Acetylcholinesterase Inhibitor Pyridostigmine Bromide Attenuates Gut Pathology and Bacterial Dysbiosis in a Murine Model of Ulcerative Colitis.

BACKGROUND: Ulcerative colitis (UC) is a Th2 inflammatory bowel disease characterized by increased IL-5 and IL-13 expression, eosinophilic/neutrophilic infiltration, decreased mucus production, impaired epithelial barrier, and bacterial dysbiosis of the colon. Acetylcholine and nicotine stimulate mucus production and suppress Th2 inflammation through nicotinic receptors in lungs but UC is rarely observed in smokers and the mechanism of the protection is unclear. METHODS: In order to evaluate whether acetylcholine can ameliorate UC-associated pathologies, we employed a mouse model of dextran sodium sulfate (DSS)-induced UC-like conditions, and a group of mice were treated with Pyridostigmine bromide (PB) to increase acetylcholine availability. The effects on colonic tissue morphology, Th2 inflammatory factors, MUC2 mucin, and gut microbiota were analyzed. RESULTS: DSS challenge damaged the murine colonic architecture, reduced the MUC2 mucin and the tight-junction protein ZO-1. The PB treatment significantly attenuated these DSS-induced responses along with the eosinophilic infiltration and the pro-Th2 inflammatory factors. Moreover, PB inhibited the DSS-induced loss of commensal Clostridia and Flavobacteria, and the gain of pathogenic Erysipelotrichia and Fusobacteria. CONCLUSIONS: Together, these data suggest that in colons of a murine model, PB promotes MUC2 synthesis, suppresses Th2 inflammation and attenuates bacterial dysbiosis therefore, PB has a therapeutic potential in UC.

Application of Electronic-Nose Technologies and VOC-Biomarkers for the Noninvasive Early Diagnosis of Gastrointestinal Diseases †.

Conventional methods utilized for clinical diagnosis of gastrointestinal (GI) diseases have employed invasive medical procedures that cause stress, anxiety and pain to patients. These methods are often expensive, time-consuming, and require sophisticated chemical-analysis instruments and advanced modeling procedures to achieve diagnostic interpretations. This paper reviews recent applications of simpler, electronic-nose (e-nose) devices for the noninvasive early diagnosis of a wide range of GI diseases by collective analysis of headspace volatile organic compound (VOC)-metabolites from clinical samples to produce disease-specific aroma signatures (VOC profiles). A different "metabolomics" approach to GI disease diagnostics, involving identifications and quantifications of disease VOC-metabolites, are compared to the electronic-nose approach based on diagnostic costs, accuracy, advantages and disadvantages. The importance of changes in gut microbiome composition that result from disease are discussed relative to effects on disease detection. A new diagnostic approach, which combines the use of e-nose instruments for early rapid prophylactic disease-screenings with targeted identification of known disease biomarkers, is proposed to yield cheaper, quicker and more dependable diagnostic results. Some priority future research needs and coordination for bringing e-nose instruments into routine clinical practice are summarized.

Alcoholic liver disease: the gut microbiome and liver cross talk.

Alcoholic liver disease (ALD) is a leading cause of morbidity and mortality worldwide. Alcoholic fatty liver disease can progress to steatohepatitis, alcoholic hepatitis, fibrosis, and cirrhosis. Patients with alcohol abuse show quantitative and qualitative changes in the composition of the intestinal microbiome. Furthermore, patients with ALD have increased intestinal permeability and elevated systemic levels of gut-derived microbial products. Maintaining eubiosis, stabilizing the mucosal gut barrier, or preventing cellular responses to microbial products protect from experimental ALD. Therefore, intestinal dysbiosis and pathological bacterial translocation appear fundamental for the pathogenesis of ALD. This review highlights causes for intestinal dysbiosis and pathological bacterial translocation, their relationship, and consequences for ALD. We also discuss how the liver affects the intestinal microbiota.

Dietary Fiber's Physicochemical Properties and Gut Bacterial Dysbiosis Determine Fiber Metabolism in the Gut.

