Journal articles: 'Symbiose intestinale'

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Bayer, Wolfgang, and Karlheiz Schmidt. "Intestinale Dysbiosen erkennen und therapieren." Ernährung & Medizin 32, no. 03 (August 30, 2017): 105–8. http://dx.doi.org/10.1055/s-0043-116347.

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ZusammenfassungEine Dysbiose bezeichnet im Gegensatz zur Eubiose, Normobiose oder Symbiose Veränderungen der intestinalen Mikrobiota (früher als Darmflora bezeichnet), die mit krankhaften, häufig entzündlichen Symptomen korreliert ist. Ursachen einer Dysbiose sind z. B. eine Überwucherung mit pathogenen Keimen, chronisch entzündliche Darmerkrankungen, aber auch Einflüsse durch Arzneimittel wie Antibiotika, Kortikosteroide etc. Vielfältige weitere Wechselwirkungen sind zu berücksichtigen wie Ernährungseinflüsse, Genussgifte (Rauchen, Alkohol) sowie auch Wechselwirkungen mit dem Hormonsystem, dem Immunsystem, dem Nervensystem und vielen weiteren Regelkreisen.

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Koga, Ryuichi, Masahiko Tanahashi, Naruo Nikoh, Takahiro Hosokawa, Xian-Ying Meng, Minoru Moriyama, and Takema Fukatsu. "Host’s guardian protein counters degenerative symbiont evolution." Proceedings of the National Academy of Sciences 118, no. 25 (June 14, 2021): e2103957118. http://dx.doi.org/10.1073/pnas.2103957118.

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Microbial symbioses significantly contribute to diverse organisms, where long-lasting associations tend to result in symbiont genome erosion, uncultivability, extinction, and replacement. How such inherently deteriorating symbiosis can be harnessed to stable partnership is of general evolutionary interest. Here, we report the discovery of a host protein essential for sustaining symbiosis. Plataspid stinkbugs obligatorily host an uncultivable and genome-reduced gut symbiont, Ishikawaella. Upon oviposition, females deposit “capsules” for symbiont delivery to offspring. Within the capsules, the fragile symbiotic bacteria survive the harsh conditions outside the host until acquired by newborn nymphs to establish vertical transmission. We identified a single protein dominating the capsule content, which is massively secreted by female-specific intestinal organs, embedding the symbiont cells, and packaged into the capsules. Knockdown of the protein resulted in symbiont degeneration, arrested capsule production, symbiont transmission failure, and retarded nymphal growth, unveiling its essential function for ensuring symbiont survival and vertical transmission. The protein originated from a lineage of odorant-binding protein-like multigene family, shedding light on the origin of evolutionary novelty regarding symbiosis. Experimental suppression of capsule production extended the female’s lifespan, uncovering a substantial cost for maintaining symbiosis. In addition to the host’s guardian protein, the symbiont’s molecular chaperone, GroEL, was overproduced in the capsules, highlighting that the symbiont’s eroding functionality is compensated for by stabilizer molecules of host and symbiont origins. Our finding provides insight into how intimate host–symbiont associations can be maintained over evolutionary time despite the symbiont’s potential vulnerability to degeneration and malfunctioning.

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Ohbayashi, Tsubasa, Kazutaka Takeshita, Wataru Kitagawa, Naruo Nikoh, Ryuichi Koga, Xian-Ying Meng, Kanako Tago, et al. "Insect’s intestinal organ for symbiont sorting." Proceedings of the National Academy of Sciences 112, no. 37 (August 31, 2015): E5179—E5188. http://dx.doi.org/10.1073/pnas.1511454112.

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Symbiosis has significantly contributed to organismal adaptation and diversification. For establishment and maintenance of such host–symbiont associations, host organisms must have evolved mechanisms for selective incorporation, accommodation, and maintenance of their specific microbial partners. Here we report the discovery of a previously unrecognized type of animal organ for symbiont sorting. In the bean bug Riptortus pedestris, the posterior midgut is morphologically differentiated for harboring specific symbiotic bacteria of a beneficial nature. The sorting organ lies in the middle of the intestine as a constricted region, which partitions the midgut into an anterior nonsymbiotic region and a posterior symbiotic region. Oral administration of GFP-labeled Burkholderia symbionts to nymphal stinkbugs showed that the symbionts pass through the constricted region and colonize the posterior midgut. However, administration of food colorings revealed that food fluid enters neither the constricted region nor the posterior midgut, indicating selective symbiont passage at the constricted region and functional isolation of the posterior midgut for symbiosis. Coadministration of the GFP-labeled symbiont and red fluorescent protein-labeled Escherichia coli unveiled selective passage of the symbiont and blockage of E. coli at the constricted region, demonstrating the organ’s ability to discriminate the specific bacterial symbiont from nonsymbiotic bacteria. Transposon mutagenesis and screening revealed that symbiont mutants in flagella-related genes fail to pass through the constricted region, highlighting that both host’s control and symbiont’s motility are involved in the sorting process. The blocking of food flow at the constricted region is conserved among diverse stinkbug groups, suggesting the evolutionary origin of the intestinal organ in their common ancestor.

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Tan, Tze Guan, Esen Sefik, Naama Geva-Zatorsky, Lindsay Kua, Debdut Naskar, Fei Teng, Lesley Pasman, et al. "Identifying species of symbiont bacteria from the human gut that, alone, can induce intestinal Th17 cells in mice." Proceedings of the National Academy of Sciences 113, no. 50 (November 23, 2016): E8141—E8150. http://dx.doi.org/10.1073/pnas.1617460113.

