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1
Nath, SameeraG, and Ranjith Raveendran. "Microbial dysbiosis in periodontitis." Journal of Indian Society of Periodontology 17, no. 4 (2013): 543. http://dx.doi.org/10.4103/0972-124x.118334.
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Hurst, John R. "Microbial dysbiosis in bronchiectasis." Lancet Respiratory Medicine 2, no. 12 (December 2014): 945–47. http://dx.doi.org/10.1016/s2213-2600(14)70223-1.
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Payne, M. A., A. Hashim, A. Alsam, S. Joseph, J. Aduse-Opoku, W. G. Wade, and M. A. Curtis. "Horizontal and Vertical Transfer of Oral Microbial Dysbiosis and Periodontal Disease." Journal of Dental Research 98, no. 13 (September 27, 2019): 1503–10. http://dx.doi.org/10.1177/0022034519877150.
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One of the hallmark features of destructive periodontal disease, well documented over the last 50 y, is a change to the quantitative and qualitative composition of the associated microbiology. These alterations are now generally viewed as transformational shifts of the microbial populations associated with health leading to the emergence of bacterial species, which are only present in low abundance in health and a proportionate decrease in the abundance of others. The role of this dysbiosis of the health associated microbiota in the development of disease remains controversial: is this altered microbiology the driving agent of disease or merely a consequence of the altered environmental conditions that invariably accompany destructive disease? In this work, we aimed to address this controversy through controlled transmission experiments in the mouse in which a dysbiotic oral microbiome was transferred either horizontally or vertically into healthy recipient mice. The results of these murine studies demonstrate conclusively that natural transfer of the dysbiotic oral microbiome from a periodontally diseased individual into a healthy individual will lead to establishment of the dysbiotic community in the recipient and concomitant transmission of the disease phenotype. The inherent resilience of the dysbiotic microbial community structure in diseased animals was further demonstrated by analysis of the effects of antibiotic therapy on periodontally diseased mice. Although antibiotic treatment led to a reversal of dysbiosis of the oral microbiome, in terms of both microbial load and community structure, dysbiosis of the microbiome was reestablished following cessation of therapy. Collectively, these data suggest that an oral dysbiotic microbial community structure is stable to transfer and can act in a similar manner to a conventional transmissible infectious disease agent with concomitant effects on pathology. These findings have implications to our understanding of the role of microbial dysbiosis in the development and progression of human periodontal disease.
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Vemuri, Ravichandra, Alistaire Ruggiero, Jordyn M. Whitfield, Greg O. Dugan, J. Mark Cline, Masha R. Block, Hao Guo, and Kylie Kavanagh. "Hypertension promotes microbial translocation and dysbiotic shifts in the fecal microbiome of nonhuman primates." American Journal of Physiology-Heart and Circulatory Physiology 322, no. 3 (March 1, 2022): H474—H485. http://dx.doi.org/10.1152/ajpheart.00530.2021.
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Hypertension specifically had detrimental effects on microbial translocation when age and metabolic syndrome criteria were evaluated as drivers of cardiovascular disease in a relevant nonhuman primate model. Intestinal barrier function exponentially decayed over time with chronic hypertension, and microbial translocation was confirmed by detection of more microbial genes in regional draining lymph nodes. Chronic hypertension resulted in fecal microbial dysbiosis and elevations of the biomarker NT-proBNP. This study provides insights on the barrier dysfunction, dysbiosis, and hypertension in controlled studies of nonhuman primates. Our study includes a longitudinal component comparing naturally occurring hypertensive to normotensive primates to confirm microbial translocation and dysbiotic microbiome development. Hypertension is an underappreciated driver of subclinical endotoxemia that can drive chronic inflammatory diseases
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Parida, Sheetal, and Dipali Sharma. "Microbial Alterations and Risk Factors of Breast Cancer: Connections and Mechanistic Insights." Cells 9, no. 5 (April 28, 2020): 1091. http://dx.doi.org/10.3390/cells9051091.
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Breast cancer-related mortality remains high worldwide, despite tremendous advances in diagnostics and therapeutics; hence, the quest for better strategies for disease management, as well as the identification of modifiable risk factors, continues. With recent leaps in genomic technologies, microbiota have emerged as major players in most cancers, including breast cancer. Interestingly, microbial alterations have been observed with some of the established risk factors of breast cancer, such as obesity, aging and periodontal disease. Higher levels of estrogen, a risk factor for breast cancer that cross-talks with other risk factors such as alcohol intake, obesity, parity, breastfeeding, early menarche and late menopause, are also modulated by microbial dysbiosis. In this review, we discuss the association between known breast cancer risk factors and altered microbiota. An important question related to microbial dysbiosis and cancer is the underlying mechanisms by which alterations in microbiota can support cancer progression. To this end, we review the involvement of microbial metabolites as effector molecules, the modulation of the metabolism of xenobiotics, the induction of systemic immune modulation, and altered responses to therapy owing to microbial dysbiosis. Given the association of breast cancer risk factors with microbial dysbiosis and the multitude of mechanisms altered by dysbiotic microbiota, an impaired microbiome is, in itself, an important risk factor.
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McHarg, Alexandra S., and Steven Leach. "The role of the gut microbiome in paediatric irritable bowel syndrome." AIMS Microbiology 8, no. 4 (2022): 454–69. http://dx.doi.org/10.3934/microbiol.2022030.
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<abstract> <p>Irritable bowel syndrome (IBS) is a common and disabling condition in children. The pathophysiology of IBS is thought to be multifactorial but remains incompletely understood. There is growing evidence implicating the gut microbiome in IBS. Intestinal dysbiosis has been demonstrated in paediatric IBS cohorts; however, no uniform or consistent pattern has been identified. The exact mechanisms by which this dysbiosis contributes to IBS symptoms remain unknown. Available evidence suggests the imbalance produces a functional dysbiosis, with altered production of gases and metabolites that interact with the intestinal wall to cause symptoms, and enrichment or depletion of certain metabolic pathways. Additional hypothesised mechanisms include increased intestinal permeability, visceral hypersensitivity and altered gastrointestinal motility; however, these remain speculative in paediatric patients, with studies limited to animal models and adult populations. Interaction between dietary components and intestinal microbiota, particularly with fermentable oligosaccharides, disaccharides, monosaccharides and polyols (FODMAPs), has drawn increasing attention. FODMAPs have been found to trigger and worsen IBS symptoms. This is thought to be related to products of their fermentation by a dysbiotic microbial population, although this remains to be proven. A low-FODMAP diet has shown promising success in ameliorating symptoms in some but not all patients. There remains much to be discovered about the role of the dysbiotic microbiome in paediatric IBS.</p> </abstract>
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Chalmers, James D. "Microbial Dysbiosis after Lung Transplantation." American Journal of Respiratory and Critical Care Medicine 194, no. 10 (November 15, 2016): 1184–86. http://dx.doi.org/10.1164/rccm.201606-1178ed.
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Molina, Nerea M., Alberto Sola-Leyva, Maria Jose Saez-Lara, Julio Plaza-Diaz, Aleksandra Tubić-Pavlović, Barbara Romero, Ana Clavero, Juan Mozas-Moreno, Juan Fontes, and Signe Altmäe. "New Opportunities for Endometrial Health by Modifying Uterine Microbial Composition: Present or Future?" Biomolecules 10, no. 4 (April 11, 2020): 593. http://dx.doi.org/10.3390/biom10040593.
