Role Of Dysbiosis Research Articles

Microbiome as an endocrine organ and its relationship with eye diseases: Effective factors and new targeted approaches.

Microbiome is an endocrine organ that refers to both the complicated biological system of microbial species that colonize our bodies and their genomes and surroundings. Recent studies confirm the connection between the microbiome and eye diseases, which are involved in the pathogenesis of eye diseases, including age-related macular disorders, diabetic retinopathy, glaucoma, retinitis pigmentosa, dry eye, and uveitis. The aim of this review is to investigate the microbiome in relation to eye health. First, a brief introduction of the characteristics of the gut microorganisms terms of composition and work, the role of dysbiosis, the gut microbiome and the eye microbiome in the progression of eye illnesses are highlighted, then the relationship among the microbiome and the function of the immune system and eye diseases, the role of inflammation and aging and the immune system, It has been reviewed and finally, the control and treatment goals of microbiome and eye diseases, the role of food factors and supplements, biotherapy and antibiotics in relation to microbiome and eye health have been reviewed.

146 The effects of antimicrobials and antimicrobial associated diarrhea on the fecal microbiome of the horse

Abstract Antibiotics are commonly given to horses to treat known bacterial infections or as prophylaxis against the development of infection. Diarrhea is a recognized adverse effect of antimicrobial administration in horses (antimicrobial associated diarrhea, AAD). In veterinary referral centers, AAD has a reported incidence of 22 to 94% (McGorum, 2010), while horses with AAD are 4.5 times more likely to die compared with horses with other types of colitis (Woods and Cohen, 1999). Although all antibiotics have potential to induce diarrhea, some have increased risk due to low oral absorption, biliary excretion, or enterohepatic recycling. The role of dysbiosis in the gut microbiota is a key feature in the pathogenesis of AAD. Disruption of commensal bacteria of the hindgut allows for pathogen overgrowth and alteration in microbial metabolic function. To date, 16S rRNA sequencing has been used to characterize the effects of penicillin, trimethoprim sulfa, doxycycline, erythromycin, ceftiofur, enrofloxacin, oxytetracycline and metronidazole on the fecal microbiome in healthy horses (Costa et al., 2015; Arnold et al., 2020; Liepman, 2022). Regardless of mechanism of action, antibiotics typically reduce diversity (species richness and evenness) and alter the bacterial community structure of the fecal microbiome, even when animals maintain normal health status and fecal character (Arnold et al., 2021). These effects typically require at least 30 days before the microbiome returns to baseline (Gomez et al, 2023). In horses with colitis, changes in the microbiome are often significant. Horses with AAD demonstrate the most severe disruption of the fecal microbiome compared with horses with Salmonella or undifferentiated colitis. These changes are evident from the phylum to species level, and include important phyla such as Bacteroidetes, Firmicutes, Fibrobacter and Verrucomicrobia (Arnold et al., 2020; Liepman, 2022; Costa et al., 2015). Alterations in the microbiota result in functional metabolic changes that are clinically manifested by diarrhea. Potential changes include alterations in the metabolism of bile acids, carbohydrates including short chain fatty acids, amino acids, lipids and proteins. There is also evidence that antimicrobials increase intestinal permeability via effects on tight junction proteins and by compromising the barrier function provided by the mucus layer between the enterocytes and gut lumen. Recent work comparing horses on antimicrobials that did and did not develop diarrhea confirm that horses with diarrhea have depletion of Verrocomicrobia and metabolites related to gastrointestinal barrier function (Arnold et al., 2021).

Gut-Gonad Perturbations in Type-1 Diabetes Mellitus: Role of Dysbiosis, Oxidative Stress, Inflammation and Energy-Dysbalance.

Type 1 diabetes mellitus is a major metabolic disorder that affects people of all age groups throughout the world. It is responsible for the alterations in male gonadal physiology in experimental models as well as in clinical cases. On the other side, diabetes mellitus has also been associated with perturbations in the gut physiology and microbiota dysbiosis. The accumulating evidence suggests a link between the gut and gonad as evident from the i) experimental data providing insights into type 1 diabetes mellitus induced gut perturbations, ii) link of gut physiology with alterations of testicular health, iii) role of gut microbiota in androgen metabolism in the intestine, and iv) epidemiological evidence linking type 1 diabetes mellitus with inflammatory bowel disease and male infertility. Considering all the pieces of evidence, it is summarized that gut dysbiosis, oxidative stress, inflammation and energy dys-balance are the prime factors involved in the gonadal damage under type 1 diabetes mellitus, in which the gut contributes significantly. Identification of novel biomarkers and intervention of suitable agents targeting these prime factors may be a step forward to restore the gonadal damage in diabetic conditions.