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Th17 cells accrue in the intestine in response to particular microbes. In rodents, segmented filamentous bacteria (SFB) induce intestinal Th17 cells, but analogously functioning microbes in humans remain undefined. Here, we identified human symbiont bacterial species, in particularBifidobacterium adolescentis, that could, alone, induce Th17 cells in the murine intestine. Similar to SFB,B. adolescentiswas closely associated with the gut epithelium and engendered cognate Th17 cells without attendant inflammation. However,B. adolescentiselicited a transcriptional program clearly distinct from that of SFB, suggesting an alternative mechanism of promoting Th17 cell accumulation. Inoculation of mice withB. adolescentisexacerbated autoimmune arthritis in the K/BxN mouse model. Several off-the-shelf probiotic preparations that includeBifidobacteriumstrains also drove intestinal Th17 cell accumulation.

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Vermehren, Cláudia Almeida Alves, and Tayna Ofelia Freitas Suarez. "Symbiosis in the microbiome of people with asd and its effects on the brain-intestine linkage." Research, Society and Development 11, no. 17 (December 20, 2022): e49111736735. http://dx.doi.org/10.33448/rsd-v11i17.36735.

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Researches show that individuals with Autistic Spectrum Disorder (ASD), present an imbalance in the intestinal microbiota, by the study carried out, there is a possibility of mitigating the characteristic symptoms of Autistic Spectrum Disorder, through the symbiosis in the intestinal microbiome. The objective of this bibliographic review is to analyze the influence of symbiosis on the microbiome in the intestine-brain axis in individuals with ASD and to verify the nutritional needs of this individual, in order to support nutritional strategies. Analyzing the gut-brain axis of children with ASD, verifying the effects of symbiosis on the microbiome and the nutritional needs of autistic people. The approach of this research was qualitative, with a basic purpose, of an observational nature, being cross-sectional bibliographic research. Studies were used to investigate the effectiveness of vitamin and mineral supplementation in the diet of children with autism spectrum disorder. The present study concludes that autistic children are more deficient in the intake of vitamins and minerals, and those who are supplemented with vitamin D had reduced or absent symptoms of ASD. Thus, it will be necessary to offer a greater variety of fruits and vegetables to obtain adequate dosages of micronutrients through food intake, helping with homeostasis in the microbiota in order to achieve a symbiosis in the intestinal microbiome of the child with ASD.

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Takahashi, Kyoko, Yutaka Sugi, Kou Nakano, Masato Tsuda, Kenta Kurihara, Akira Hosono, and Shuichi Kaminogawa. "Epigenetic Control of the Host Gene by Commensal Bacteria in Large Intestinal Epithelial Cells." Journal of Biological Chemistry 286, no. 41 (August 23, 2011): 35755–62. http://dx.doi.org/10.1074/jbc.m111.271007.

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Intestinal epithelial cells (IECs) are continuously exposed to large numbers of commensal bacteria but are relatively insensitive to them, thereby averting an excessive inflammatory reaction. We have previously reported that the hyporesponsiveness of a human IEC line to LPS was primarily the result of a down-regulation of TLR4 gene transcription through epigenetic mechanisms. In the present study we show that DNA methylation in the 5′ region of the TLR4 gene is significantly higher in IECs than in splenic cells in vivo. The methylation was shown to be dependent on the differentiation state of the IECs, as the differentiated IEC population that expressed higher levels of intestinal alkaline phosphatase (IAP) also displayed greater methylation and lower expression of the TLR4 gene than the undifferentiated population. The IAPhigh, differentiated population also showed less abundant expression of CDX2, the transcription factor required for the development of the intestine, than the IAPlow, undifferentiated population. Overexpression of CDX2 in an IEC line decreased the methylation level of the TLR4 gene, increased transcriptional promoter activity of the gene, and increased responsiveness to the TLR4 ligand. Furthermore, the methylation level of the TLR4 gene was significantly lower in IECs of the large intestine of germ-free mice than in those of conventional mice, whereas the level in IECs of the small intestine was almost equal between these mice, indicating that commensal bacteria contribute to the maintenance of intestinal symbiosis by controlling epigenetic modification of the host gene in the large intestine.

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Kolopp-Sarda, Marie-Nathalie. "Système immunitaire muqueux et microbiote intestinal : Histoire d’une symbiose." Revue Francophone des Laboratoires 2016, no. 484 (July 2016): 39–47. http://dx.doi.org/10.1016/s1773-035x(16)30222-2.

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Franke, Maximilian, Benedikt Geier, Jörg U. Hammel, Nicole Dubilier, and Nikolaus Leisch. "Coming together—symbiont acquisition and early development in deep-sea bathymodioline mussels." Proceedings of the Royal Society B: Biological Sciences 288, no. 1957 (August 18, 2021): 20211044. http://dx.doi.org/10.1098/rspb.2021.1044.

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How and when symbionts are acquired by their animal hosts has a profound impact on the ecology and evolution of the symbiosis. Understanding symbiont acquisition is particularly challenging in deep-sea organisms because early life stages are so rarely found. Here, we collected early developmental stages of three deep-sea bathymodioline species from different habitats to identify when these acquire their symbionts and how their body plan adapts to a symbiotic lifestyle. These mussels gain their nutrition from chemosynthetic bacteria, allowing them to thrive at deep-sea vents and seeps worldwide. Correlative imaging analyses using synchrotron-radiation based microtomography together with light, fluorescence and electron microscopy revealed that the pediveliger larvae were aposymbiotic. Symbiont colonization began during metamorphosis from a planktonic to a benthic lifestyle, with the symbionts rapidly colonizing first the gills, the symbiotic organ of adults, followed by all other epithelia of their hosts. Once symbiont densities in plantigrades reached those of adults, the host's intestine changed from the looped anatomy typical for bivalves to a straightened form. Within the Mytilidae, this morphological change appears to be specific to Bathymodiolus and Gigantidas , and is probably linked to the decrease in the importance of filter feeding when these mussels switch to gaining their nutrition largely from their symbionts.