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Current knowledge suggests that the uterus harbours its own microbiota, where the microbes could influence the uterine functions in health and disease; however, the core uterine microbial composition and the host-microbial relationships remain to be fully elucidated. Different studies are indicating, based on next-generation sequencing techniques, that microbial dysbiosis could be associated with several gynaecological disorders, such as endometriosis, chronic endometritis, dysfunctional menstrual bleeding, endometrial cancer, and infertility. Treatments using antibiotics and probiotics and/or prebiotics for endometrial microbial dysbiosis are being applied. Nevertheless there is no unified protocol for assessing the endometrial dysbiosis and no optimal treatment protocol for the established dysbiosis. With this review we outline the microbes (mostly bacteria) identified in the endometrial microbiome studies, the current treatments offered for bacterial dysbiosis in the clinical setting, and the future possibilities such as pro- and prebiotics and microbial transplants for modifying uterine microbial composition.
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Park, Kiwoong, Suhyeon Park, Arulkumar Nagappan, Navin Ray, Juil Kim, Sik Yoon, and Yuseok Moon. "Probiotic Escherichia coli Ameliorates Antibiotic-Associated Anxiety Responses in Mice." Nutrients 13, no. 3 (March 1, 2021): 811. http://dx.doi.org/10.3390/nu13030811.
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Despite the beneficial actions of antibiotics against bacterial infections, the use of antibiotics is a crucial etiological factor influencing microbial dysbiosis-associated adverse outcomes in human health. Based on the assumption that gut microbial dysbiosis can provoke behavioral or psychological disorders, the present study evaluated anxiety-linked behavioral changes in a mouse model of streptomycin-induced dysbiosis. Measuring anxiety-like behavior using the light–dark box and elevated plus maze tests indicated that streptomycin treatment caused acute anxiety in mice. As an intervention for dysbiosis-associated distress, the probiotic strain Escherichia coli Nissle 1917 (EcN) was evaluated for its effects on streptomycin-induced behavioral changes in mice. EcN supplementation persistently ameliorated anxiety responses in mice with streptomycin-induced dysbiosis. As an outcome of anxiety, body weight changes were marginally affected by antibiotic treatment. However, mice supplemented with EcN displayed acute retardation of body weight gain, since EcN is known to reduce food intake and increase energy expenditure. Taken together, EcN treatment prominently counteracted streptomycin-induced anxiety in mice, with the metabolically beneficial retardation of body weight gain. The present model simulates psychological disorders in antibiotic users. As a promising intervention, EcN treatment can facilitate psychological relief under conditions of dysbiotic stress by blocking the pathologic gut–brain circuit.
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Srivastava, Shivani, Archana Singh, Kumar Sandeep, and Durgavati Yadav. "Epigenetic Regulation of Gut Microbial Dysbiosis." Indian Journal of Microbiology 61, no. 2 (February 11, 2021): 125–29. http://dx.doi.org/10.1007/s12088-021-00920-y.
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Loke, P’ng, and Yvonne A. L. Lim. "Can Helminth Infection Reverse Microbial Dysbiosis?" Trends in Parasitology 31, no. 11 (November 2015): 534–35. http://dx.doi.org/10.1016/j.pt.2015.10.001.
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Wang, Fuyuan, and Sabita Roy. "Gut Homeostasis, Microbial Dysbiosis, and Opioids." Toxicologic Pathology 45, no. 1 (November 28, 2016): 150–56. http://dx.doi.org/10.1177/0192623316679898.
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Gut homeostasis plays an important role in maintaining animal and human health. The disruption of gut homeostasis has been shown to be associated with multiple diseases. The mutually beneficial relationship between the gut microbiota and the host has been demonstrated to maintain homeostasis of the mucosal immunity and preserve the integrity of the gut epithelial barrier. Currently, rapid progress in the understanding of the host–microbial interaction has redefined toxicological pathology of opioids and their pharmacokinetics. However, it is unclear how opioids modulate the gut microbiome and metabolome. Our study, showing opioid modulation of gut homeostasis in mice, suggests that medical interventions to ameliorate the consequences of drug use/abuse will provide potential therapeutic and diagnostic strategies for opioid-modulated intestinal infections. The study of morphine’s modulation of the gut microbiome and metabolome will shed light on the toxicological pathology of opioids and its role in the susceptibility to infectious diseases.
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Tiffany, Connor R., and Andreas J. Bäumler. "Dysbiosis: from fiction to function." American Journal of Physiology-Gastrointestinal and Liver Physiology 317, no. 5 (November 1, 2019): G602—G608. http://dx.doi.org/10.1152/ajpgi.00230.2019.
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Advances in data collection technologies reveal that an imbalance (dysbiosis) in the composition of host-associated microbial communities (microbiota) is linked to many human illnesses. This association makes dysbiosis a central concept for understanding how the human microbiota contributes to health and disease. However, it remains problematic to define the term dysbiosis by cataloguing microbial species names. Here, we discuss how incorporating the germ-organ concept, ecological assumptions, and immunological principles into a theoretical framework for microbiota research provides a functional definition for dysbiosis. The generation of such a framework suggests that the next logical step in microbiota research will be to illuminate the mechanistic underpinnings of dysbiosis, which often involves a weakening of immune mechanisms that balance our microbial communities.
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Gagliardi, Antonella, Valentina Totino, Fatima Cacciotti, Valerio Iebba, Bruna Neroni, Giulia Bonfiglio, Maria Trancassini, Claudio Passariello, Fabrizio Pantanella, and Serena Schippa. "Rebuilding the Gut Microbiota Ecosystem." International Journal of Environmental Research and Public Health 15, no. 8 (August 7, 2018): 1679. http://dx.doi.org/10.3390/ijerph15081679.
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A microbial ecosystem in which bacteria no longer live in a mutualistic association is called dysbiotic. Gut microbiota dysbiosis is a condition related with the pathogenesis of intestinal illnesses (irritable bowel syndrome, celiac disease, and inflammatory bowel disease) and extra-intestinal illnesses (obesity, metabolic disorder, cardiovascular syndrome, allergy, and asthma). Dysbiosis status has been related to various important pathologies, and many therapeutic strategies aimed at restoring the balance of the intestinal ecosystem have been implemented. These strategies include the administration of probiotics, prebiotics, and synbiotics; phage therapy; fecal transplantation; bacterial consortium transplantation; and a still poorly investigated approach based on predatory bacteria. This review discusses the various aspects of these strategies to counteract intestinal dysbiosis.
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V, Nikhra. "The Nutritional Links for Gut Microbial Dysbiosis and its Metabolic and Endocrinal Fallouts." Gastroenterology & Hepatology International Journal 7, no. 2 (August 30, 2022): 1–6. http://dx.doi.org/10.23880/ghij-16000198.