Role of microbiota-derived corisin in coagulation activation during SARS-CoV-2 infection

BackgroundCoagulopathy is a major cause of morbidity and mortality in COVID-19 patients. Hypercoagulability in COVID-19 results in deep vein thrombosis, thromboembolic complications, and diffuse intravascular coagulation. Microbiome dysbiosis influences the clinical course of COVID-19. However, the role of dysbiosis in COVID-19-associated coagulopathy is not fully understood. ObjectivesThe present study tested the hypothesis that the microbiota-derived proapoptotic corisin is involved in the coagulation system activation during SARS-CoV-2 infection. MethodsThis cross-sectional study included 47 consecutive patients who consulted for symptoms of COVID-19. A mouse acute lung injury model was used to recapitulate the clinical findings. A549 alveolar epithelial, THP-1, and human umbilical vein endothelial cells were used to evaluate procoagulant and anticoagulant activity of corisin. ResultsCOVID-19 patients showed significantly high circulating levels of corisin, thrombin-antithrombin complex, D-dimer, tumor necrosis factor-α, and monocyte-chemoattractant protein-1 with reduced levels of free protein S compared with healthy subjects. The levels of thrombin-antithrombin complex, D-dimer, and corisin were significantly correlated. A monoclonal anticorisin-neutralizing antibody significantly inhibited the inflammatory response and coagulation system activation in a SARS-CoV-2 spike protein-associated acute lung injury mouse model, and the levels of corisin and thrombin-antithrombin complex were significantly correlated. In an in vitro experiment, corisin increased the tissue factor activity and decreased the anticoagulant activity of thrombomodulin in epithelial, endothelial, and monocytic cells. ConclusionThe microbiota-derived corisin is significantly increased and correlated with activation of the coagulation system during SARS-CoV-2 infection, and corisin may directly increase the procoagulant activity in epithelial, endothelial, and monocytic cells.

The intestinal microbiome of inflammatory bowel disease across the pediatric age range

ABSTRACT Dysbiosis is associated with pediatric and adult-onset inflammatory bowel disease (IBD), but the role of dysbiosis and the microbiome in very early onset IBD (VEO-IBD) has not yet been described. Here, we aimed to demonstrate the impact of age and inflammation on microbial community structure using shotgun metagenomic sequencing in children with VEO-IBD, pediatric-onset IBD, and age-matched pediatric healthy controls (HC) observed longitudinally over the course of 8 weeks. We found disease-related differences in alpha and beta diversity between HC and children with IBD or VEO-IBD. Using a healthy microbial maturity index modeled from HC across the age range to characterize their gut microbiota, we found that children with pediatric-onset IBD and VEO-IBD had lower maturity than their age-matched HC groups, suggesting a disease effect on the microbial community. In addition, patients with pediatric IBD had significantly lower maturity than those with VEO-IBD, who had more heterogeneity at the youngest ages, highlighting differences in these two cohorts that were not captured in standard comparisons of alpha and beta diversity. These results demonstrate that young age and inflammation independently impact microbial community structure. However, the effect is not additive in the youngest patients, likely because of the heterogeneous and dynamic stool microbiome in this population.

The Role of Dysbiosis and Chronic Viral Infection in Autoimmune Rheumatic Diseases

Autoimmune diseases are a diverse group of approximately 100 disorders that are characterized by abnormal reactivity of B and T cells against self-antigens.1 Clinical manifestations can vary greatly, from organ-specific to systemic, and from life-threatening to subclinical. Autoimmune conditions affect about 5-9% of the world’s population,2 and occur more frequently in women than men.3,4 A 2020 study of the prevalence of antinuclear antibodies (ANAs) found a 50% overall increase in this biomarker of autoimmunity over the course of 25 years, suggesting that autoimmunity is on the rise in the United States.5 Interestingly, the increase in ANA prevalence was notable among adolescents (ages 12-19), lending some credence to the hygiene hypothesis, which posits that improved hygiene practices and cleaner environments in childhood reduce exposure to immune challenges, and may result in aberrant immune responses when exposed to infections later in life.