A fiber-rich diet is considered beneficial for gut health. An inflamed gut with a dysbiotic bacterial community can result in altered fiber metabolism depending on the fiber's physicochemical properties. This study examined the effect of fiber's physicochemical properties on fiber fermentation in the presence of healthy and colitis-associated bacteria. Sixteen fibers with different levels of solubility, complexity, and fermentation rate were used in in vitro fermentation with healthy human gut bacteria. Resistant maltodextrins (RMD), pectin (HMP), inulin (ChIn), and wheat bran (WB) were selected for fermentation using ulcerative colitis (UC)-associated bacteria to assess bacterial dysbiosis effect. UC-associated gut microbiota showed a significant reduction in α-and ß-diversity indices compared to healthy-associated microbiota. The differences in the gut microbiota composition and diversity between the donors resulted in decreased fermentation rates with UC-associated bacteria. Fiber fermentation metabolites, short-chain fatty acids (SCFA) and gas production were significantly lower in the presence of UC-associated bacteria for all four fibers tested. Overall, we conclude that dietary fiber properties and microbial dysbiosis are influential in fiber fermentation and metabolite production in the gut.

Application of PCR-Based Techniques for the Identification of Genetic Fingerprint Diversity of Dominant Bacteria in Fecal Samples of Children with Diarrhea in Vietnam.

In Vietnam, diarrhea, especially persistent diarrhea, is one of the most common diseases in children, while a significant proportion of cases are negative with pathogens; thus, there is an urgent need to understand gut bacterial dysbiosis. In this study, bacteria in the fecal samples of five healthy and ten diarrheal children were separated from other residues, then adopted to extract their metagenomic DNA for evaluating their diversity based on V3 and V6-V8 regions and the 16S rRNA gene by PCR-RFLP and PCR-DGGE. As a result, bacterial metagenomic DNAs with high quality, quantity and diversity were successfully extracted using a GeneJET kit and a chemical protocol. A sequence analysis of 73 representative DNA fragments from gels indicated a remarkable bacterial dysbiosis in all groups of diarrhea. Viral diarrhea was characterized by extremely reduced bacterial diversity with the blossom of Bifidobacterium and Streptococcus. Streptococcus was also the most abundant in persistent diarrhea. Beneficial bacteria that may play a role in the self- rebalance in intestinal bacterial communities, such as Bifidobacterium, Lactobacillus, and Enterococcus, were seen in all diarrheal groups, while Bacteroides and Akkermansia muciniphila were seen in the healthy group but absent in the diarrheal groups. This study provides additional evidence for a relationship between intestinal bacterial dysbiosis and diarrhea in children, emphasizing an increase in Streptococcus.

Polycystic ovary syndrome and iron overload: biochemical link and underlying mechanisms with potential novel therapeutic avenues.

Polycystic ovary syndrome (PCOS) is an endocrine and metabolic disorder in women with components of significant genetic predisposition and possibly multiple, but not yet clearly defined, triggers. This disorder shares several clinical features with hemochromatosis, a genetically defined inheritable disorder of iron overload, which includes insulin resistance, increased adiposity, diabetes, fatty liver, infertility, and hyperandrogenism. A notable difference between the two disorders, however, is that the clinical symptoms in PCOS appear at much younger age whereas they become evident in hemochromatosis at a much later age. Nonetheless, noticeable accumulation of excess iron in the body is a common finding in both disorders even at adolescence. Hepcidin, the iron-regulatory hormone secreted by the liver, is reduced in both disorders and consequently increases intestinal iron absorption. Recent studies have shown that gut bacteria play a critical role in the control of iron absorption in the intestine. As dysbiosis is a common finding between PCOS and hemochromatosis, changes in bacterial composition in the gut may represent another cause for iron overload in both diseases via increased iron absorption. This raises the possibility that strategies to prevent accumulation of excess iron with iron chelators and/or probiotics may have therapeutic potential in the management of polycystic ovary syndrome.

Recurrent Bacterial Vaginosis: A Case Report and Review of Management.

Recurrent and refractory bacterial vaginosis is a potentially hazardous condition that affects the age-bearing population of women. We report the case of a 33-year-old patient presenting with recurrent bacterial vaginosis after attempting multiple regimens for the past three years. The patient had a history significant for ectopic pregnancy and multiple sexually transmitted diseases. Successfully managing this condition in the female population is crucial to prevent uncommon complications. Furthermore, introducing healthy vaginal microbiota can be the best course of action amongst patients with long-term recurrence of bacterial vaginosis.

Gut Microbiome Remains Static in Functional Abdominal Pain Disorders Patients Compared to Controls: Potential for Diagnostic Tools.