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Hagymási, Krisztina, Anna Bacsárdi, Anna Egresi, Evelin Berta, Zsolt Tulassay, and Gabriella Lengyel. "A bélflóra patofiziológai jelentősége és szerepe mint terápiás célpont májbetegségekben." Orvosi Hetilap 159, no. 36 (September 2018): 1465–74. http://dx.doi.org/10.1556/650.2018.31178.

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Abstract: The community of microorganisms in the intestine, namely gut microbiome lives in symbiosis with the host, contributing to its homeostasis and influencing it simultaneously. It can be suspected that gut microbiome plays a central role in the pathophysiology of intestinal and extraintestinal diseases: determining their development, progress and complications. Recently, intestinal microbiome has become a highlighted field of interest and important topic in research, especially in hepatology. It is in the focus of relevant research as the liver is the organ which meets nutrients, bacterial components, toxins and metabolites at first, as a filter. The evolvement of different liver diseases – just like alcoholic and non-alcoholic fatty liver disease, steatohepatitis, cirrhosis or hepatocellular carcinoma – correlates with the changed composition and activity of gut microbiome. Thus, it can be hypothesized that pre-, pro- and antibiotics could have an impact on the treatment of these diseases. In our review article, the relationship between intestinal flora and liver diseases with different etiologies as well as therapeutic possibilities are discussed. Orv Hetil. 2018; 159(36): 1465–1474.

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Lindner, Cornelia, Benjamin Wahl, Lisa Föhse, Sebastian Suerbaum, Andrew J. Macpherson, Immo Prinz, and Oliver Pabst. "Age, microbiota, and T cells shape diverse individual IgA repertoires in the intestine." Journal of Experimental Medicine 209, no. 2 (January 16, 2012): 365–77. http://dx.doi.org/10.1084/jem.20111980.

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Intestinal immunoglobulin A (IgA) ensures host defense and symbiosis with our commensal microbiota. Yet previous studies hint at a surprisingly low diversity of intestinal IgA, and it is unknown to what extent the diverse Ig arsenal generated by somatic recombination and diversification is actually used. In this study, we analyze more than one million mouse IgA sequences to describe the shaping of the intestinal IgA repertoire, its determinants, and stability over time. We show that expanded and infrequent clones combine to form highly diverse polyclonal IgA repertoires with very little overlap between individual mice. Selective homing allows expanded clones to evenly seed the small but not large intestine. Repertoire diversity increases during aging in a dual process. On the one hand, microbiota-, T cell–, and transcription factor RORγt–dependent but Peyer’s patch–independent somatic mutations drive the diversification of expanded clones, and on the other hand, new clones are introduced into the repertoire of aged mice. An individual’s IgA repertoire is stable and recalled after plasma cell depletion, which is indicative of functional memory. These data provide a conceptual framework to understand the dynamic changes in the IgA repertoires to match environmental and intrinsic stimuli.

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Ciche, Todd A., Kwi-suk Kim, Bettina Kaufmann-Daszczuk, Ken C. Q. Nguyen, and David H. Hall. "Cell Invasion and Matricide during Photorhabdus luminescens Transmission by Heterorhabditis bacteriophora Nematodes." Applied and Environmental Microbiology 74, no. 8 (February 15, 2008): 2275–87. http://dx.doi.org/10.1128/aem.02646-07.

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ABSTRACT Many animals and plants have symbiotic relationships with beneficial bacteria. Experimentally tractable models are necessary to understand the processes involved in the selective transmission of symbiotic bacteria. One such model is the transmission of the insect-pathogenic bacterial symbionts Photorhabdus spp. by Heterorhabditis bacteriophora infective juvenile (IJ)-stage nematodes. By observing egg-laying behavior and IJ development, it was determined that IJs develop exclusively via intrauterine hatching and matricide (i.e., endotokia matricida). By transiently exposing nematodes to fluorescently labeled symbionts, it was determined that symbionts infect the maternal intestine as a biofilm and then invade and breach the rectal gland epithelium, becoming available to the IJ offspring developing in the pseudocoelom. Cell- and stage-specific infection occurs again in the pre-IJ pharyngeal intestinal valve cells, which helps symbionts to persist as IJs develop and move to a new host. Synchronous with nematode development are changes in symbiont and host behavior (e.g., adherence versus invasion). Thus, Photorhabdus symbionts are maternally transmitted by an elaborate infectious process involving multiple selective steps in order to achieve symbiont-specific transmission.

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Pédron, Thierry, Giulia Nigro, and Philippe J. Sansonetti. "From homeostasis to pathology: decrypting microbe–host symbiotic signals in the intestinal crypt." Philosophical Transactions of the Royal Society B: Biological Sciences 371, no. 1707 (November 5, 2016): 20150500. http://dx.doi.org/10.1098/rstb.2015.0500.

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Metagenomic analysis of the human intestinal microbiome has provided a wealth of information that allowed an exceptionally detailed description of its microbial content and physiological potential. It also set the basis for studies allowing correlation of alterations in the balance of this microbiota and the occurrence of a certain number of emerging diseases, such as inflammatory bowel diseases, obesity and diabetes, and possibly colorectal cancer. The time has come to give the intestinal microbiota in symbiosis with its host an experimental dimension. This brief review summarizes our attempt at developing a cellular microbiology of the mutualistic symbiosis established between the gut microbiota and the host intestinal surface. Particular attention is paid to the intestinal crypt, due to its role in epithelial regeneration. This article is part of the themed issue ‘The new bacteriology’.

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Bukharin, O. V., E. V. Ivanova, N. B. Perunova, and I. A. Nikiforov. "FUNCTIONAL GROUPS OF BIFIDOFLORA OF INTESTINAL MICROBIOTA IN ASSOCIATIVE SYMBIOSIS OF HUMAN." Journal of microbiology epidemiology immunobiology, no. 1 (February 28, 2018): 3–9. http://dx.doi.org/10.36233/0372-9311-2018-1-3-9.