Unveiling the interplay between NSAID-induced dysbiosis and autoimmune liver disease in children: insights into the hidden gateway to autism spectrum disorders. Evidence from ex vivo, in vivo, and clinical studies.

Autism spectrum disorders (ASD) represent a diverse group of neuropsychiatric conditions, and recent evidence has suggested a connection between ASD and microbial dysbiosis. Immune and gastrointestinal dysfunction are associated with dysbiosis, and there are indications that modulating the microbiota could improve ASD-related behaviors. Additionally, recent findings highlighted the significant impact of microbiota on the development of autoimmune liver diseases, and the occurrence of autoimmune liver disease in children with ASD is noteworthy. In the present study, we conducted both an in vivo study and a clinical study to explore the relationship between indomethacin-induced dysbiosis, autoimmune hepatitis (AIH), and the development of ASD. Our results revealed that indomethacin administration induced intestinal dysbiosis and bacterial translocation, confirmed by microbiological analysis showing positive bacterial translocation in blood cultures. Furthermore, indomethacin administration led to disturbed intestinal permeability, evidenced by the activation of the NLRP3 inflammasomes pathway and elevation of downstream biomarkers (TLR4, IL18, caspase 1). The histological analysis supported these findings, showing widened intestinal tight junctions, decreased mucosal thickness, inflammatory cell infiltrates, and collagen deposition. Additionally, the disturbance of intestinal permeability was associated with immune activation in liver tissue and the development of AIH, as indicated by altered liver function, elevated ASMA and ANA in serum, and histological markers of autoimmune hepatitis. These results indicate that NSAID-induced intestinal dysbiosis and AIH are robust triggers for ASD existence. These findings were further confirmed by conducting a clinical study that involved children with ASD, autoimmune hepatitis (AIH), and a history of NSAID intake. Children exposed to NSAIDs in early life and complicated by dysbiosis and AIH exhibited elevated serum levels of NLRP3, IL18, liver enzymes, ASMA, ANA, JAK1, and IL6. Further, the correlation analysis demonstrated a positive relationship between the measured parameters and the severity of ASD. Our findings suggest a potential link between NSAIDs, dysbiosis-induced AIH, and the development of ASD. The identified markers hold promise as indicators for early diagnosis and prognosis of ASD. This research highlights the importance of maintaining healthy gut microbiota and supports the necessity for further investigation into the role of dysbiosis and AIH in the etiology of ASD.

Gut and airway microbiota dysbiosis and their role in COVID-19 and long-COVID.

The gut microbiota plays a crucial role in human health and disease. Gut dysbiosis is known to be associated with increased susceptibility to respiratory diseases and modifications in the immune response and homeostasis of the lungs (the so-called gut-lung axis). Furthermore, recent studies have highlighted the possible role of dysbiosis in neurological disturbances, introducing the notion of the "gut-brain axis." During the last 2 years, several studies have described the presence of gut dysbiosis during coronavirus disease 2019 (COVID-19) and its relationship with disease severity, SARS-CoV-2 gastrointestinal replication, and immune inflammation. Moreover, the possible persistence of gut dysbiosis after disease resolution may be linked to long-COVID syndrome and particularly to its neurological manifestations. We reviewed recent evidence on the association between dysbiosis and COVID-19, investigating the possible epidemiologic confounding factors like age, location, sex, sample size, the severity of disease, comorbidities, therapy, and vaccination status on gut and airway microbial dysbiosis in selected studies on both COVID-19 and long-COVID. Moreover, we analyzed the confounding factors strictly related to microbiota, specifically diet investigation and previous use of antibiotics/probiotics, and the methodology used to study the microbiota (α- and β-diversity parameters and relative abundance tools). Of note, only a few studies focused on longitudinal analyses, especially for long-term observation in long-COVID. Lastly, there is a lack of knowledge regarding the role of microbiota transplantation and other therapeutic approaches and their possible impact on disease progression and severity. Preliminary data seem to suggest that gut and airway dysbiosis might play a role in COVID-19 and in long-COVID neurological symptoms. Indeed, the development and interpretation of these data could have important implications for future preventive and therapeutic strategies.