Background: Functional Abdominal Pain disorders (FAPDs) are a group of heterogeneous gastrointestinal disorders with unclear pathophysiology. In children, FAPDs are more common in the winter months than summer months. The possible influence of school stressors has been proposed. Previously, our group showed differences in bacterial relative abundances and alpha diversity in the gut microbiome and its relationship with stressors in a cross-sectional evaluation of children suffering from FAPDs compared to a healthy control group. We present longitudinal data to assess whether the gut microbiome changes over school terms in the control and FAPDs groups. Methods: The longitudinal study included children with FAPDs (n = 28) and healthy controls (n = 54). Gastrointestinal symptoms, as well as stool microbiome, were assessed in both groups. Stool samples were serially collected from all participants during both the school term and summer vacation. The stool samples were subjected to total genomic extraction, 16S rRNA amplicon sequencing, and bioinformatics analysis. The gut microbiome was compared at school and during vacation. Other metrics, alpha diversity, and beta diversity, were also compared between the two school terms in every group. Results: In the healthy group, there were differences in microbiome composition between school terms and summer vacation. Conversely, we found no differences in the FAPDs group between the two terms. The healthy control group revealed differences (p-value < 0.05) in 55 bacterial species between the school term and vacation. Several of the differentially abundant identified bacteria were involved in short-chain fatty acids production (SCFAs), inflammation reduction, and gut homeostasis. Alpha diversity metrics, such as the Shannon index, were different in the control group and remained unchanged in the FAPDs group. Conclusion: Although preliminary, our findings suggest that the gut microbiome is static in FAPDs. This compares with a more dynamic healthy gut microbiome. Further studies are warranted to corroborate this and understand the interplay between stress, symptoms, and a less diverse and static microbiome. Future studies will also account for different variables such as diet and other patient demographic criteria that were missing in the current study.

Immune activation of characteristic gut mycobiota Kazachstania pintolopesii on IL-23/IL-17R signaling in ankylosing spondylitis.

It is very important to understand the communication and interaction mechanisms between the host and its resident microorganisms on host physiology and for precise diagnosis and treatment. Although intestinal fungi and bacteria dysbiosis is increasingly linked to ankylosing spondylitis (AS), their mechanisms of action have been rarely illustrated. In this paper, fecal samples from 10 AS monkeys and 10 healthy controls were collected to systematically characterize the gut mycobiota and microbiota in AS monkeys by 16S rRNA and ITS2 DNA sequencing. Our results showed the gut fungi of Kazachstania pintolopesii, Saccharomycetaceae, Kazachstania, and Saccharomyceteles. Saccharomycetes were specially enriched in AS, and the microbiota of AS monkeys was characterized by an increased abundance of Clostridia, Clostridiales, Ruminococcaceae, and Prevotella 2, using Line Discriminant Analysis Effect Size. Compared to healthy controls, decreased ITS2/16S biodiversity ratios and altered bacterial-fungal interkingdom networks were observed in AS monkeys. Oral administration of K. pintolopesii activates IL-17RA pathway and induce inflammatory reaction in the colonic tissue of C57BL/6 mice, as well as multiple AS phenotypes, including fungal and bacterial dysbiosis, immune responses of NK cells, platelets, T cells, leukocytes, B-cell activation, rheumatoid arthritis, and inflammatory bowel disease. We also found the secreted products of K. pintolopesii could activate the IL-17RA pathway, which induces PANoptosis in macrophage RAW264.7 cells. Much worse, the PANoptosis products could promote the proliferation and morphological changes of K. pintolopesii, which resulted in much more K. pintolopesii and a severe inflammatory reaction. Interestingly, the inflammatory factor TNF-α can promote the morphological transformation of Candida albicans and K. pintolopesii, which is worthy of further study. The characteristic fungi in all these findings implied that fungal and bacterial dysbiosis have a close link to AS and that their communication and interaction indeed play an important role in autoimmune responses, and K. pintolopesii could be a potential marker microorganism in AS, although its specific mechanism is not fully elucidated.

The Association of Microbiome Dysbiosis With Colorectal Cancer.