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The Human Gut Microbiome: The gastro-intestinal tract, skin and genitals, and various other body organs, harbour large and diverse communities of bacteria, viruses, and other microscopic life. In the human gut, a nutrient-rich environment, reside ~ 100 trillion microbes, the vast majority of which is present in the colon. There inhabit microbial members as residents (autochthonous), while others (allochthonous) are from ingested food, water, and other components of the environment. The adult human gut microbiota is dominated by mainly two bacteria, the Bacteroidetes and Firmicutes, and an archea, Metanobrevibacter smithii. The microbial ecosystems throughout the body interact with the molecular processes, which have been linked to various aspects of human physiology. The understanding about microbiota is evolving and presents as an important research avenue. The Gut Biosphere and Ecosystem: In general, the gut microbial communities depend on their specific enzymes and molecules to utilize available nutrients, cell-surface molecular appendages to attach on to their right habitat, to evade bacteriophages, with ability to deal with immune system and avoid washout and genetic mutability to stay well-adapted. The microbiota influences various biological processes and organ physiology, including gastrointestinal processes, energy metabolism and insulin resistance, and thus influence weight gain, development of diabetes, and aging. The intestinal epithelium actively senses various bacteria and plays an essential role in maintaining host-microbial homeostasis at the mucosal interface. On the other hand, the host factors, such as dietary factors influence the host-microbial and microbial-microbial relationships. Microbiota, Health and Disease States: The evidence from clinical studies and animal models shows a link between the gut microbiome and human health. There exists a bidirectional microbiota–gut–brain communication which modulates brain function and behaviours. The research in mice and humans is beginning to establish a link between the composition of microbes in the gut and immune response to tumor cells. Certain metabolites or antigens presented by members of that microbiome may help uplift the sensitivity of immune system to tumour cells, whereas dysbiosis may lead to the loss of antitumor immunity. On the other hand, the gut microbes harbour enzymes and secrete molecules that can influence drug activation, efficacy, and metabolism. Dietary Constituents and Microbiome: The dietary components influence the gut microbiota. It has been documented that a change in diet can alter the degradative activity of the colonic microbiota in vivo and in a physiologically relevant setting influence the expression of various microbial genes. The complex plant polysaccharides in diet are not digested and enter the colon as a potential food source for the gut microorganisms, which harbour a multitude of genes involved in catabolism of carbohydrates. The reduced availability of dietary polysaccharides and fibre can trigger dysbiosis and degradation of intestinal mucin layer and affect intestinal health. The microbial production of short chain fatty acids and other metabolites has been shown to influence immune system.
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Richard Samuelson, Derrick, Vincent Maffei, Eugene Blanchard, Meng Luo, Christopher Taylor, Judd Shellito, Martin Ronis, Patricia Molina, and David Welsh. "2262." Journal of Clinical and Translational Science 1, S1 (September 2017): 4–5. http://dx.doi.org/10.1017/cts.2017.32.
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OBJECTIVES/SPECIFIC AIMS: Alcohol consumption perturbs the normal intestinal microbial communities (alcohol dysbiosis). To begin to investigate the relationship between alcohol-mediated dysbiosis and host defense we developed an alcohol dysbiosis fecal adoptive transfer model, which allows us to isolate the host immune response to a pathogenic challenge at a distal organ (ie, the lung). This model system allowed us to determine whether the host immune responses to Klebsiella pneumoniae are altered by ethanol-associated dysbiosis, independent of alcohol use. We hypothesized that alcohol-induced changes in intestinal microbial communities would impair pulmonary host defenses against K. pneumoniae. METHODS/STUDY POPULATION: Mice were treated with a cocktail of antibiotics daily for 2 weeks. Microbiota-depleted mice were then recolonized by gavage for 3-days with intestinal microbiota from ethanol-fed or pair-fed animals. Following recolonization groups of mice were sacrificed prior to and 48 hours post respiratory infection with K. pneumoniae. We then assessed susceptibility to Klebsiella infection by determining colony counts for pathogen burden in the lungs. We also determined lung and intestinal immunology, intestinal permeability, as well as, liver damage and inflammation. RESULTS/ANTICIPATED RESULTS: We found that increased susceptibility to K. pneumoniae is, in part, mediated by the intestinal microbiota, as animals recolonized with an alcohol-induced dysbiotic intestinal microbial community have significantly higher lung burdens of K. pneumoniae (5×104 CFU vs. 1×103 CFU) independent of EtOH. We also found that increased susceptibility in alcohol-dysbiosis recolonized animals was associated with a decrease in the recruitment and/or proliferation of CD4+ and CD8+ T-cells (1.5×109 cells vs. 2.5×109 cells) in the lung following Klebsiella infection. However, there were increased numbers of T-cells in the intestinal tract following Klebsiella infection, which may suggest that T cells are being sequestered in the intestinal tract to the detriment of host defense in the lung. Interestingly, mice recolonized with an alcohol-dysbiotic microbiota had increased intestinal permeability as measured by increased levels of serum intestinal fatty acid binding protein (55 vs. 30 ng/mL). Alcohol-dysbiotic microbiota also increased liver steatosis (Oil Red-O staining) and liver inflammation (>2-fold expression of IL-17 and IL-23). DISCUSSION/SIGNIFICANCE OF IMPACT: Our findings suggest that the commensal intestinal microbiota support mucosal host defenses against infectious agents by facilitating normal immune responses to pulmonary pathogens. Our data also suggest that increased intestinal permeability coupled with increased liver inflammation may impair the recruitment/proliferation of immune cells in the respiratory tract following infection. The role of the microbiota during host defense will be important areas of future research directed at understanding the effects of microbial dysbiosis in patients with AUDs.
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Tain, You-Lin, and Chien-Ning Hsu. "Role of the Gut Microbiota in Children with Kidney Disease." Children 10, no. 2 (January 31, 2023): 269. http://dx.doi.org/10.3390/children10020269.
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Disruption of the composition and structure of the gut microbiota, namely dysbiosis, dictates the pathophysiology of kidney diseases. The bidirectional kidney–gut axis is of interest in chronic kidney disease (CKD); the uremic milieu leads to intestinal dysbiosis and gut microbial metabolites and toxins implicated in the loss of kidney function and increased comorbidity burden. Considering that kidney diseases can originate in childhood or even earlier in fetal life, identification of the pathogenetic connection between gut microbiota dysbiosis and the development of pediatric renal diseases deserves more attention. This review concentrates on the pathogenic link between dysbiotic gut microbiota and pediatric renal diseases, covering CKD, kidney transplantation, hemodialysis and peritoneal dialysis, and idiopathic nephrotic syndrome. Gut microbiota-targeted therapies including dietary intervention, probiotics, prebiotics, postbiotics and fecal microbial transplantation are discussed for their potential for the treatment of pediatric renal diseases. A deeper understanding of gut microbiota in pediatric renal diseases will aid in developing innovative gut microbiota-targeted interventions for preventing or attenuating the global burden of kidney diseases.
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Oliver, L., S. Ramió-Pujol, M. Malagón, M. Serrano, A. Bahí, D. Busquets, L. Torrealba, M. Serra-Pagès, X. Aldeguer, and J. Garcia-Gil. "P687 Development of a panel of microbial markers to distinguish transient from pathological dysbiosis." Journal of Crohn's and Colitis 15, Supplement_1 (May 1, 2021): S606. http://dx.doi.org/10.1093/ecco-jcc/jjab076.807.