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Aim. Aim of the research is the identification of functional groups of human gut bifidoflora based on analysis of the spectrum of metabolites features, proteome, bioprofile, immunoregulatory properties and the ability to differentiate «self/non-self» among the associative microbiota. Materials and methods. The materials are 260 strains ofbifidobacteria isolated from 122 intestinal microsymbiocenoses. Experimental studies were carried out using bacteriological, chromatographic and immunological methods. Statistical processing of material is carried out by means of the package Statistica 10.0 using of k-cluster analysis and discriminant method. Results. As a result ofthe work, 3 clusters containing strains of various types of bifidobacteria were identified. The first cluster was represented by B. bifidum and was characterized by the antipeptide activity of the strains with respect to FNO-a and INF-y, IL-10. In the second cluster of the B. longum culture predominated, where the parameters of the backbone factor of microsymbiocenosis, the ability to microbial recognition, antagonistic activity and production of acetic acid were significant. In the third cluster the species composition of bifidobacteria was diverse and products of butyric, caproic acids and their isoforms were the informative tests. Conclusion. The key function of bifido-flora in the regulation of the homeostasis of the intestinal biotope is realized by the formation of functional clusters, among which the first group participates in the formation of the cytokine balance, the second group is responsible for the discrimination of associative microbiota and direct protection of the biotope from pathogens, and the third is necessary to maintain the barrier metabolic function of enterocytes in the human large intestine.

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Dudun, Andrei A., Dariana V. Chesnokova, Vera V. Voinova, Anton P. Bonartsev, and Garina A. Bonartseva. "Changes in the Gut Microbiota Composition during Implantation of Composite Scaffolds Based on Poly(3-hydroxybutyrate) and Alginate on the Large-Intestine Wall." Polymers 15, no. 17 (September 4, 2023): 3649. http://dx.doi.org/10.3390/polym15173649.

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The development of biopolymer scaffolds for intestine regeneration is one of the most actively developing areas in tissue engineering. However, intestinal regenerative processes after scaffold implantation depend on the activity of the intestinal microbial community that is in close symbiosis with intestinal epithelial cells. In this work, we study the impact of different scaffolds based on biocompatible poly(3-hydroxybutyrate) (PHB) and alginate (ALG) as well as PHB/ALG scaffolds seeded with probiotic bacteria on the composition of gut microbiota of Wistar rats. Implantation of PHB/ALG scaffolds on the large-intestine wall to close its injury showed that alpha diversity of the gut microbiota was not reduced in rats implanted with different PHB/ALG scaffolds except for the PHB/ALG scaffolds with the inclusion of Lactobacillus spheres (PHB/ALG-L). The composition of the gut microbiota of rats implanted with PHB/ALG scaffolds with probiotic bacteria or in simultaneous use of an antimicrobial agent (PHB/ALG-AB) differed significantly from other experimental groups. All rats with implanted scaffolds demonstrated shifts in the composition of the gut microbiota by individual operational taxonomic units. The PHB/ALG-AB construct led to increased abundance of butyrate-producing bacteria: Ileibacterium sp. dominated in rats with implanted PHB/ALG-L and Lactobacillus sp. and Bifidobacterium sp. dominated in the control group. In addition, the PHB/ALG scaffolds had a favourable effect on the growth of commensal bacteria. Thus, the effect of implantation of the PHB/ALG scaffold compared to other scaffolds on the composition of the gut microbiota was closest to the control variant, which may demonstrate the biocompatibility of this device with the microbiota.

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Bobyr, V. V., L. O. Stechenko, V. P. Shirobokov, O. A. Nazarchuk, and O. V. Rymsha. "The role of sorbents and probiotics in prevention of structural and morphological disorders in the small intestine of animals developing in dysbiosis." Reports of Morphology 26, no. 2 (October 12, 2020): 45–50. http://dx.doi.org/10.31393/morphology-journal-2020-26(2)-07.

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The past decade is characterized by a noticeable increase in the interest of physicians in all areas of activity in the development of new and improvement of existing approaches to the correction of dysbiotic disorders. Among them, the concept of using probiotics occupies a leading position. At the same time, some enterosorbents, the mechanism of action of which is largely due to the sanitation of the intestinal lumen and due to this improvement of conditions for the vital activity of the physiological microbiota, can be attributed to the group of means of improving the normal microflora. In the context of an increase in the level of resistance to antibacterial agents, the inclusion of enterosorbents in the complex therapy of dysbiosis is an important and pathogenetically justified approach. The aim of the work was to clarify the effectiveness of the use of sorbents and probiotics for the prevention of structural and morphological disorders in the small intestine of white mice developing against the background of antibiotic-induced dysbiosis. Electron-microscopic methods showed that in the mucous membrane of the small intestine of mice after using the probiotic “Simbiter” the extinction of manifestations of cytodestructive disorders is observed. In addition, the obtained electron microscopic data, indicating the ability of probiotic drugs with the simultaneous introduction into the body of animals with a complex of antibiotics, to stimulate the body’s immune response. As a result of ultrastructural analysis of the mucous membrane of the small intestine of mice, the formation of dysbiosis in which occurred against the background of the use of enterosorbents, a decrease in the severity of structural damage was found, compared with the group of animals that received only antibiotics. After using “Symbiogel”, activation of plasma cells was registered, which can be an indicator of the inflammatory process and the activity of the immune response in general, as evidenced by the detection of plasma cells with dilated tubules. In general, it should be noted that the use of “Symbiogel” for the prevention of dysbiotic disorders contributes to the formation of a more pronounced immune response, compared with probiotic drugs. So, on the model of antibiotic-induced dysbiosis at the ultrastructural level, the ability of multiprobiotics “Simbiter®” and sorbent “Symbiogel” to reduce cytodestructive changes in the mucous membrane of the small intestine of mice and normalize morphoimunogenesis was proved.