Many studies have been conducted to identify the causative organisms in colorectal cancer (CRC) and compare the microbiota of healthy individuals and those with CRC. The pathways by which the microbiota promotes CRC development are not yet fully understood. The hypothesized mechanisms include damage to the DNA, production of carcinogenic metabolites, and promotion of chronic inflammation. In a state of dysbiosis, the gut loses protective bacteria and is enriched with pathogenic and cancer-promoting bacteria, which promotes functions associated with cancer such as angiogenesis, loss of apoptosis, and cell proliferation. We have established a strong link between microbiota dysbiosis and certain species of bacteria and even viruses involved in tumorigenesis. In this review, we look at some of the major identified species and how they are related to CRC. Future research should include and even focus on mycobiome and virome on CRC development. Due to the diversity of the gut microbiome, there is a high possibility that the gain and loss of bacteria and their metabolic functions lead to CRC.

Protein Tyrosine and Serine/Threonine Phosphorylation in Oral Bacterial Dysbiosis and Bacteria-Host Interaction.

The human oral cavity harbors approximately 1,000 microbial species, and dysbiosis of the microflora and imbalanced microbiota-host interactions drive many oral diseases, such as dental caries and periodontal disease. Oral microbiota homeostasis is critical for systemic health. Over the last two decades, bacterial protein phosphorylation systems have been extensively studied, providing mounting evidence of the pivotal role of tyrosine and serine/threonine phosphorylation in oral bacterial dysbiosis and bacteria-host interactions. Ongoing investigations aim to discover novel kinases and phosphatases and to understand the mechanism by which these phosphorylation events regulate the pathogenicity of oral bacteria. Here, we summarize the structures of bacterial tyrosine and serine/threonine kinases and phosphatases and discuss the roles of tyrosine and serine/threonine phosphorylation systems in Porphyromonas gingivalis and Streptococcus mutans, emphasizing their involvement in bacterial metabolism and virulence, community development, and bacteria-host interactions.

Periodontal dysbiosis associates with reduced CSF Aß42 in cognitively normal elderly.

INTRODUCTION: Periodontal disease is a chronic, inflammatory bacterial dysbiosis that is associated with both Alzheimer's disease (AD) and Down syndrome. METHODS: A total of 48 elderly cognitively normal subjects were evaluated for differences in subgingival periodontal bacteria (assayed by 16S rRNA sequencing) between cerebrospinal fluid (CSF) biomarker groups of amyloid and neurofibrillary pathology. A dysbiotic index (DI) was defined at the genus level as the abundance ratio of known periodontal bacteria to healthy bacteria. Analysis of variance/analysis of covariance (ANOVA/ANCOVA), linear discriminant effect-size analyses (LEfSe) were used to determine the bacterial genera and species differences between the CSF biomarker groups. RESULTS: At genera and species levels, higher subgingival periodontal dysbiosis was associated with reduced CSF amyloid beta (Aß)42 (P = 0.02 and 0.01) but not with P-tau. DISCUSSION: We show a selective relationship between periodontal disease bacterial dysbiosis and CSF biomarkers of amyloidosis, but not for tau. Further modeling is needed to establish the direct link between oral bacteria and Aß.

Bacterial dysbiosis incites Th17 cell revolt in irradiated gut.

Th17 cells are critical members in mediating immune responses of adaptive immunity. In humans and mice, gut is a main site where Th17 cells are resided, and Th17 cell polarization also occurs in the gut. This process can be mediated by many factors, such as commensal bacteria, dendritic cells and cytokines, such as TGF-ß and IL-6. Physiologically, polarized Th17 cells function in anti-infection and maintaining the integrity of intestinal epithelium. However, Th17 cells are plastic. For example, they will become pro-inflammatory cells if being exposed to IL-23. The pathogenic roles of Th17 cells have been well documented in inflammatory bowel disease. Besides, Th17 cells can accumulate in irradiated gut as well. Critically, radiation enteritis and inflammatory bowel disease present several similarities in disease pathology and pathophysiology. Herein, bacterial dysbiosis highly correlates with the pathogenicity of Th17 cells in inflammatory bowel disease. To our knowledge, radiation serves as a factor in inducing bacterial dysbiosis. Using this action, can Th17 cells be incited to promote inflammation in irradiated gut? In this review, we will sequentially introduce polarization of Th17 cells at steady state, radiation-induced Th17 accumulation in the gut, and advances in the management of radiation enteritis by using pharmacological therapy for bacterial dysbiosis.

Niche Specific Microbiota-Dependent and Independent Bone Loss around Dental Implants and Teeth.