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Abstract Background Dysbiosis is a widely used but unspecific term. It has been defined as any change in the composition of resident microbial communities relative to the ones found in healthy individuals. But it is still unclear which are the appropriate communities to define it and the reference values to measure it. Different studies have described dysbiosis in various diseases such as Inflammatory Bowel Disease (IBD), diabetes, rheumatoid arthritis, and autism, among others. Besides, the microbiota can be altered by transient factors such as antibiotics, diet, stress, or infections. Therefore, different degrees of severity can be associated with the term dysbiosis from which pathological and transient dysbiosis can be differentiated. This work aimed at defining more specifically the term intestinal dysbiosis and to differentiate both transient and pathological dysbiosis. Methods Fifteen key microbial markers belonging to the principal families, classes and orders found in the human intestinal microbiota were accurately selected based on its functionality: F. prausnitzii (Fpra), E. coli (Eco), Firmicutes (Fir), Bacteroidetes (Bac), A. muciniphila (Akk), Ruminococcus sp. (Rum), Roseburia sp. (Ros), Gammaproteobacteria (Gam), Clostridia cluster I (Clo), Clostridia cluster XIV (XIV), Enterococcus sp., Lactobacillus sp. (Lac), C. albicans (Can), M. smithii (Msm), and the total bacterial load (Eub). The dysbiosis was defined using stool samples in a cohort of healthy subjects (n=24) and then validated with 9 patients diagnosed with intestinal diseases 4 IBD and 2 Irritable Bowel Syndrome (IBS)). Total DNA was extracted and the abundance of microbial markers was analysed by qPCR. Together with the establishment of the most common range in which each microbial marker was found, an index to define the pathological dysbiosis was calculated. Results Almost all healthy subjects analysed presented one or two slightly altered markers. The affected microbial markers in this “transient dysbiosis” were Fpra, Akk, and Ros, which are indicative of the mucous layer state, Firm as indicative of the lifestyle and fiber intake, Gam as characteristic of the pro-inflammatory state of the gut, and Msm as an altered intestinal habit and gas production. All patients analyzed (IBD and IBS) presented alterations mainly of the bacteria inhabiting the mucosa and an alteration of the opportunistic species related to the disrupted mucous layer and defining “pathological dysbiosis”. Conclusion This study establishes an appropriate abundance range of key microbial markers in the gut, leading to a specific definition of dysbiosis which allows to differentiate the pathological from the transient dysbiosis. These results need further validation in a larger patient cohort.
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Salas Garcia, Mariana C., Alyson L. Yee, Jack A. Gilbert, and Melissa Dsouza. "Dysbiosis in Children Born by Caesarean Section." Annals of Nutrition and Metabolism 73, Suppl. 3 (2018): 24–32. http://dx.doi.org/10.1159/000492168.
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The rate of Caesarean-section delivery in the United States has increased by 60% from 1996 through to 2013 and now accounts for > 30% of births [CDC, 2017]. The purpose of this review is to present the current understanding of both the microbial risk factors that increase the likelihood of a Caesarean-section delivery and the microbial dysbiosis that is thought to result from the Caesarean section. We provide examples of research into the impact of early-life microbial dysbiosis on infant development and long-term health outcomes, as well as consider the efficacy and the long-term implications of microbiome-based therapies to mitigate this dysbiosis. The steep rise in the Caesarean-section delivery rate makes it imperative to understand the potential of microbiota modulation for the treatment of dysbiosis.
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Jun, Shelly, Kelsea Drall, Brittany Matenchuk, Cara McLean, Charlene Nielsen, Chinwe Obiakor, Aaron van der Leek, and Anita Kozyrskyj. "Sanitization of Early Life and Microbial Dysbiosis." Challenges 9, no. 2 (December 18, 2018): 43. http://dx.doi.org/10.3390/challe9020043.
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Childbearing and infant care practices have dramatically evolved since the 15th century. Shifting away from traditional home-based experiences, with the emergence of the microbial aware era and the hospital as a quintessential sanitizing machine, early life has now long been characterized as a condition to be medically managed. Paradoxically, this ‘germ-free’ march towards a healthier early life environment has opened the door to greater microbial susceptibility and dysbiosis. Many studies have now established that infant exposure to excessive sanitation and hygiene regimens are associated with an increased risk for and onset of childhood immune system diseases. In this paper, we explore the ways in which biomedical-centered efforts to enhance early life have come at a cost to planetary health, in relation to infant microbial succession. We examine three major areas of early life that have been subject to the ‘ripple effect’ of hygiene and sanitation concerns—childbirth, home environment, and breastfeeding.
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Thomas, Karen R., Jacob Watt, Chuen Mong J. Wu, Adejoke Akinrinoye, Sairah Amjad, Lucy Colvin, Rachel Cowe, Sylvia H. Duncan, Wendy R. Russell, and Patrice Forget. "Pain and Opioid-Induced Gut Microbial Dysbiosis." Biomedicines 10, no. 8 (July 28, 2022): 1815. http://dx.doi.org/10.3390/biomedicines10081815.
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Opioid-induced dysbiosis (OID) is a specific condition describing the consequences of opioid use on the bacterial composition of the gut. Opioids have been shown to affect the epithelial barrier in the gut and modulate inflammatory pathways, possibly mediating opioid tolerance or opioid-induced hyperalgesia; in combination, these allow the invasion and proliferation of non-native bacterial colonies. There is also evidence that the gut-brain axis is linked to the emotional and cognitive aspects of the brain with intestinal function, which can be a factor that affects mental health. For example, Mycobacterium, Escherichia coli and Clostridium difficile are linked to Irritable Bowel Disease; Lactobacillaceae and Enterococcacae have associations with Parkinson’s disease, and Alistipes has increased prevalence in depression. However, changes to the gut microbiome can be therapeutically influenced with treatments such as faecal microbiota transplantation, targeted antibiotic therapy and probiotics. There is also evidence of emerging therapies to combat OID. This review has collated evidence that shows that there are correlations between OID and depression, Parkinson’s Disease, infection, and more. Specifically, in pain management, targeting OID deserves specific investigations.
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Sobhani, Iradj, Julien Tap, Françoise Roudot-Thoraval, Jean P. Roperch, Sophie Letulle, Philippe Langella, Gérard Corthier, Jeanne Tran Van Nhieu, and Jean P. Furet. "Microbial Dysbiosis in Colorectal Cancer (CRC) Patients." PLoS ONE 6, no. 1 (January 27, 2011): e16393. http://dx.doi.org/10.1371/journal.pone.0016393.
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Dicker, Alison J., and James D. Chalmers. "Microbial Dysbiosis in Bronchiectasis and Cystic Fibrosis." Archivos de Bronconeumología (English Edition) 53, no. 9 (September 2017): 471–72. http://dx.doi.org/10.1016/j.arbr.2017.01.010.
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Valverde-Molina, José, and Luis García-Marcos. "Microbiome and Asthma: Microbial Dysbiosis and the Origins, Phenotypes, Persistence, and Severity of Asthma." Nutrients 15, no. 3 (January 17, 2023): 486. http://dx.doi.org/10.3390/nu15030486.
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The importance of the microbiome, and of the gut-lung axis in the origin and persistence of asthma, is an ongoing field of investigation. The process of microbial colonisation in the first three years of life is fundamental for health, with the first hundred days of life being critical. Different factors are associated with early microbial dysbiosis, such as caesarean delivery, artificial lactation and antibiotic therapy, among others. Longitudinal cohort studies on gut and airway microbiome in children have found an association between microbial dysbiosis and asthma at later ages of life. A low a-diversity and relative abundance of certain commensal gut bacterial genera in the first year of life are associated with the development of asthma. Gut microbial dysbiosis, with a lower abundance of Phylum Firmicutes, could be related with increased risk of asthma. Upper airway microbial dysbiosis, especially early colonisation by Moraxella spp, is associated with recurrent viral infections and the development of asthma. Moreover, the bacteria in the respiratory system produce metabolites that may modify the inception of asthma and is progression. The role of the lung microbiome in asthma development has yet to be fully elucidated. Nevertheless, the most consistent finding in studies on lung microbiome is the increased bacterial load and the predominance of proteobacteria, especially Haemophilus spp. and Moraxella catarrhalis. In this review we shall update the knowledge on the association between microbial dysbiosis and the origins of asthma, as well as its persistence, phenotypes, and severity.
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Zenobia, Camille, Hatice Hasturk, Daniel Nguyen, Thomas E. Van Dyke, Alpdogan Kantarci, and Richard P. Darveau. "Porphyromonas gingivalis Lipid A Phosphatase Activity Is Critical for Colonization and Increasing the Commensal Load in the Rabbit Ligature Model." Infection and Immunity 82, no. 2 (November 25, 2013): 650–59. http://dx.doi.org/10.1128/iai.01136-13.