On the Oral Microbiome of Oral Potentially Malignant and Malignant Disorders: Dysbiosis, Loss of Diversity, and Pathogens Enrichment.

The role of dysbiosis in the development and progression of oral potentially malignant disorders (OPMDs) remains largely unknown. Here, we aim to characterize and compare the oral microbiome of homogeneous leucoplakia (HL), proliferative verrucous leukoplakia (PVL), oral squamous cell carcinoma (OSCC), and OSCC preceded by PVL (PVL-OSCC). Fifty oral biopsies from HL (n = 9), PVL (n = 12), OSCC (n = 10), PVL-OSCC (n = 8), and healthy (n = 11) donors were obtained. The sequence of the V3-V4 region of the 16S rRNA gene was used to analyze the composition and diversity of bacterial populations. In the cancer patients, the number of observed amplicon sequence variants (ASVs) was lower and Fusobacteriota constituted more than 30% of the microbiome. PVL and PVL-OSCC patients had a higher abundance of Campilobacterota and lower Proteobacteria than any other group analyzed. A penalized regression was performed to determine which species were able to distinguish groups. HL is enriched in Streptococcus parasanguinis, Streptococcus salivarius, Fusobacterium periodonticum, Prevotella histicola, Porphyromonas pasteri, and Megasphaera micronuciformis; PVL is enriched in Prevotella salivae, Campylobacter concisus, Dialister pneumosintes, and Schaalia odontolytica; OSCC is enriched in Capnocytophaga leadbetteri, Capnocytophaga sputigena, Capnocytophaga gingivalis, Campylobacter showae, Metamycoplasma salivarium, and Prevotella nanceiensis; and PVL-OSCC is enriched in Lachnospiraceae bacterium, Selenomonas sputigena, and Prevotella shahii. There is differential dysbiosis in patients suffering from OPMDs and cancer. To the best of our knowledge, this is the first study comparing the oral microbiome alterations in these groups; thus, additional studies are needed.

A Novel Probiotic Combination Ameliorates Crohn's Disease-Like Ileitis by Increasing Short-Chain Fatty Acid Production and Modulating Essential Adaptive Immune Pathways.

Crohn's disease (CD) represents a significant public health challenge. We identified a combination of beneficial probiotic strains (Saccharomyces boulardii, Lactobacillus rhamnosus, Lactobacillus acidophilus, and Bifidobacterium breve) and amylase that may antagonize elevated bacterial pathogens in the inflamed gut. Our aim was to characterize the effect(s) of this novel probiotic supplement in SAMP1/YitFc (SAMP) mice with CD-like ileitis. Three groups of 7-week-old SAMP mice were used in this study. The first experimental group was administered 1 dose of the probiotic supplement (probiotic strains + amylase) diluted in sterile phosphate-buffered saline (PBS) (0.25 mg in 100 µL of PBS) every day for 56 days through the gavage technique, the second group had a probiotic supplement (probiotic strains without amylase), and the third group was a control group in which animals were administered sterile PBS. At the end of the treatment, mice were sacrificed and ilea were collected for histological scoring of ileitis and NanoString analysis. Stool samples were evaluated by 16S ribosomal RNA and gas chromatography-mass spectrometry analyses. Histology scores showed that mice treated with probiotics + amylase had a significant decrease of ileitis severity compared with the other 2 groups. 16S ribosomal RNA and gas chromatography-mass spectrometry analysis showed that abundance of species belonging to genus Lachnoclostridium and Mucispirillum schaedleri were significantly increased compared with the other 2 groups, and this increase was associated with augmented production of short-chain fatty acids. NanoString data showed that 21 genes involved in B memory cell development and T cell infiltration were significantly upregulated in probiotic-treated mice and that 3 genes were significantly downregulated. Our data provide experimental proof for a beneficial effect of the designed probiotic formulation on the severity of CD-like ileitis in the SAMP mouse model, involving both alteration of intestinal genetic pathways and microbial rearrangements. Thus, we propose that this novel probiotic mixture should be further tested as an adjuvant therapy in the treatment of biofilm-associated disorders such as CD, in which it has been proven that polymicrobial imbalance plays a critical role in dysbiosis and gut inflammation.