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Aytbaev, K. A., I. T. Murkamilov, and R. R. Kaliev. "Chronic kidney disease: pathophysiological role of dysbiosis of intestine and renoprotective effectiveness of interventions concerning its modulation." Medical Journal of the Russian Federation 22, no. 3 (June 15, 2016): 157–62. http://dx.doi.org/10.18821/0869-2106-2016-22-4-157-162.

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The review presents data concerning disorders of quantitative and qualitative content of intestinal microbiota in patients with chronic kidney disease. The causes enhancing development of intestinal dysbiosis and sub-clinical inflammation under chronic disease of kidneys are considered. The results of preliminary studies concerning investigation of particular approaches to therapy of chronic kidney disease directed to restoring of intestinal symbiosis and neutralization of bacterial endotoxins and adsorption of uremic toxins of intestinal origin are presented.

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Mayatskaya, T. A., L. A. Kharitonova, O. V. Papysheva, and A. M. Zatevalov. "Formation of intestinal microbiocenosis in children born to mothers with gestational diabetes mellitus." Experimental and Clinical Gastroenterology 1, no. 1 (March 17, 2021): 96–105. http://dx.doi.org/10.31146/1682-8658-ecg-185-1-96-105.

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Rationale. The global medical community currently studies the influence of microbiocenosis on macroorganism. The metabolome of the human gut microbiome may be a factor in the development of pathology in tissues and organs.Objective. To improve the early diagnosis of intestinal microecology disorders in infants by determining the species composition and functional activity of the intestinal microflora to predict the health status of children born to mothers with diabetes.Materials and methods. We studied the intestinal microbiocenosis in 60 infants aged 1–28 days, including 22 infants by healthy mothers (control group) and 38 infants by mothers with diabetes (study group). The following was evaluated: the species composition of the intestinal microbiocenosis; its functional state by concentrations of short-chain fatty acids (SCFA); the content of elastase and simple carbohydrates in feces. The species composition was studied by fecal next generation sequencing (NGS), SCFA concentration was studied by gas-liquid chromatography of acidified fecal supernatant, pancreatic elastase in fecal samples was quantified by ELISA, and fecal carbohydrate content was determined by Benedict’s test. The gut dysbiosis was measured by the biodiversity of the microbial community quantified in biology by Shannon index according to the formula: where and corresponds to the number of microbial species in the intestinal microbial community. Normalized Shannon index has a range of values from 0 to 1, convenient for the interpretation of the microbiocenosis condition. An increase in the biodiversity of the microbial community was associated with an increase in dysbiotic changes of the gut microbiocenosis. Statistical analysis was performed with Statistica 8.0 and MS Office Excel 2010.Results. In children born by mothers with diabetes, the formation of microbial community at the stage of intestinal tract settlement occurs because of the increase of species biodiversity and formation of strong correlation between different classes of microorganisms, indicating a decrease of symbiont relationships of microbiocenosis with macroorganism normally mediated by intestinal epithelial cells condition and cooperation of the cells with intestinal mucosal barrier components. Due to the pronounced biodiversity and interspecies symbiosis of bacteria, compensatory mechanisms are formed in the colon for coexistence of macroorganism and microbiota. Thus, not only the butyric acid is produced in sufficient quantities but also the microbiota consumes SCFA releasing an increased amounts of iso-acids and promoting the growth of putrefactive microbial flora.

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Mazmanian, Sarkis K., June L. Round, and Dennis L. Kasper. "A microbial symbiosis factor prevents intestinal inflammatory disease." Nature 453, no. 7195 (May 2008): 620–25. http://dx.doi.org/10.1038/nature07008.

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Anhê, Fernando F., Nicole G. Barra, and Jonathan D. Schertzer. "Glucose alters the symbiotic relationships between gut microbiota and host physiology." American Journal of Physiology-Endocrinology and Metabolism 318, no. 2 (February 1, 2020): E111—E116. http://dx.doi.org/10.1152/ajpendo.00485.2019.

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Bacteria and mammals exhibit all aspects of symbiosis. Metabolic flux in bacteria and in specific host cells can influence host-microbe symbiotic relationships and tip the balance between mutualism, commensalism, and parasitism. The relationship between microbes and host metabolism is bidirectional: microbes can influence host blood glucose, but glucose levels can influence the microbiota and host response to specific bacteria. A key consideration determining symbiotic relationships is compartmentalization of bacterial niches by mucosal, chemical, and physical barriers of the gut. We propose that compartmentalization of glucose levels in the blood versus the intestinal lumen is another important factor dictating host-microbe symbiosis. Host glucose and specific bacteria can modify the intestinal barrier, immune function, and antimicrobial defenses, which can then break down compartmentalization of microbes, alter glucose levels and impact symbiosis. Determining how glucose metabolism promotes mutualistic, commensal, and parasitic relationships within the entire microbiota community is relevant to glucose control in diabetes and enteric infections, which occur more often and have worse outcomes in diabetics.

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Gebhart, C. J., S. McOrist, G. H. K. Lawson, J. E. Collins, and G. E. Ward. "Specific in situ Hybridization of the Intracellular Organism of Porcine Proliferative Enteropathy." Veterinary Pathology 31, no. 4 (July 1994): 462–67. http://dx.doi.org/10.1177/030098589403100409.

