. Through pathogen load detection and pathological evaluation, we confirmed that IHNV successfully invaded the rainbow trout, causing severe damage to the epidermis of the skin. qPCR analyses revealed that IHNV invasion significantly upregulated antiviral genes and elicited strong innate immune responses. Transcriptome analyses indicated that IHNV challenge induced strong antiviral responses mediated by pattern recognition receptor (PRR) signaling pathways in the early stage of the infection (4 days post-infection (dpi)), and an extremely strong antibacterial immune response occurred at 14 dpi. Our 16S rRNA sequencing results indicated that the skin microbial community of IHNV-infected fish was significantly richer and more diverse. Particularly, the infected fish exhibited a decrease in Proteobacteria accompanied by an increase in Actinobacteria. Furthermore, IHNV invasion favored the colonization of opportunistic pathogens such as Rhodococcus and Vibrio on the skin, especially in the later stage of infection, leading to dysbiosis. Our findings suggest that IHNV invasion is associated with skin microbiota dysbiosis and could thus lead to secondary bacterial infection.
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40

Perugini, Paola, Camilla Grignani, Giorgia Condrò, Harald van der Hoeven, Annamaria Ratti, Antonella Mondelli, Antonio Colpani, and Mariella Bleve. "Skin Microbiota: Setting up a Protocol to Evaluate a Correlation between the Microbial Flora and Skin Parameters." Biomedicines 11, no. 3 (March 21, 2023): 966. http://dx.doi.org/10.3390/biomedicines11030966.

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The concept of skin microbiota is not really clear and more accurate approaches are necessary to explain how microbial flora can influence skin biophysical parameters in healthy individuals and in pathology patients with non-infectious skin disease. The aim of this work is to provide a suitable, fast and reproducible protocol to correlate skin parameters with the composition of skin microbiota. For this purpose, the work was split into two main phases. The first phase was focused on the selection of volunteers by the administration of a specific questionnaire. The skin microbiota was then collected from the forehead of selected volunteers as a test area and from the shoulder as control area. On the same skin area, the biophysical parameters, such as trans-epidermal water loss (TEWL), sebum level (SL), porphyrin intensity, keratin content and stratum corneum water content were taken. All parameters were taken at t0 and after 15 days without changes in the volunteers’ lifestyle. A strong correlation was found between forehead and shoulder area for porphyrin intensity, pH and TEWL parameters, and between Cutibacterium acnes and some biophysical parameters both in the forehead and the shoulder area. The procedural setup in this work represents the starting point for evaluating problematic skins and the efficacy of cosmetic products or treatment against skin dysbiosis.
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Tustumi, Francisco, Vitor Pelogi Arienzo, Isabela Roskamp Sunye, Phellipe Fabbrini Santos Lucas, Bárbara Buccelli Colonno, Julia Grams Quintas, Elis Nogara Lisboa, and Daniel José Szor. "Esophageal Dysbiosis in Achalasia and Cancer Development: A Critical Review." Genes 14, no. 8 (July 26, 2023): 1521. http://dx.doi.org/10.3390/genes14081521.

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Background: Microorganisms provide various benefits to their human hosts, including assisting with digestion, synthesizing certain vitamins, developing the gastrointestinal and immune systems, regulating metabolism, and protecting against some pathogens. However, microbial imbalances can cause tissue damage and contribute to inflammatory disorders and cancers. Microbial dysbiosis refers to an imbalance or disruption in the normal composition and function of the microbial communities that inhabit various body parts, including the gut, oral cavity, skin, and reproductive tract. Emerging research suggests that microbial dysbiosis plays a significant role in cancer development and progression. This issue is particularly relevant in achalasia, in which food stasis, changes in endoluminal pH, and poor esophageal clearance might contribute to esophageal microbial dysbiosis. This study aimed to evaluate the association between dysbiosis and esophageal cancer development, focused on esophageal dysmotility disorders. Methods: This study is a critical review, gathering the current evidence for the association between dysbiosis and the development of esophageal cancer. Results: Studies have shown that microbiota play a role in cancer development, although the mechanisms for how they do so are not yet fully understood. One possible explanation is that microbiota alterations can lead to chronic inflammation, promoting cancer cell growth. Additionally, some bacteria produce toxins that can damage DNA and cause genomic instability, and certain bacterial products can promote tumor growth. Conclusion: Despite the close relationship between dysbiosis and cancer development in esophageal dysmotility disorders, further investigations are still needed to elucidate the precise mechanisms by which dysbiosis contributes to cancer development and to identify potential therapeutic interventions targeting the microbiota to prevent or treat cancer.
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Luo, Jialiang, Zhengyumeng Zhu, Yumeng Zhai, Junxiang Zeng, Lei Li, Di Wang, Fan Deng, Bo Chang, Jia Zhou, and Ledong Sun. "The Role of TSLP in Atopic Dermatitis: From Pathogenetic Molecule to Therapeutical Target." Mediators of Inflammation 2023 (April 15, 2023): 1–8. http://dx.doi.org/10.1155/2023/7697699.