Porphyromonas gingivalis diffusible signaling molecules enhance Fusobacterium nucleatum biofilm formation via gene expression modulation

ABSTRACT Background Periodontitis is caused by a dysbiotic shift in the dental plaque microbiome. Fusobacterium nucleatum is involved in the colonization of Porphyromonas gingivalis, which plays a key role in dysbiosis, via coaggregation and synergy with this microorganism. Aim We investigated the effect of diffusible signaling molecules from P. gingivalis ATCC 33277 on F. nucleatum TDC 100 to elucidate the synergistic mechanisms involved in dysbiosis. Methods The two species were cocultured separated with an 0.4-µm membrane in tryptic soy broth, and F. nucleatum gene expression profiles in coculture with P. gingivalis were compared with those in monoculture. Results RNA sequencing revealed 139 genes differentially expressed between the coculture and monoculture. The expression of 52 genes was upregulated, including the coaggregation ligand-coding gene. Eighty-seven genes were downregulated. Gene Ontology analysis indicated enrichment for the glycogen synthesis pathway and a decrease in de novo synthesis of purine and pyrimidine. Conclusion These results indicate that diffusible signaling molecules from P. gingivalis induce metabolic changes in F. nucleatum, including an increase in polysaccharide synthesis and reduction in de novo synthesis of purine and pyrimidine. The metabolic changes may accelerate biofilm formation by F. nucleatum with P. gingivalis. Further, the alterations may represent potential therapeutic targets for preventing dysbiosis.

Role of dysbiosis and leaky gut syndrome in allergic manifestations

Role of dysbiosis and leaky gut syndrome in allergic manifestations

(R)Evolution in Allergic Rhinitis Add-On Therapy: From Probiotics to Postbiotics and Parabiotics.

Starting from the “Hygiene Hypothesis” to the “Microflora hypothesis” we provided an overview of the symbiotic and dynamic equilibrium between microbiota and the immune system, focusing on the role of dysbiosis in atopic march, particularly on allergic rhinitis. The advent of deep sequencing technologies and metabolomics allowed us to better characterize the microbiota diversity between individuals and body sites. Each body site, with its own specific environmental niches, shapes the microbiota conditioning colonization and its metabolic functionalities. The analysis of the metabolic pathways provides a mechanistic explanation of the remote mode of communication with systems, organs, and microflora of other body sites, including the ecosystem of the upper respiratory tract. This axis may have a role in the development of respiratory allergic disease. Notably, the microbiota is significant in the development and maintenance of barrier function; influences hematopoiesis and innate immunity; and shows its critical roles in Th1, Th2, and Treg production, which are necessary to maintain immunological balance and promote tolerance, taking part in every single step of the inflammatory cascade. These are microbial biotherapy foundations, starting from probiotics up to postbiotics and parabiotics, in a still-ongoing process. When considering the various determinants that can shape microbiota, there are several factors to consider: genetic factors, environment, mode of delivery, exposure to antibiotics, and other allergy-unrelated diseases. These factors hinder the engraftment of probiotic strains but may be upgradable with postbiotic and parabiotic administration directly on molecular targets. Supplementation with postbiotics and parabiotics could represent a very exciting perspective of treatment, bypassing probiotic limitations. At present, this avenue remains theoretical and to be explored, but it will certainly be a fascinating path to follow.

How primary care providers can help prevent food allergies

IgE-mediated food allergy rates have increased in recent decades, yet treatment options remain limited. Prevention strategies are thus essential. We will review recent research and consensus guidelines for food allergy prevention. Research has continued to support that early introduction of allergens via the gastrointestinal tract induces tolerance and prevents development of food allergy. In contrast, allergen sensitization may occur via transcutaneous allergen exposure. This is supported by research that shows a decreased risk of food allergy with aggressive treatment of atopic dermatitis. More recent research suggests that transcutaneous sensitization could also be facilitated by frequent emollient use in the absence of atopic dermatitis but definitive research is lacking. Murine models have shown a likely role of dysbiosis, or disruption of the body's normal healthy microbiome, in development of food allergy, yet human studies have yet to show a conclusive benefit of probiotics in the prevention of food allergy. Important approaches for food allergy prevention are: introduction of peanut and cooked egg at 4-6 months, early introduction of other allergenic foods, and early diagnosis and treatment of atopic dermatitis (because of a predisposition to food sensitization through the damaged skin barrier). More research is needed to clarify the role, if any, of emollient use and probiotics.