Oral mucosal homeostasis is achieved by complex immunologic mechanisms, orchestrating host immunity to adapt to the physiologic functions of the various specialized niches in the oral cavity. Dental implants introduce a novel mucosal niche to the immune system to deal with. Nevertheless, the immune mechanisms engaged toward implants and whether they have broader effects are not well defined. Using a murine model, we found an accumulation of neutrophils and RANKL-expressing T and B lymphocytes in the implant-surrounding mucosa, accompanied by local bone loss. Surprisingly, the presence of implants had an impact on remote periodontal sites, as elevated inflammation and accelerated bone loss were detected in intact distant teeth. This was due to microbial dysbiosis induced by the implants, since antibiotic treatment prevented bone loss around teeth. However, antibiotic treatment failed to prevent the loss of implant-supporting bone, highlighting the distinct mechanisms mediating bone loss at each site. Further analysis revealed that implants induced chronic lymphocyte activation and increased mRNA expression of IFN-α and accumulation of IFN-α-producing plasmacytoid dendritic cells, which we previously reported as bone-destructive immune responses. Collectively, this study demonstrates that implants have a strong and broad impact on oral mucosal homeostasis, inducing periodontal bone loss in a niche-specific manner that is both microbiota dependent and independent.

Ursolic Acid Improves Intestinal Damage and Bacterial Dysbiosis in Liver Fibrosis Mice.

Liver fibrosis is a reversible process of extracellular matrix deposition or scar formation after liver injury. Intestinal damage and bacterial dysbiosis are important concomitant intestinal changes in liver fibrosis and may in turn accelerate the progression of liver fibrosis through the gut-liver axis. RhoA, an important factor in the regulation of the cytoskeleton, plays an important role in intestinal damage. We investigated the effects of ursolic acid (UA), a traditional Chinese medicine with anti-fibrotic effects, on intestinal damage and bacterial disorder through the RhoA pathway. UA treatment reduced intestinal damage by inhibiting the inflammatory factor TNF-α and increasing the expression of tight junction proteins and antibacterial peptides to protect the intestinal barrier. Moreover, the corrective effect of UA on bacterial dysbiosis was also confirmed by sequencing of the 16S rRNA gene. Potential beneficial bacteria, such as the phylum Firmicutes and the genera Lactobacillus and Bifidobacterium, were increased in the UA group compared to the CCl4 group. In liver fibrosis mice with RhoA inhibition via injection of adeno-associated virus, the liver fibrosis, intestinal damage, and flora disturbances were improved. Moreover, UA inhibited the expression of RhoA pathway components. In conclusion, UA improves intestinal damage and bacterial dysbiosis partly via the RhoA pathway. This may be a potential mechanism by which UA exerts its anti-fibrotic effects and provides effective theoretical support for the future use of UA in clinical practice.

Culture-independent studies on bacterial dysbiosis in oral and oropharyngeal squamous cell carcinoma: A systematic review.

Imbalance within the resident bacterial community (dysbiosis), rather than the presence and activity of a single organism, has been proposed to be associated with, and to influence, the development and progression of various diseases; however, the existence and significance of dysbiosis in oral/oropharyngeal cancer is yet to be clearly established. A systematic search (conducted on 25/01/2018 and updated on 25/05/2018) was performed on three databases (Pubmed, Web of Science & Scopus) to identify studies employing culture-independent methods which investigated the bacterial community in oral/oropharyngeal cancer patients compared to control subjects. Of the 1546 texts screened, only fifteen publications met the pre-determined selection criteria. Data extracted from 731 cases and 809 controls overall, could not identify consistent enrichment of any particular taxon in oral/oropharyngeal cancers, although common taxa could be identified between studies. Six studies reported the enrichment of Fusobacteria in cancer at different taxonomic levels whereas four studies reported an increase in Parvimonas. Changes in microbial diversity remained inconclusive, with four studies showing a higher diversity in controls, three studies showing a higher diversity in tumors and three additional studies showing no difference between tumors and controls. Even though most studies identified a component of dysbiosis in oral/oropharyngeal cancer, methodological and analytical variations prevented a standardized summary, which highlights the necessity for studies of superior quality and magnitude employing standardized methodology and reporting. Indeed an holistic metagenomic approach is likely to be more meaningful, as is understanding of the overall metabolome, rather than a mere enumeration of the organisms present.