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ABSTRACTPeriodontitis is a disease of polymicrobial etiology characterized by inflammation, degradation of host tissue, and bone that irreversibly destroys the supporting apparatus of teeth.Porphyromonas gingivaliscontains lipid A with structural heterogeneity that has been postulated to contribute to the initiation of dysbiosis in oral communities by modulating the host response, thereby creating a permissive environment for its growth. We examined twoP. gingivalislipid A phosphatase mutants which contain different “locked” lipid A structures that induce different host cellular responses for their ability to induce dysbiosis and periodontitis in rabbits. Lipopolysaccharide (LPS) preparations obtained from these strains were also examined. After repeated applications of all strains and their respective LPS preparations,P. gingivaliswild type, but not the lipid A mutants, had a significant impact on both the oral commensal microbial load and composition. In contrast, in rabbits exposed to the mutant strains or the LPS preparations, the microbial load did not increase, and yet significant changes in the oral microbial composition were observed. All strains and their respective LPS preparations induced periodontitis. Therefore, the ability to alter the lipid A composition in response to environmental conditions by lipid A phosphatases is required for both colonization of the rabbit and increases in the microbial load. Furthermore, the data demonstrate that multiple dysbiotic oral microbial communities can elicit periodontitis.
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Nagaraja, T. G. "98 Gut Microbiome: Implications on gut Health." Journal of Animal Science 100, Supplement_3 (September 21, 2022): 45. http://dx.doi.org/10.1093/jas/skac247.088.
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Abstract The rumen and the hindgut, which includes cecum and colon, of cattle are inhabited by a diverse microbial community, which is composed mainly of bacteria, but also includes archaea, protozoa, fungi and viruses. Most reside in the lumen, but also colonize the epithelial surface and their compositions are a critical component of the host health. Recent advances in sequencing techniques and biological computational tools have further underscored the complexity of the microbial community. The vast repertoire of the gut microbiome provides the host complementary genetic resources to harvest energy, provide proteins and vitamins, contribute to the development of gut epithelium and gut-associated lymphoid system, and to the overall gut health. The gut epithelium-vascular interface allows secretions, and absorption and metabolism of fermentation products and serves as a selective barrier to prevent translocation and systemic dissemination of microbes, microbial toxins, and immunogens. The barrier function includes protection form mechanical damage caused by feedstuffs, chemical damage from acidity, toxins and microbial invasion, especially pathogens. The mechanisms employed likely differ between the two fermentative regions of the gut, given the dramatic difference in epithelial structures. Rumen is lined by stratified squamous epithelium compared a single layer of columnar epithelium interspersed with mucus-producing goblet cells in the hindgut. The mucus layer is the first barrier the pathogen has to overcome for colonization and translocation. An imbalance in the composition of gut microbiota, called dysbiosis, leads to gut functional disorders. The dysbiosis can range from a change in one to a few species to the perturbation of entire microbial community. The assessment of gut microbial dysbiosis is a challenge because of the complexity and huge variations in the community composition, including animal-to-animal. The gut barrier function determines whether the dysbiotic changes are contained within the lumen or disseminated systemically to affect the health and productivity.
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Guo, Yang, Yang Zhang, Markus Gerhard, Juan-Juan Gao, Raquel Mejias-Luque, Lian Zhang, Michael Vieth, et al. "Effect of Helicobacter pylori on gastrointestinal microbiota: a population-based study in Linqu, a high-risk area of gastric cancer." Gut 69, no. 9 (December 19, 2019): 1598–607. http://dx.doi.org/10.1136/gutjnl-2019-319696.
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ObjectiveGastrointestinal microbiota may be involved in Helicobacter pylori-associated gastric cancer development. The aim of this study was to explore the possible microbial mechanisms in gastric carcinogenesis and potential dysbiosis arising from H. pylori infection.DesignDeep sequencing of the microbial 16S ribosomal RNA gene was used to investigate alterations in paired gastric biopsies and stool samples in 58 subjects with successful and 57 subjects with failed anti-H. pylori treatment, relative to 49 H. pylori negative subjects.ResultsIn H. pylori positive subjects, richness and Shannon indexes increased significantly (both p<0.001) after successful eradication and showed no difference to those of negative subjects (p=0.493 for richness and p=0.420 for Shannon index). Differential taxa analysis identified 18 significantly altered gastric genera after eradication. The combination of these genera into a Microbial Dysbiosis Index revealed that the dysbiotic microbiota in H. pylori positive mucosa was associated with advanced gastric lesions (chronic atrophic gastritis and intestinal metaplasia/dysplasia) and could be reversed by eradication. Strong coexcluding interactions between Helicobacter and Fusobacterium, Neisseria, Prevotella, Veillonella, Rothia were found only in advanced gastric lesion patients, and were absent in normal/superficial gastritis group. Changes in faecal microbiota included increased Bifidobacterium after successful H. pylori eradication and more upregulated drug-resistant functional orthologs after failed treatment.ConclusionH. pylori infection contributes significantly to gastric microbial dysbiosis that may be involved in carcinogenesis. Successful H. pylori eradication potentially restores gastric microbiota to a similar status as found in uninfected individuals, and shows beneficial effects on gut microbiota.
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Risovannaya, O. N., and Z. V. Lalieva. "Influence of psychoemotional stress on microbal landscape of gingival furrow." Medical alphabet 2, no. 11 (November 23, 2019): 46–49. http://dx.doi.org/10.33667/2078-5631-2019-2-11(386)-46-49.
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Relevance of the research topic. The oral cavity is one of the most diverse microbiomes in the human body, which is divided into several biotopes: oral mucosa, dental plaque, gingival fluid and gingival sulcus zone and others. The biotope of the gingival sulcus is unique in that quantitative and qualitative changes in the microbial communities of this microecological system can lead to the development of the main dental diseases — gingivitis, periodontitis and caries. Purpose. To study the influence of emotional stress on the microbal landscape of the gingival furrow, which is in a state of eubiosis and dysbiosis. Materials and methods. The study involved 67 aged by 30–49 years. A microbiological study was made of the general microbial contamination of the gingival furrow and its colonization by individual microbal species using aerobic and anaerobic cultivation methods. Results. In the state of relative dormancy, 100 % of people without gum disease were found to have an eubiotic condition of the gingival microbal, at 100 % of persons with periodontis the microbal of the gingival groove was in a state of dysbiosis. Summary. The influence of the stressor on the disorder of the balance of the microbial homeostasis of the dental gingival slit causes an increase in the imbalance of microbial associations in the form of a decrease in the comensal microflora and an increase in the opportunistic pathogenicity. Highlights. 1. Emotional stress may cause the development of periodontal diseases in people who work in the field of law enforcement. 2. On a background of emotional stress the dysbalance of microbial associations increases.
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Coker, Olabisi Oluwabukola, Zhenwei Dai, Yongzhan Nie, Guijun Zhao, Lei Cao, Geicho Nakatsu, William KK Wu, et al. "Mucosal microbiome dysbiosis in gastric carcinogenesis." Gut 67, no. 6 (August 1, 2017): 1024–32. http://dx.doi.org/10.1136/gutjnl-2017-314281.