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The identity of the intracellular bacteria found in the enterocytes of pigs with proliferative enteropathy was investigated using specific DNA probes to various Campylobacter species and to a novel organism, ileal symbiont intracellularis. The ilea from pigs (Nos. 1–7) that were diagnosed by routine histopathology as having proliferative enteropathy were used. Diagnosis was made on the basis of proliferation of the enterocytes on hematoxylin and cosin-stained sections and the presence of large numbers of intracellular curved organisms on Warthin-Starry silver-stained sections. Four of these pigs (Nos. 1–4) had the chronic form of the disease, porcine intestinal adenomatosis, and three (Nos. 5–7) had the acute form, proliferative hemorrhagic enteropathy. An additional three normal pigs (Nos. 8–10) were obtained from three separate farms with no history of proliferative enteropathy. Frozen ileal sections were examined by in situ hybridization with DNA probes specific for ileal symbiont intracellularis and the three porcine intestinal Campylobacter species, C. coli, C. hyointestinalis, and C. mucosalis. In all seven pigs with either the intestinal adenomatosis or hemorrhagic enteropathy form of the disease, a DNA probe specific for ileal symbiont intracellularis hybridized to localized foci in the apical cytoplasm of ileal enterocytes. These hybridization sites corresponded to the location of intracellular bacteria in silver-stained sections of adjacent tissue. Sections from the three normal pigs tested with this probe and from all pigs tested with the Campylobacter species-specific DNA probes showed no specific hybridization reactions. The identity of the intracellular organism in these diseased pigs is ileal symbiont intracellularis.

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Yunker, Rebecca, Geon Goo Han, Hien Luong, and Shipra Vaishnava. "Intestinal Epithelial Cell Intrinsic Zinc Homeostasis is Critical for Host-Microbiome Symbiosis." Journal of Immunology 210, no. 1_Supplement (May 1, 2023): 82.18. http://dx.doi.org/10.4049/jimmunol.210.supp.82.18.

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Abstract A robust intestinal barrier is essential for maintaining host-microbiome symbiosis. Defects in the intestinal barrier are associated with a broad range of inflammatory and metabolic diseases. Pharmacological doses of Zinc (Zn) are widely used to improve intestinal barrier function; however, the precise cellular role of Zn in regulating the intestinal barrier during health and disease is not known. A better understanding of how Zn regulates the gut barrier and intestinal epithelial cells (IEC) could enable the development of targeted Zn-based therapeutic approaches. To understand the impact of Zn homeostasis we developed a mouse model with the transcription factor MTF-1 specifically deleted in IECs (MTF ΔIEC). MTF-1 controls the expression of many different zinc importers and exporters. We find that MTF ΔIECmice had reduced expression of Zn homeostasis machinery, demonstrated a leaky barrier, and showed heightened neutrophil activation in the periphery. Additionally, MTF ΔIECmice had a higher bacterial load at the mucosa and were more susceptible to infection by Crohn’s disease associated adherent invasive E.coli. MTF ΔIECmice showed a striking loss of Paneth cells (PCs) from the small intestinal crypts. PCs are specialized antimicrobial-secreting cells with a unique requirement for Zn, but the exact role of Zn in PCs is not known. Based on our findings we conclude that Zn homeostasis is needed for regulating host-microbiome interaction via modulation of intestinal barrier permeability and maintenance of Paneth cells.Our work demonstrating the impact of zinc homeostasis on host-microbe interactions lays the groundwork for understanding zinc in the context of inflammatory bowel disease and dysbiosis in the mucosal microbiome. This work was supported by the NIH [R01DK113265] to Shipra Vaishnava

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Wang, Shuai, Qianhong Ye, Xiangfang Zeng, and Shiyan Qiao. "Functions of Macrophages in the Maintenance of Intestinal Homeostasis." Journal of Immunology Research 2019 (March 18, 2019): 1–8. http://dx.doi.org/10.1155/2019/1512969.

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Intestinal macrophages constitute the largest pool of macrophages in the body and have emerged as crucial sentinels for pathogen recognition and elimination. The source and development of intestinal macrophages, as well as their distinct properties have been well documented. Intestinal macrophages exert their functions in the maintenance of intestinal homeostasis by shaping host-microbiota symbiosis, managing gut inflammation, crosstalking with T cells, and facilitating wound repair. Recently, nutritional regulation of intestinal macrophages has attracted substantial attention and is becoming a promising approach to disease prevention and control. Understanding the mechanisms employed by intestinal macrophages in mediating intestinal immune homeostasis and inflammation, as well as the mode of action of dietary nutrients in the modulating functions of intestinal macrophages, represents an opportunity to prevent and control inflammatory bowel diseases.

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Chen, Yuezhou, Neha Chaudhary, Nicole Yang, Alessandra Granato, Jacob A. Turner, Shannon L. Howard, Colby Devereaux, et al. "Microbial symbionts regulate the primary Ig repertoire." Journal of Experimental Medicine 215, no. 5 (March 27, 2018): 1397–415. http://dx.doi.org/10.1084/jem.20171761.

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The ability of immunoglobulin (Ig) to recognize pathogens is critical for optimal immune fitness. Early events that shape preimmune Ig repertoires, expressed on IgM+ IgD+ B cells as B cell receptors (BCRs), are poorly defined. Here, we studied germ-free mice and conventionalized littermates to explore the hypothesis that symbiotic microbes help shape the preimmune Ig repertoire. Ig-binding assays showed that exposure to conventional microbial symbionts enriched frequencies of antibacterial IgM+ IgD+ B cells in intestine and spleen. This enrichment affected follicular B cells, involving a diverse set of Ig-variable region gene segments, and was T cell–independent. Functionally, enrichment of microbe reactivity primed basal levels of small intestinal T cell–independent, symbiont-reactive IgA and enhanced systemic IgG responses to bacterial immunization. These results demonstrate that microbial symbionts influence host immunity by enriching frequencies of antibacterial specificities within preimmune B cell repertoires and that this may have consequences for mucosal and systemic immunity.

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Sears, Cynthia L. "Enterotoxigenic Bacteroides fragilis: a Rogue among Symbiotes." Clinical Microbiology Reviews 22, no. 2 (April 2009): 349–69. http://dx.doi.org/10.1128/cmr.00053-08.