29-LB: Investigating the Molecular Basis of the Microbiota-Mediated Regulation of Postprandial Chylomicron Production

Obesity and insulin resistance have been identified as major global health concerns. They are associated with increased intestinal chylomicron production and subsequent remnant lipoprotein accumulation which lead to postprandial dyslipidemia. Dietary composition influences metabolic output of the gut microbiota by digesting dietary nutrients and producing various metabolites, which affects host metabolism. Understanding the mechanistic roles of the microbiota in regulating host lipid metabolism is therefore critical in addressing the pathogenesis of dyslipidemia. In this study, we aimed to investigate the effects of microbiota on lipid and lipoprotein metabolism in Syrian golden hamsters which is a more relevant animal model to human. Microbiota depletion was induced in male and female hamsters given either standard chow or a low fat/high fructose (HF) diet via antibiotic oral gavage administration. The results showed that feeding a HF diet increased plasma triglyceride (TG) and cholesterol (CH) levels while substantially reduced microbiota in antibiotic-administered groups led to significant reduction in circulating TG and CH in both diets. Then, we intended to look at the role of dysbiosis on postprandial lipid accumulation. Interestingly, in both sexes postprandial and TRL-TG levels were dramatically reduced after antibiotic administration; the effect was associated with significantly decreased ApoB48 protein levels. These changes appear to be due to a modulation of genes involved in farnesoid X receptor (FXR) receptor signaling in the ileum. Additionally, some critical genes implicated in lipid synthesis and absorption were also altered in the jejunum, with the most remarkable discovery being the extremely substantial down regulation of Scavenger Receptor Class B type 1“SR-B1” at both the mRNA and protein levels in all antibiotic-treated groups independent of sex and diet. In summary, our results suggest a novel role for the gut microbiota in regulating lipid and lipoprotein metabolism in the gut, urging further studies to determine the underlying mechanisms. Disclosure N. H. S. Abdalqadir: None. K. Adeli: None. Funding Canadian Institutes of Health Research

Alzheimer's Disease-Related Dysbiosis Might Be Triggered by Certain Classes of Antibiotics with Time-Lapse: New Insights into the Pathogenesis?

Several putative factors are identified in the literature as causative agents or risk factors for the development of Alzheimer's disease (AD). The amyloid cascade hypothesis has been the main hypothesis about the pathophysiology of AD for decades, but recent studies raised the possible role of dysbiosis in the development of AD, which prevents memory loss. Finding possible associations between antibiotic consumption patterns and the prevalence of AD in European countries. Antibiotic consumption (European Centre for Disease Prevention and Control, ECDC) for 1997-2007, 2008-2018, and as the whole 1997-2018 period, has been compared to the AD prevalence for 2018 expressed in percentage of the population and statistically analyzed by Pearson calculation. A significant positive correlation has been found between the AD prevalence (2018) and the average quinolone consumption for the years 1997-2007 (r: 0.37, p: 0.044). A similar association was not observed for the entire 22 years (1997-2018) of the average quinolone consumption, and the years 2008-2018, indicating 10-20 years of time-lapse between the antibiotic exposure and the development of AD. The ratio of broad-spectrum and narrow-spectrum antibiotics (B/N) estimated in the ECDC database for the years of 2008-2018 showed a strong positive association with AD prevalence (2018) (r: 0.406, p: 0.026) and a positive correlation tendency for the entire 22 years 1997-2018 (r: 0.344, p: 0.063), but none for the years 1997-2007 (r: 0.256, p: 0.241). Our study indicated the possible sequential role of certain classes of antibiotics in the development of dysbiosis leading to amyloid deposits of AD, which strengthen the possible role of different mediator molecules (short-chain fatty acids, lipopolysaccharides, etc.) produced by the altered microbiome in the development of AD.

Gut Dysbiosis and Clostridioides difficile Infection in Neonates and Adults.