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ObjectivesWe aimed to characterise the microbial changes associated with histological stages of gastric tumourigenesis.DesignWe performed 16S rRNA gene analysis of gastric mucosal samples from 81 cases including superficial gastritis (SG), atrophic gastritis (AG), intestinal metaplasia (IM) and gastric cancer (GC) from Xi’an, China, to determine mucosal microbiome dysbiosis across stages of GC. We validated the results in mucosal samples of 126 cases from Inner Mongolia, China.ResultsWe observed significant mucosa microbial dysbiosis in IM and GC subjects, with significant enrichment of 21 and depletion of 10 bacterial taxa in GC compared with SG (q<0.05). Microbial network analysis showed increasing correlation strengths among them with disease progression (p<0.001). Five GC-enriched bacterial taxa whose species identifications correspond to Peptostreptococcus stomatis, Streptococcus anginosus, Parvimonas micra, Slackia exigua and Dialister pneumosintes had significant centralities in the GC ecological network (p<0.05) and classified GC from SG with an area under the receiver-operating curve (AUC) of 0.82. Moreover, stronger interactions among gastric microbes were observed in Helicobacter pylori-negative samples compared with H. pylori-positive samples in SG and IM. The fold changes of selected bacteria, and strengths of their interactions were successfully validated in the Inner Mongolian cohort, in which the five bacterial markers distinguished GC from SG with an AUC of 0.81.ConclusionsIn addition to microbial compositional changes, we identified differences in bacterial interactions across stages of gastric carcinogenesis. The significant enrichments and network centralities suggest potentially important roles of P. stomatis, D. pneumosintes, S. exigua, P. micra and S. anginosus in GC progression.
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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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Lu, Junying, Lingxin Xiong, Xiaohao Zhang, Zhongmin Liu, Shiji Wang, Chao Zhang, Jingtong Zheng, et al. "The Role of Lower Airway Dysbiosis in Asthma: Dysbiosis and Asthma." Mediators of Inflammation 2017 (2017): 1–10. http://dx.doi.org/10.1155/2017/3890601.
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With the development of culture-independent techniques, numerous studies have demonstrated that the lower airway is not sterile in health and harbors diverse microbial communities. Furthermore, new evidence suggests that there is a distinct lower airway microbiome in those with chronic respiratory disease. To understand the role of lower airway dysbiosis in the pathogenesis of asthma, in this article, we review the published reports about the lung microbiome of healthy controls, provide an outlook on the contribution of lower airway dysbiosis to asthma, especially steroid-resistant asthma, and discuss the potential therapies targeted for lower airway dysbiosis.
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Gomez-Ramirez, Uriel, Pedro Valencia-Mayoral, Sandra Mendoza-Elizalde, Juan Rafael Murillo-Eliosa, Fortino Solórzano Santos, Araceli Contreras-Rodríguez, Gerardo Zúñiga, et al. "Role of Helicobacter pylori and Other Environmental Factors in the Development of Gastric Dysbiosis." Pathogens 10, no. 9 (September 16, 2021): 1203. http://dx.doi.org/10.3390/pathogens10091203.
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Microbiomes are defined as complex microbial communities, which are mainly composed of bacteria, fungi, and viruses residing in diverse regions of the human body. The human stomach consists of a unique and heterogeneous habitat of microbial communities owing to its anatomical and functional characteristics, that allow the optimal growth of characteristic bacteria in this environment. Gastric dysbiosis, which is defined as compositional and functional alterations of the gastric microbiota, can be induced by multiple environmental factors, such as age, diet, multiple antibiotic therapies, proton pump inhibitor abuse, H. pylori status, among others. Although H. pylori colonization has been reported across the world, chronic H. pylori infection may lead to serious consequences; therefore, the infection must be treated. Multiple antibiotic therapy improvements are not always successful because of the lack of adherence to the prescribed antibiotic treatment. However, the abuse of eradication treatments can generate gastric dysbiotic states. Dysbiosis of the gastric microenvironment induces microbial resilience, due to the loss of relevant commensal bacteria and simultaneous colonization by other pathobiont bacteria, which can generate metabolic and physiological changes or even initiate and develop other gastric disorders by non-H. pylori bacteria. This systematic review opens a discussion on the effects of multiple environmental factors on gastric microbial communities.
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Ferreira, Rui M., Joana Pereira-Marques, Ines Pinto-Ribeiro, Jose L. Costa, Fatima Carneiro, Jose C. Machado, and Ceu Figueiredo. "Gastric microbial community profiling reveals a dysbiotic cancer-associated microbiota." Gut 67, no. 2 (November 4, 2017): 226–36. http://dx.doi.org/10.1136/gutjnl-2017-314205.
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ObjectiveGastric carcinoma development is triggered by Helicobacter pylori. Chronic H. pylori infection leads to reduced acid secretion, which may allow the growth of a different gastric bacterial community. This change in the microbiome may increase aggression to the gastric mucosa and contribute to malignancy. Our aim was to evaluate the composition of the gastric microbiota in chronic gastritis and in gastric carcinoma.DesignThe gastric microbiota was retrospectively investigated in 54 patients with gastric carcinoma and 81 patients with chronic gastritis by 16S rRNA gene profiling, using next-generation sequencing. Differences in microbial composition of the two patient groups were assessed using linear discriminant analysis effect size. Associations between the most relevant taxa and clinical diagnosis were validated by real-time quantitative PCR. Predictive functional profiling of microbial communities was obtained with PICRUSt.ResultsThe gastric carcinoma microbiota was characterised by reduced microbial diversity, by decreased abundance of Helicobacter and by the enrichment of other bacterial genera, mostly represented by intestinal commensals. The combination of these taxa into a microbial dysbiosis index revealed that dysbiosis has excellent capacity to discriminate between gastritis and gastric carcinoma. Analysis of the functional features of the microbiota was compatible with the presence of a nitrosating microbial community in carcinoma. The major observations were confirmed in validation cohorts from different geographic origins.ConclusionsDetailed analysis of the gastric microbiota revealed for the first time that patients with gastric carcinoma exhibit a dysbiotic microbial community with genotoxic potential, which is distinct from that of patients with chronic gastritis.
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Hoang, Tung, Min Jung Kim, Ji Won Park, Seung-Yong Jeong, Jeeyoo Lee, and Aesun Shin. "Abstract 3062: Modifiable factors and gut microbiome alteration among colorectal cancer patients." Cancer Research 82, no. 12_Supplement (June 15, 2022): 3062. http://dx.doi.org/10.1158/1538-7445.am2022-3062.
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Abstract Background: Previous study have indicated an association of microbial dysbiosis with stages of colorectal cancer (CRC). Meanwhile, higher microbial stochasticity has been introduced as the Anna Karenina principle (AKP) effect, which originates from the opening line of Leo Tolstoy and is translated in the microbiome as “all healthy microbiomes are similar; each dysbiotic microbiome is dysbiotic in its own way”. Here, we aim to elucidate the effect of modifiable factors on microbiome stochasticity related to dysbiosis in CRC. Methods: Fecal samples from 331 CRC patients, were collected prior to their surgery at Seoul National University Hospital. Bacteria that were enriched in early- and late-stage CRC groups were identified by linear discrimination analysis effect size (LEfSE) method, which was then used to calculate microbial dysbiosis index (MDI). The association of dietary choices with microbiome variability was addressed using the LEfSE analysis. The difference of intra-sample similarity index among lifestyle factors and metabolic diseases was tested to examine the AKP effect. A tree-based analysis of food choices was constructed. We then applied Procrustes framework to analyze the shape of dietary diversity and microbiome. Results: The LEfSE identified Leuconostoc, Oxalobacter, Acidaminococcus, and Methanobrevibacter were enriched in early-stage CRC, whereas Bacteroides, Fusobacterium, Lachnoanaerobaculum, Clostridium, and Granulicatella were enriched in late-stage CRC patients. The MDI derived from these bacteria had 64.2% predictive ability for CRC stages, with sensitivity and specificity of 61% and 69%, respectively. The AKP effect was found for history of smoking, alcohol consumption, and diabetes, whereas obesity and hypertension showed anti-AKP effect. For dietary choices, the hierarchical tree of foods and nutrients did not shape the microbial between-sample diversity. Additionally, high MDI was related with a high intake of pizza/hamburger, poultry, and light-vegetable combination. Conclusion: Our study contributed to current evidence of the microbiome structure and dysbiosis at different stages of CRC. Furthermore, history of smoking, alcohol consumption, and diabetes showed AKP effect in CRC patients. Non-significant association between dietary choices and microbiome diversity supported a small variation of microbiome profiles explained by dietary intake at the population level. Citation Format: Tung Hoang, Min Jung Kim, Ji Won Park, Seung-Yong Jeong, Jeeyoo Lee, Aesun Shin. Modifiable factors and gut microbiome alteration among colorectal cancer patients [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2022; 2022 Apr 8-13. Philadelphia (PA): AACR; Cancer Res 2022;82(12_Suppl):Abstract nr 3062.