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SUMMARY Enterotoxigenic Bacteroides fragilis (ETBF) strains are strains of B. fragilis that secrete a 20-kDa heat-labile zinc-dependent metalloprotease toxin termed the B. fragilis toxin (BFT). BFT is the only recognized virulence factor specific for ETBF. ETBF strains are associated with inflammatory diarrheal disease in children older than 1 year of age and in adults; limited data suggest an association of ETBF colonization with inflammatory bowel disease flare-ups and colorectal cancer. ETBF secretes one of three highly related BFT isoforms. The relationship between BFT isoform and disease expression is unknown. Although the mechanism of action of BFT is incompletely understood, available data suggest that BFT binds to a specific intestinal epithelial cell receptor, stimulating intestinal cell signal transduction pathways that result in cell morphology changes, cleavage of E-cadherin, reduced colonic barrier function, and increased epithelial cell proliferation and cytokine expression (such as the proinflammatory chemokine interleukin-8). Together, the data suggest that in some hosts, ETBF acts via secretion of BFT to induce colitis. However, the full spectrum of clinical disease related to ETBF and the impact of chronic ETBF colonization on the host remain to be defined.

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Semydotska, Zh, I. Chernyakova, and O. Avdeyeva. "Kidneys and microbiota." Ukrainian Journal of Nephrology and Dialysis, no. 1(65) (November 14, 2019): 48–57. http://dx.doi.org/10.31450/ukrjnd.1(65).2020.07.

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The review article analyzes the results of studies of the bi-directional relationship of the intestinal microbiota and kidneys, the so-called colorenal interactive axis of interaction. The intestinal microbiota is considered as a kind of organ that influences the brain, cardiovascular and immune systems, as well as the kidneys of the "host". Short-chain fatty acids (SCFA) formed in the colon as the result of microbial metabolism from plant components of dietary fiber and acting as ligands for the olfactory receptor, paired G-proteins in the kidneys are recognized as the markers of this symbiosis. With the help of modern omix technologies, the development of dysbiosis taking into account patients with chronic kidney disease (CKD) has been proved, which leads to the accumulation of precursors of uremic toxins, a decrease in the production of SCFA, which have nephroprotective properties and play a key role in energy homeostasis. Changes in the composition of the intestinal microbiota in CKD, an increase in the content of uremic toxins in the intestinal lumen contribute to the appearance of the “leaky” intestinal barrier syndrome, the movement of bacteria from the intestine into the general circulation, the development of systemic inflammation, oxidative stress, comorbidity, the progression of CKD, and an increase in mortality. Diets with restriction of protein and potassium quotas, violation of nutritional status lead to the development of dysbiosis in CKD. A decrease in the diet of vegetables and fruit causes the expansion of bacteria producing uricase and urease, which are enzymes in the formation of uremic toxins and reduce the number and variety of bacteria producing short-chain fatty acids. Potential targeted effects on the axis of “intestinal microbiota - chronic kidney disease” are being discussed: the use of a diet enriched in plant fibers, heat-treated, then chilled potatoes and rice as prebiotics (sources of resistant starch), nuts, plant seeds, and pro-, pre-, synbiotics, fecal transplantation. Most of the proposed interventions in the structure and functions of the microbiota are not dangerous, side effects are minimal.

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Palmer-Young, Evan C., Thomas R. Raffel, and Quinn S. McFrederick. "Temperature-mediated inhibition of a bumblebee parasite by an intestinal symbiont." Proceedings of the Royal Society B: Biological Sciences 285, no. 1890 (October 31, 2018): 20182041. http://dx.doi.org/10.1098/rspb.2018.2041.

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Competition between organisms is often mediated by environmental factors, including temperature. In animal intestines, nonpathogenic symbionts compete physically and chemically against pathogens, with consequences for host infection. We used metabolic theory-based models to characterize differential responses to temperature of a bacterial symbiont and a co-occurring trypanosomatid parasite of bumblebees, which regulate body temperature during flight and incubation. We hypothesized that inhibition of parasites by bacterial symbionts would increase with temperature, due to symbionts having higher optimal growth temperatures than parasites. We found that a temperature increase over the range measured in bumblebee colonies would favour symbionts over parasites. As predicted by our hypothesis, symbionts reduced the optimal growth temperature for parasites, both in direct competition and when parasites were exposed to symbiont spent medium. Inhibitory effects of the symbiont increased with temperature, reflecting accelerated growth and acid production by symbionts. Our results indicate that high temperatures, whether due to host endothermy or environmental factors, can enhance the inhibitory effects of symbionts on parasites. Temperature-modulated manipulation of microbiota could be one explanation for fever- and heat-induced reductions of infection in animals, with consequences for diseases of medical and conservation concern.

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Pickard, Joseph M., and Alexander V. Chervonsky. "Intestinal Fucose as a Mediator of Host–Microbe Symbiosis." Journal of Immunology 194, no. 12 (June 5, 2015): 5588–93. http://dx.doi.org/10.4049/jimmunol.1500395.

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Tarnecki, A. M., F. A. Burgos, C. L. Ray, and C. R. Arias. "Fish intestinal microbiome: diversity and symbiosis unravelled by metagenomics." Journal of Applied Microbiology 123, no. 1 (May 10, 2017): 2–17. http://dx.doi.org/10.1111/jam.13415.

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Fast, David, Kristina Petkau, Meghan Ferguson, Minjeong Shin, Anthony Galenza, Benjamin Kostiuk, Stefan Pukatzki, and Edan Foley. "Vibrio cholerae-Symbiont Interactions Inhibit Intestinal Repair in Drosophila." Cell Reports 30, no. 4 (January 2020): 1088–100. http://dx.doi.org/10.1016/j.celrep.2019.12.094.

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Solomon, Alla, and Yurii Polyevoda. "PROBIOTICS AND THEIR ROLE IN THE PRODUCTION OF SPIRITUAL PRODUCTS OF SPECIAL PURPOSE." ENGINEERING, ENERGY, TRANSPORT AIC, no. 3(106) (November 29, 2019): 56–65. http://dx.doi.org/10.37128/2520-6168-2019-3-7.