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Atopic dermatitis (AD) is a kind of chronic skin disease with inflammatory infiltration, characterized by skin barrier dysfunction, immune response dysregulation, and skin dysbiosis. Thymic stromal lymphopoietin (TSLP) acts as a regulator of immune response, positively associated with AD deterioration. Mainly secreted by keratinocytes, TSLP interacts with multiple immune cells (including dendritic cells, T cells, and mast cells), following induction of Th2-oriented immune response during the pathogenesis of AD. This article primarily focuses on the TSLP biological function, the relationship between TSLP and different cell populations, and the AD treatments targeting TSLP.
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43

Khasiev, N. D., E. B. Shaposhnikova, N. I. Shevchuk, and I. V. Mironov. "Features of the skin microbiota in patients with diabetes." Bulletin of the Russian Military Medical Academy 20, no. 4 (December 15, 2018): 76–78. http://dx.doi.org/10.17816/brmma12276.

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The assessment of the skin microbiota state in elderly people with diabetes mellitus is given. For the research and development of quantitative and specific indicators of deep microbiota of the skin used the method of agar imprints. The revealed changes in the skin microbiota in patients with diabetes mellitus are of interest as adaptive characteristics of the organism, and also serve as a harbinger of deviations in the clinical and physiological status of patients and give reason to present the basic laws of skin biocenosis in elderly people suffering from diabetes mellitus. It was found that the species composition of the microbiota does not change in the control group in the deep layers of the forearm skin, and the number of colony-forming units increased, which corresponds to skin dysbiosis of the I degree. It was also found that representatives of Staphylococcus spp occupy a dominant position in the skin microbiota in persons with diabetes mellitus, both in frequency of occurrence and in quantitative measure. At the same time, in the observed patients, regardless of the type and stage of diabetes mellitus, an increase in the number of colony-forming units by 1 cm2 of the deep layers of the forearm skin was revealed, which corresponds to the dysbacteriosis of the skin of the III degree. This is 2,6 times greater than in healthy individuals. This increase is directly correlated with the severity of diabetes. It is shown that dysbiosis can manifest itself by clinical local symptoms, and then by General disorders, which aggravate the course of the underlying disease and complicate treatment. An integrated approach to this problem can be used for a more differentiated assessment of the prognosis of complications in patients with diabetes mellitus and to improve the effectiveness of treatment and preventive care.
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Dong, X., L. S. Miller, N. Archer, L. Garza, and X. Dong. "LB972 Defensins and neutrophil-specific defensin receptors prevent skin dysbiosis and infection." Journal of Investigative Dermatology 142, no. 8 (August 2022): B24. http://dx.doi.org/10.1016/j.jid.2022.05.995.

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Dong, X., G. Wang, L. Miller, B. S. Kim, L. A. Garza, N. K. Archer, and X. Dong. "218 Neutrophil-specific defensin receptors that prevent skin dysbiosis and bacterial infection." Journal of Investigative Dermatology 141, no. 5 (May 2021): S39. http://dx.doi.org/10.1016/j.jid.2021.02.239.

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Lee, Hyun-Ji, and Miri Kim. "Skin Barrier Function and the Microbiome." International Journal of Molecular Sciences 23, no. 21 (October 28, 2022): 13071. http://dx.doi.org/10.3390/ijms232113071.

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Human skin is the largest organ and serves as the first line of defense against environmental factors. The human microbiota is defined as the total microbial community that coexists in the human body, while the microbiome refers to the collective genome of these microorganisms. Skin microbes do not simply reside on the skin but interact with the skin in a variety of ways, significantly affecting the skin barrier function. Here, we discuss recent insights into the symbiotic relationships between the microbiome and the skin barrier in physical, chemical, and innate/adaptive immunological ways. We discuss the gut-skin axis that affects skin barrier function. Finally, we examine the effects of microbiome dysbiosis on skin barrier function and the role of these effects in inflammatory skin diseases, such as acne, atopic dermatitis, and psoriasis. Microbiome cosmetics can help restore skin barrier function and improve these diseases.
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Szczepańska, Milena, Leszek Blicharz, Joanna Nowaczyk, Karolina Makowska, Mohamad Goldust, Anna Waśkiel-Burnat, Joanna Czuwara, Zbigniew Samochocki, and Lidia Rudnicka. "The Role of the Cutaneous Mycobiome in Atopic Dermatitis." Journal of Fungi 8, no. 11 (October 31, 2022): 1153. http://dx.doi.org/10.3390/jof8111153.