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Рисованная, Ольга, Olga Risovannaya, Зарина Лалиева, and Zarina Lalieva. "A STUDY OF THE INFLUENCE OF PSYCHOEMOTIONAL STRESS ON MICROBFL LANDSCAPE OF THE GINGIVAL FURROW IN STUDENTS." Actual problems in dentistry 15, no. 2 (August 9, 2019): 135–40. http://dx.doi.org/10.18481/2077-7566-2019-15-2-135-140.
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Relevance of the research topic. The oral cavity is one of the most diverse microbiomes in the human body, which is divided into several biotopes: oral mucosa, dental plaque, gingival fluid and gingival sulcus zone and others. The biotope of the gingival sulcus is unique in that quantitative and qualitative changes in the microbial communities of this microecological system can lead to the development of the main dental diseases - gingivitis, periodontitis and caries. The scientific literature on the etiology of these diseases determines the microbial landscape of the gingival sulcus as the dominant causative factor. A significant influence on the microflora of periodontal tissues is exerted by various stressors of a modern person.
Purpose ― to study the influence of emotional stress on the microbal landscape of the gingival furrow, which is in a state of eubiosis and dysbiosis.
Materials and methods. The study involved 67 aged by 35―44 years. A microbiological study was made of the general microbial contamination of the gingival furrow and its colonization by individual microbal species using aerobic and anaerobic cultivation methods.
Results. In the state of relative dormancy, 100 % of people without gum disease were found to have an eubiotic condition of the gingival microbal, 100 % of persons with periodontis - the microbal of the gingival groove were in a state of dysbiosis.
Summary. The influence of the stressor on the disorder of the balance of the microbial homeostasis of the dental gingival slit causes an increase in the imbalance of microbial associations in the form of a decrease in the comensal microflora and an increase in the opportunistic pathogenicity.
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Suvorov, A. N. "Microbial personified therapy as an instrument of medical doctor in the future." Russian Journal for Personalized Medicine 2, no. 1 (April 4, 2022): 51–62. http://dx.doi.org/10.18705/2782-3806-2022-2-1-51-62.
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The review discusses modern concepts of microbiota, its organization and significance for the functioning of the human body. The data on the significance of changes in the microbial composition in the case of dysbiosis and the strategies of a modern clinician aimed at restoring the microbial community inherent in each person are presented. The author’s position in relation to microbial therapy by means of exogenously grown microorganisms (probiotics, autoprobiotics and fecal transplantation) being introduced into the human body under conditions of dysbiosis are described.
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Battaglioli, Eric J., Vanessa L. Hale, Jun Chen, Patricio Jeraldo, Coral Ruiz-Mojica, Bradley A. Schmidt, Vayu M. Rekdal, et al. "Clostridioides difficileuses amino acids associated with gut microbial dysbiosis in a subset of patients with diarrhea." Science Translational Medicine 10, no. 464 (October 24, 2018): eaam7019. http://dx.doi.org/10.1126/scitranslmed.aam7019.
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The gut microbiota plays a critical role in pathogen defense. Studies using antibiotic-treated mice reveal mechanisms that increase susceptibility toClostridioides difficileinfection (CDI), but risk factors associated with CDI in humans extend beyond antibiotic use. Here, we studied the dysbiotic gut microbiota of a subset of patients with diarrhea and modeled the gut microbiota of these patients by fecal transplantation into germ-free mice. When challenged withC. difficile, the germ-free mice transplanted with fecal samples from patients with dysbiotic microbial communities showed increased gut amino acid concentrations and greater susceptibility to CDI. AC. difficilemutant that was unable to use proline as an energy source was unable to robustly infect germ-free mice transplanted with a dysbiotic or healthy human gut microbiota. Prophylactic dietary intervention using a low-proline or low-protein diet in germ-free mice colonized by a dysbiotic human gut microbiota resulted in decreased expansion of wild-typeC. difficileafter challenge, suggesting that amino acid availability might be important for CDI. Furthermore, a prophylactic fecal microbiota transplant in mice with dysbiosis reduced proline availability and protected the mice from CDI. Last, we identified clinical risk factors that could potentially predict gut microbial dysbiosis and thus greater susceptibility to CDI in a retrospective cohort of patients with diarrhea. Identifying at-risk individuals and reducing their susceptibility to CDI through gut microbiota–targeted therapies could be a new approach to preventingC. difficileinfection in susceptible patients.
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Shapiro, Hagit, Kim Goldenberg, Karina Ratiner, and Eran Elinav. "Smoking-induced microbial dysbiosis in health and disease." Clinical Science 136, no. 18 (September 2022): 1371–87. http://dx.doi.org/10.1042/cs20220175.
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Abstract Smoking is associated with an increased risk of cancer, pulmonary and cardiovascular diseases, but the precise mechanisms by which such risk is mediated remain poorly understood. Additionally, smoking can impact the oral, nasal, oropharyngeal, lung and gut microbiome composition, function, and secreted molecule repertoire. Microbiome changes induced by smoking can bear direct consequences on smoking-related illnesses. Moreover, smoking-associated dysbiosis may modulate weight gain development following smoking cessation. Here, we review the implications of cigarette smoking on microbiome community structure and function. In addition, we highlight the potential impacts of microbial dysbiosis on smoking-related diseases. We discuss challenges in studying host–microbiome interactions in the context of smoking, such as the correlations with smoking-related disease severity versus causation and mechanism. In all, understanding the microbiome’s role in the pathophysiology of smoking-related diseases may promote the development of rational therapies for smoking- and smoking cessation-related disorders, as well as assist in smoking abstinence.
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Kumar, Purnima S. "Microbial dysbiosis: The root cause of periodontal disease." Journal of Periodontology 92, no. 8 (July 2021): 1079–87. http://dx.doi.org/10.1002/jper.21-0245.
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Mandal, Supratim, Shrabasti Bandyopadhyay, Komal Tyagi, and Adhiraj Roy. "Human microbial dysbiosis as driver of gynecological malignancies." Biochimie 197 (June 2022): 86–95. http://dx.doi.org/10.1016/j.biochi.2022.02.005.
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Xuan, Caiyun, Jaime M. Shamonki, Alice Chung, Maggie L. DiNome, Maureen Chung, Peter A. Sieling, and Delphine J. Lee. "Microbial Dysbiosis Is Associated with Human Breast Cancer." PLoS ONE 9, no. 1 (January 8, 2014): e83744. http://dx.doi.org/10.1371/journal.pone.0083744.