5-Aminosalicylic Acid Alters the Gut Bacterial Microbiota in Patients With Ulcerative Colitis.

Background: The aim of this study was to clarify the effect of 5-aminosalicylic acid (5-ASA) treatment on gut bacterial microbiota in patients with ulcerative colitis (UC). Methods: A total of 57 UC patients, including 20 untreated and 37 5-ASA-treated, were recruited into an exploration cohort. We endoscopically collected both non-inflamed and inflamed mucosal samples from all patients, and compared the gut bacterial profiles using 16S rDNA sequencing. Ten untreated UC patients were then treated with 5-ASA and subsequently recruited for an independent validation study to confirm the acquired data. Results: In untreated UC patients, compared with those in non-inflamed mucosae, Firmicutes (such as Enterococcus) were decreased and Proteobacteria (e.g., Escherichia-Shigella) were increased in the inflamed mucosae. Compared with the inflamed mucosae of untreated UC patients, there was a higher abundance of Firmicutes (e.g., Enterococcus) and lower Proteobacteria (Escherichia-Shigella) in the inflamed mucosae of 5-ASA treated UC patients. In the validation cohort, after administration of 5-ASA, bacterial alteration was consistent with these data. Furthermore, there was a skewed negative correlation between Escherichia-Shigella and bacterial genera of Firmicutes in the inflamed mucosae. 5-ASA treatment decreased the strength of bacterial correlation and weakened the skewed negative correlation pattern. Conclusion: The microbial dysbiosis (mainly characterized by an increased abundance in the Escherichia-Shigella genus) and the skewed negative correlation between Escherichia-Shigella and bacterial genera of Firmicutes are two characteristics of the inflamed mucosae of UC patients. 5-ASA treatment decreases Escherichia-Shigella and weakens the skewed correlations, which may be related to its treatment efficiency.

Keeping it tight: The relationship between bacterial dysbiosis, septate junctions, and the intestinal barrier in Drosophila.

Maladaptive changes in the intestinal flora, typically referred to as bacterial dysbiosis, have been linked to intestinal aging phenotypes, including an increase in intestinal stem cell (ISC) proliferation, activation of inflammatory pathways, and increased intestinal permeability1,2. However, the causal relationships between these phenotypes are only beginning to be unravelled. We recently characterized the age-related changes that occur to septate junctions (SJ) between adjacent, absorptive enterocytes (EC) in the fly intestine. Changes could be observed in the overall level of SJ proteins, as well as the localization of a subset of SJ proteins. Such age-related changes were particularly noticeable at tricellular junctions (TCJ)3. Acute loss of the Drosophila TCJ protein Gliotactin (Gli) in ECs led to rapid activation of stress signalling in stem cells and an increase in ISC proliferation, even under axenic conditions; a gradual disruption of the intestinal barrier was also observed. The uncoupling of changes in bacteria from alterations in ISC behaviour and loss of barrier integrity has allowed us to begin to explore the interrelationship of these intestinal aging phenotypes in more detail and has shed light on the importance of the proteins that contribute to maintenance of the intestinal barrier.

Traumatic Brain Injury in Mice Induces Acute Bacterial Dysbiosis Within the Fecal Microbiome.

The secondary injury cascade that is activated following traumatic brain injury (TBI) induces responses from multiple physiological systems, including the immune system. These responses are not limited to the area of brain injury; they can also alter peripheral organs such as the intestinal tract. Gut microbiota play a role in the regulation of immune cell populations and microglia activation, and microbiome dysbiosis is implicated in immune dysregulation and behavioral abnormalities. However, changes to the gut microbiome induced after acute TBI remains largely unexplored. In this study, we have investigated the impact of TBI on bacterial dysbiosis. To test the hypothesis that TBI results in changes in microbiome composition, we performed controlled cortical impact (CCI) or sham injury in male 9-weeks old C57BL/6J mice. Fresh stool pellets were collected at baseline and at 24 h post-CCI. 16S rRNA based microbiome analysis was performed to identify differential abundance in bacteria at the genus and species level. In all baseline vs. 24 h post-CCI samples, we evaluated species-level differential abundances via clustered and annotated operational taxonomic units (OTU). At a high-level view, we observed significant changes in two genera after TBI, Marvinbryantia, and Clostridiales. At the species-level, we found significant decreases in three species (Lactobacillus gasseri, Ruminococcus flavefaciens, and Eubacterium ventriosum), and significant increases in two additional species (Eubacterium sulci, and Marvinbryantia formatexigens). These results pinpoint critical changes in the genus-level and species-level microbiome composition in injured mice compared to baseline; highlighting a previously unreported acute dysbiosis in the microbiome after TBI.