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Atopic dermatitis is a chronic inflammatory skin disorder characterized by eczematous lesions, itch, and a significant deterioration in the quality of life. Recently, microbiome dysbiosis has been implicated in the pathogenesis of atopic dermatitis. Changes in the fungal microbiome (also termed mycobiome) appear to be an important factor influencing the clinical picture of this entity. This review summarizes the available insights into the role of the cutaneous mycobiome in atopic dermatitis and the new research possibilities in this field. The prevalence and characteristics of key fungal species, the most important pathogenesis pathways, as well as classic and emerging therapies of fungal dysbiosis and infections complicating atopic dermatitis, are presented.
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48

Murashkin, Nikolay N., Leyla S. Namazova-Baranova, Leonid A. Opryatin, Roman V. Epishev, Alexander I. Materikin, Eduard T. Ambarchian, Roman A. Ivanov, Dmitriy V. Fedorov, and Daria S. Kukoleva. "Biologic Therapy of Moderate and Severe Forms of Atopic Dermatitis in Children." Current Pediatrics 19, no. 6 (December 27, 2020): 432–43. http://dx.doi.org/10.15690/vsp.v19i6.2145.

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Atopic dermatitis (AD) is the disease with chronic inflammation, epidermal barrier dysfunction and microbial dysbiosis. AD is widespread, including pediatric population. The article discusses the disease’s pathogenesis: skin barrier deficiency, immunological causes of chronic inflammation, characteristics of normal skin microbiome and its disorders on both affected and unaffected skin of children with AD. Main principles of systemic treatment for moderate and severe forms of disease are considered. Features of targeted therapy with dupilumab (IL 4/IL 13 inhibitor) in children with moderate and severe forms of AD are discussed. The overview of the research results on the dupilumab efficacy and safety is presented.
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49

Khalil, Alaa, Aamina Batool, and Sania Arif. "Healthy Cattle Microbiome and Dysbiosis in Diseased Phenotypes." Ruminants 2, no. 1 (February 23, 2022): 134–56. http://dx.doi.org/10.3390/ruminants2010009.

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Cattle farming is an ancient practice, with roots in the early Neolithic era that has retained a major status in the food industry, with global beef market revenue amounting to $385.7B (as of 2018). Hence, cattle maintenance is essential for catering to the nutritional requirements of modern civilization. This extensive review aims to provide a holistic overview of the cattle microbiome, analyzing the native microbial composition within the respiratory tract, gastrointestinal tract, reproductive tract, and skin of cattle. The dysbiosis associated with various diseases such as bovine respiratory disease, bovine digital dermatitis, mastitis, Johne’s disease, uterine diseases (metritis and endometritis), and metabolic disorders (ruminal acidosis and ketosis) have been discussed. Moreover, various non-antibiotic microbial therapies including phage therapy, prebiotics, and probiotics have been examined as potential means to reduce disease-associated dysbiosis. In general, this review highlights the importance of the microbiome in the maintenance of health in cattle and its potential in alleviating bovine diseases, with an aim to enhance cattle health and production.
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Haasbroek, Kyle, Masayuki Yagi, and Yoshikazu Yonei. "Staphylococcus aureus Biofilm Inhibiting Activity of Advanced Glycation Endproduct Crosslink Breaking and Glycation Inhibiting Compounds." Antibiotics 11, no. 10 (October 14, 2022): 1412. http://dx.doi.org/10.3390/antibiotics11101412.

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Staphylococcus aureus is a Gram-positive bacterium that plays a role in the pathogenesis of skin lesions in diabetes mellitus, atopic dermatitis, and psoriasis, all of which are associated with elevated non-enzymatic glycation biomarkers. The production of biofilm protects resident bacteria from host immune defenses and antibiotic interventions, prolonging pathogen survival, and risking recurrence after treatment. Glycated proteins formed from keratin and glucose induce biofilm formation in S. aureus, promoting dysbiosis and increasing pathogenicity. In this study, several glycation-inhibiting and advanced glycation endproduct (AGE) crosslink-breaking compounds were assayed for their ability to inhibit glycated keratin-induced biofilm formation as preliminary screening for clinical testing candidates. Ascorbic acid, astaxanthin, clove extract, n-phenacylthiazolium bromide, and rosemary extract were examined in an in vitro static biofilm model with S. aureus strain ATCC 12600. Near complete biofilm inhibition was achieved with astaxanthin (ED50 = 0.060 mg/mL), clove extract (ED50 = 0.0087 mg/mL), n-phenacylthiazolium bromide (ED50 = 5.3 mg/mL), and rosemary extract (ED50 = 1.5 mg/mL). The dosage necessary for biofilm inhibition was not significantly correlated with growth inhibition (R2 = 0.055. p = 0.49). Anti-glycation and AGE breaking compounds with biofilm inhibitory activity are ideal candidates for treatment of S. aureus dysbiosis and skin infection that is associated with elevated skin glycation.
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