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Hov, Johannes Roksund. "Editorial: proton pump inhibition - microbial complications beyond dysbiosis." Alimentary Pharmacology & Therapeutics 50, no. 8 (October 2019): 962–63. http://dx.doi.org/10.1111/apt.15495.
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Shin, Na-Ri, Tae Woong Whon, and Jin-Woo Bae. "Proteobacteria: microbial signature of dysbiosis in gut microbiota." Trends in Biotechnology 33, no. 9 (September 2015): 496–503. http://dx.doi.org/10.1016/j.tibtech.2015.06.011.
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Singh, V. P., S. D. Proctor, and B. P. Willing. "Koch's postulates, microbial dysbiosis and inflammatory bowel disease." Clinical Microbiology and Infection 22, no. 7 (July 2016): 594–99. http://dx.doi.org/10.1016/j.cmi.2016.04.018.
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Olsen, Ingar. "Oral microbial dysbiosis precedes development of pancreatic cancer." Journal of Oral Microbiology 9, no. 1 (January 1, 2017): 1374148. http://dx.doi.org/10.1080/20002297.2017.1374148.
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Topcuoglu, Nursen, Arzu Pınar Erdem, Ilker Karacan, and Guven Kulekci. "Oral microbial dysbiosis in patients with Kostmann syndrome." Journal of Medical Microbiology 68, no. 4 (April 1, 2019): 609–15. http://dx.doi.org/10.1099/jmm.0.000964.
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Kaakoush, N. O., A. S. Day, K. D. Huinao, S. T. Leach, D. A. Lemberg, S. E. Dowd, and H. M. Mitchell. "Microbial Dysbiosis in Pediatric Patients with Crohn's Disease." Journal of Clinical Microbiology 50, no. 10 (July 25, 2012): 3258–66. http://dx.doi.org/10.1128/jcm.01396-12.
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Taguchi, Kensei, Kei Fukami, Bertha C. Elias, and Craig R. Brooks. "Dysbiosis-Related Advanced Glycation Endproducts and Trimethylamine N-Oxide in Chronic Kidney Disease." Toxins 13, no. 5 (May 19, 2021): 361. http://dx.doi.org/10.3390/toxins13050361.
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Chronic kidney disease (CKD) is a public health concern that affects approximately 10% of the global population. CKD is associated with poor outcomes due to high frequencies of comorbidities such as heart failure and cardiovascular disease. Uremic toxins are compounds that are usually filtered and excreted by the kidneys. With the decline of renal function, uremic toxins are accumulated in the systemic circulation and tissues, which hastens the progression of CKD and concomitant comorbidities. Gut microbial dysbiosis, defined as an imbalance of the gut microbial community, is one of the comorbidities of CKD. Meanwhile, gut dysbiosis plays a pathological role in accelerating CKD progression through the production of further uremic toxins in the gastrointestinal tracts. Therefore, the gut-kidney axis has been attracting attention in recent years as a potential therapeutic target for stopping CKD. Trimethylamine N-oxide (TMAO) generated by gut microbiota is linked to the progression of cardiovascular disease and CKD. Also, advanced glycation endproducts (AGEs) not only promote CKD but also cause gut dysbiosis with disruption of the intestinal barrier. This review summarizes the underlying mechanism for how gut microbial dysbiosis promotes kidney injury and highlights the wide-ranging interventions to counter dysbiosis for CKD patients from the view of uremic toxins such as TMAO and AGEs.
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Khatri, Gauri S., Christine Kurian, Asha Anand, and Paari KA. "Gut Homeostasis; Microbial Cross Talks in Health and Disease Management." Current Research in Nutrition and Food Science Journal 9, no. 3 (December 30, 2021): 1017–45. http://dx.doi.org/10.12944/crnfsj.9.3.28.
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The human gut is a densely populated region comprising a diverse collection of microorganisms. The number, type and function of the diverse gut microbiota vary at different sites along the entire gastrointestinal tract. Gut microbes regulate signaling and metabolic pathways through microbial cross talks. Host and microbial interactions mutually contribute for intestinal homeostasis. Rapid shift or imbalance in the microbial community disrupts the equilibrium or homeostatic state leading to dysbiosis and causes many gastrointestinal diseases viz., Inflammatory Bowel Disease, Obesity, Type 2 diabetes, Metabolic endotoxemia, Parkinson’s disease and Fatty liver disease etc. Intestinal homeostasis has been confounded by factors that disturb the balance between eubiosis and dysbiosis. This review correlates the consequences of dysbiosis with the incidence of various diseases. Impact of microbiome and its metabolites on various organs such as liver, brain, kidney, large intestine, pancreas etc are discussed. Furthermore, the role of therapeutic approaches such as ingestion of nutraceuticals (probiotics, prebiotics and synbiotics), Fecal Microbial Treatment, Phage therapy and Bacterial consortium treatment in restoring the eubiotic state is elaborately reviewed.
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Hu, S., A. R. Bourgonje, R. Gacesa, B. H. Jansen, A. Bangma, I. Hidding, E. A. M. Festen, et al. "P086 Mucosal microbiota modulate host intestinal immune signatures in Inflammatory Bowel Disease." Journal of Crohn's and Colitis 16, Supplement_1 (January 1, 2022): i185—i186. http://dx.doi.org/10.1093/ecco-jcc/jjab232.215.
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Abstract Background Host intestinal immune gene signatures and microbial dysregulations expose potential mechanisms in the pathogenesis of inflammatory bowel diseases (IBD). Profiling of mucosa-attached microbiota allows the understanding of locally present microbial communities and their immediate impact on the host. This study evaluated interactions between host mucosal gene expression and intestinal mucosa-attached microbiota in IBD. Methods Intestinal mucosal bulk RNA-sequencing data was combined with mucosal 16S rRNA gene sequencing data from 696 intestinal biopsies derived from 337 patients with IBD (181 with Crohn’s disease [CD] and 156 with ulcerative colitis [UC]) and 16 non-IBD controls. Hierarchical all-against-all associations testing (HAllA) was used to assess factors affecting host gene expressions and microbiota. Mucosal cell enrichments were predicted by deconvolution. Linear mixed interaction models were used to investigate host-microbiota interactions, adjusting for age, sex, BMI and batch effects. Variation explanation analysis was performed by Lasso regression. Results In total, 15,934 intestinal genes and 113 microbial taxa were identified and included in subsequent analyses. Host intestinal gene expressions were characterized by tissue- and inflammation-specificity, whereas intraindividual variability of the mucosal microbiota dominated over disease location and inflammation effects. We observed forty associations between the mucosal expression of genes and the abundance of specific microbes independent of dysbiosis (FDR<0.05). Examples include a positive association between aryl hydrocarbon receptor (AHR) and Bifidobacterium, and a negative association between interleukin 18 receptor 1 (IL18R1) and Lachnoclostridium. Furthermore, 112 gene-microbiota interactions changed in patients with microbial dysbiosis compared to non-dysbiosis (FDR<0.05). These interactions were enriched in immune-related and extracellular matrix organization pathways. For example, the IL1R1 gene was positively associated with Collinsella abundance in non-dysbiotic patients, whereas an inverse association was observed in high dysbiosis. Finally, the presence of mucosal microbial taxa explained up to 10% of the variation in cell type enrichment, affecting epithelial cells, macrophages and regulatory T-cells. Conclusion Interactions between host intestinal gene expressions and mucosa-attached microbiota are disrupted in patients with IBD. Furthermore, mucosal microbiota are highly personalized and potentially contribute to intestinal cell type alterations. Our study unravels key immune-mediated molecular pathways and relevant bacteria in intestinal tissue, which may guide drug development and precision medicine in IBD.