Colonización fúngica y síntomas gastrointestinales en niños con trastorno del espectro autista y neurotípicos / Fungical colonization and gastrointestinal symptoms in children with autistic spectrum disorder and neurotipic

Introducción: los síntomas digestivos pudiesen presentarse por colonización fúngica, alteraciones en la barrera intestinal y microbiota bacteriana, enfermedades alérgicas, autoinmunes y disbiosis. Objetivo: investigar la presencia de colonización fúngica y síntomas gastrointestinales en niños con trastorno del espectro autista y neurotípicos. Metodología: estudio prospectivo, aleatorio, comparativo y transversal Grupo A: niños con trastorno del espectro Autista (TEA) y grupo B: niños neurotípicos. variables: edad, sexo, síntomas gastrointestinales, perfil de disbiosis básico e identificación de hongos. Resultados: grupo A, 28 niños, 7,11+3,07 años (rango 2-13), 25 (89,28%) masculino. Síntomas: distensión abdominal, estreñimiento y flatulencia fétida; grupo B, 16 niños, 5,55+3,20 años (rango 2-11), 10 (62,25%) femenino. Síntomas: dolor abdominal y alteración del patrón evacuatorio. Se encontró mayor colonización fúngica en el grupo A, 22/28 (78,57%) con respecto al grupo B, 5/16 (31,25%), p=0.0034. Se obtuvo microbiota fúngica 11/28 como comensal y 11/28 patógena en el grupo A y grupo B, 3/16 comensal y 2/16 como patógeno, diferencia significativa, p=0.0103. La cándida fue el hongo más aislado. Grupo A, 20/22 (90,90%) y grupo B, 5/16 (31,25%). disbiosis fúngica, 11/22 del grupo A, 5 (45,45%) grado III, 4 (36,36%) grado II y 2 (18,18%) grado I, y grupo B, 2/5 grado I, no se encontraron diferencias p=0,538. Hubo disbiosis simultánea fúngica y bacteriana, sin diferencias entre los grupos, p=0,5366. Conclusiones: los niños con TEA y síntomas digestivos presentan con mayor frecuencia colonización fúngica y disbiosis que los niños neurotípicos. un nuevo abordaje se encuentra al alcance con el estudio de la microbiota fúngica, además de la bacteriana(AU)

Introduction: digestive symptoms may occur due to fungal colonization, alterations in the intestinal barrier, bacterial microbiota, allergic and autoimmune diseases, and dysbiosis. Objective: to investigate the presence of fungal colonization and gastrointestinal symptoms in children with Autism spectrum disorder (ASD) and neurotypic children. Methodology: Prospective, randomized, comparative and cross-sectional study, Group A: children with Asd) and group B: neurotypic children. variables: age, sex, gastrointestinal symptoms, basic dysbiosis profile and fungal identification. Results: group A, 28 children, 7.11 + 3.07 years (range 2-13), 25 (89.28%) male. symptoms: abdominal distension, constipation and fetid flatulence; group B, 16 children, 5.55 + 3.20 years (range 2-11), 10 (62.25%) female. symptoms: abdominal pain and abnormal evacuation pattern. Greater fungal colonization was found in group A, 22/28 (78.57%) vs group B, 5/16 (31.25%), p = 0.0034. Fungic microbiota 11/28 was obtained as commensal and 11/28 as pathogenic in group A (group B, 3/16 commensal and 2/16 pathogen), p = 0.0103. candida was the most isolated fungus. Group A: 20/22 (90.90%), Group B: 5/16 (31.25%). Fungal dysbiosis, 11/22 group A, 5 (45.45%) grade III, 4 (36.36%) grade II and 2 (18.18%) grade I; group B, 2/5 grade I, no differences were found p = 0.1538. there was simultaneous fungal and bacterial dysbiosis, without differences between the groups, p = 0.5366. Conclusions: children with Asd and digestive symptoms have more frequent fungal colonization and dysbiosis than neurotypic children. A new approach is within reach with the study of the fungal microbiota, in addition to the bacterial one(AU)