In this review, we focus on gut microbiota profiles in infants and adults colonized (CDC) or infected (CDI) with Clostridioides difficile. After a short update on CDI epidemiology and pathology, we present the gut dysbiosis profiles associated with CDI in adults and infants, as well as the role of dysbiosis in C. difficile spores germination and multiplication. Both molecular and culturomic studies agree on a significant decrease of gut microbiota diversity and resilience in CDI, depletion of Firmicutes, Bacteroidetes, and Actinobacteria phyla and a high abundance of Proteobacteria, associated with low butyrogenic and high lactic acid-bacteria levels. In symptomatic cases, microbiota deviations are associated with high levels of inflammatory markers, such as calprotectin. In infants, colonization with Bifidobacteria that trigger a local anti-inflammatory response and abundance of Ruminococcus, together with lack of receptors for clostridial toxins and immunological factors (e.g., C. difficile toxins neutralizing antibodies) might explain the lack of clinical symptoms. Gut dysbiosis amelioration through administration of “biotics” or non-toxigenic C. difficile preparations and fecal microbiota transplantation proved to be very useful for the management of CDI.

Emerging Role of Microbiome in the Prevention of Urinary Tract Infections in Children.

The microbiome of the urinary tract plays a significant role in maintaining health through the impact on bladder homeostasis. Urobiome is of great importance in maintaining the urothelial integrity and preventing urinary tract infection (UTI), as well as promoting local immune function. Dysbiosis in this area has been linked to an increased risk of UTIs, nephrolithiasis, and dysfunction of the lower urinary tract. However, the number of studies in the pediatric population is limited, thus the characteristic of the urobiome in children, its role in a child’s health, and pediatric urologic diseases are not completely understood. This review aims to characterize the healthy urobiome in children, the role of dysbiosis in urinary tract infection, and to summarize the strategies to modification and reshape disease-prone microbiomes in pediatric patients with recurrent urinary tract infections.

Роль пробиотиков в коррекции нежелательных явлений на фоне химиотерапии у пациенток со злокачественными новообразованиями яичников

Introduction. Increasing the effectiveness of chemotherapy for ovarian cancer is an important task of modern oncogynecology. A serious disadvantage of chemotherapeutic drugs used in the treatment of malignant ovarian neoplasms is a low selectivity and the associated high systemic toxicity which manifests itself as a combination of undesirable side effects of chemotherapy (functional disorders of the gastrointestinal tract, toxic effects on various organs and the blood system). In recent years, the role of dysbiosis as a factor affecting the tolerability of chemotherapy has been studied. Aim. To compare the severity of the developing adverse events in patients with malignant ovarian neoplasms receiving chemotherapy with the use of probiotics and without them. Materials and methods. The study involved 25 patients diagnosed with stage II–IV ovarian cancer. The patients of the study group (10 women) underwent combined treatment (cytoreductive surgery + 6 courses of chemotherapy). During 3 cycles of chemotherapy, the patients of this group received VedaBiotic, an innovative domestic multisynbiotic drug containing 11 strains of probiotics a prebiotic, vitamin C, and a natural sorbent. The comparison group consisted of 15 patients diagnosed with stage II–IV ovarian cancer, who received the same treatment as the patients in the study group but without taking probiotic preparations. To study the effectiveness of taking probiotics, the following were assessed: condition of patients according to the Karnofsky Performance Scale (indicator – Karnofsky performance score); quality of life of patients according to the EORTC QLQ-C30 questionnaire (version 3.0); results of full blood count and blood chemistry. Results. The assessment of patients’ general status on the Karnofsky Performance Scale showed a significant improvement in the well-being of patients in the study group. Patients who took VedaBiotic had significantly less pronounced subjective complaints such as dyspnea, pain, sleep disturbance, asthenia, loss of appetite, nausea, vomiting, diarrhea. According to the results of blood chemistry, the level of liver enzymes was significantly lower in the study group. Conclusion. These data may indicate the possibility of a chemoprotective effect on the part of the microbiota of the large intestine. In the authors’ opinion, VedaBiotic can be recommended for the inclusion into the diet of oncological patients receiving anticancer therapy to effectively restore the microbiota of the large intenstine.

S159 The Role of Dysbiosis in Neurological Disorders

S159 The Role of Dysbiosis in Neurological Disorders