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In ensuring the proper functioning of the human body, an important role is played by the microorganisms that enter into it with symbiosis. Between them and the microorganism - symbiote, special relationships are formed, including metabolism exchange, internal ecological relations are created, which is a prerequisite for the existence of the macroorganism. These microorganisms ferment nutrients that have not been digested in the upper gastrointestinal tract, forming a variety of chemical compounds that exert both a positive and a negative effect on the human body. Disturbance of normal activity of intestinal microflora leads to serious physiological disorders and can be the cause of a number of diseases. Therefore, the key to human health is, in particular, maintaining the gut microbiota in a normal state. Most of the human gut microbial organisms are obligate anaerobes, optional anaerobes are presented in a much smaller number. In recent years, there has been a growing interest in dairy products containing probiotics and prebiotics. The article deals with the main tendencies of development of modern special purpose fermented milk products and the criteria for evaluation of promising probiotic cultures and the main factors that influence the ability of bacteria to survive and maintain activity in the product before entering the gastrointestinal tract. In this scientific work we use general scientific methods of research: analysis, synthesis, abstraction, monographic and special methods of research - statistical and calculation. Information base of the research - current legislative and regulatory acts of Ukraine, scientific works of domestic and foreign scientists, own observations of the authors.

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Bhunia, Rima, Varsha Singh, Srijan Das, Anindya Krishna Basu, and Dolanchapa Sikdar. "PROBIOTICS: A SIGNIFICANT APPROACH TO HEALTH." International Journal of Engineering Applied Sciences and Technology 7, no. 11 (March 1, 2023): 104–13. http://dx.doi.org/10.33564/ijeast.2023.v07i11.019.

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This report deals with the study that Probiotics have been with us for as long as people have eaten fermented milks, but their collaboration with health benefits have only come in the century when Metchnikoff gave idea of replacing dangerous microbes by useful ones in order to modify our gut flora. Later based on assumption that colonization of the gut was essential, used intestinal strains of Lactobacillus acidophilus for treatment of constipation, digestive hazards. According to Food and agriculture organisation of United Nations (UN) probiotics are live microorganisms which on administering in proper amount produces useful effects to the host when consumed orally. Probiotics were found to effectively influence the host by enhancing their microbial balance of intestine, thus suppressing pathogens and toxin forming bacteria. Hence, probiotics with boosting the functioning of the immune system also naturally help in fighting bad bacteria by providing the body with sufficient good to keep the body in symbiosis. It doesn't have any risk of overdose too that leads to the need for a prescription or the monitoring of a physician.

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HU, Haiming, Ke LAN, and Hongtao LIU. "Human symbiont Bacteroides xylanisolvens attenuates NASH through intestinal nicotine catabolism." Chinese Journal of Natural Medicines 21, no. 2 (February 2023): 81–82. http://dx.doi.org/10.1016/s1875-5364(23)60387-5.

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Rutz, Sascha, Christian Neumann, Jonas Blume, Axel Kalies, and Alexander Scheffold. "c-Maf-dependent Treg cell control of intestinal TH17 cells and IgA establishes host-microbiota homeostasis." Journal of Immunology 202, no. 1_Supplement (May 1, 2019): 57.19. http://dx.doi.org/10.4049/jimmunol.202.supp.57.19.

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Abstract Foxp3+T regulatory (Treg) cells are crucial to maintain immune homeostasis both in lymphoid and non-lymphoid tissues. Here we demonstrate that the ability of intestinal Treg cells to constrain microbiota-dependent interleukin 17–producing T helper cell (TH17) and immunoglobulin A (IgA) responses critically required the expression of the transcription factor c-Maf. The terminal differentiation and function of several intestinal Treg cell populations, including RORgt+Tregcells and T follicular regulatory cells, was c-Maf-dependent. c-Maf controlled Treg cell-derived interleukin 10 (IL-10) production and prevented excessive phosphatidylinositol-3-OH kinase (PI(3)K)–kinase Akt–mechanistic target of rapamycin (mTORC1) signaling and inflammatory cytokine expression in intestinal Treg cells. c-Maf-deficiency in Treg cells led to a profound dysbiosis of the intestinal microbiota, which when transferred to germ-free mice, was sufficient to induce exacerbated intestinal TH17 responses, even in a c-Maf-competent environment. Thus, c-Maf acts to preserve the identity and function of intestinal Treg cells, which is essential for the establishment of host-microbial symbiosis.

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Barra, Nicole G., Fernando F. Anhê, Joseph F. Cavallari, Anita M. Singh, Darryl Y. Chan, and Jonathan D. Schertzer. "Micronutrients impact the gut microbiota and blood glucose." Journal of Endocrinology 250, no. 2 (August 1, 2021): R1—R21. http://dx.doi.org/10.1530/joe-21-0081.

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Micronutrients influence hormone action and host metabolism. Dietary minerals, trace elements, and vitamins can alter blood glucose and cellular glucose metabolism, and several micronutrients are associated with the risk and progression of type 2 diabetes. Dietary components, microbes, and host immune, endocrine, and metabolic responses all interact in the intestine. There has been a focus on macronutrients modifying the host-microbe relationship in metabolic disease. Micronutrients are positioned to alter host-microbe symbiosis that participates in host endocrine control of glucose metabolism. Minerals and trace elements can alter the composition of the intestinal microbiota, gut barrier function, compartmentalized metabolic inflammation, cellular glucose transport, and endocrine control of glucose metabolism, including insulin and thyroid hormones. Dietary vitamins also influence the composition of the intestinal microbiota and vitamins can be biotransformed by gut microbes. Host-microbe regulation of vitamins can alter immunity, lipid and glucose metabolism, and cell fate and function of pancreatic beta cells. Causal effects of micronutrients in host-microbe metabolism are still emerging, and the mechanisms linking dietary excess or deficiency of specific micronutrients to changes in gut microbes directly linked to metabolic disease risk are not yet clear. Dietary fiber, fat, protein, and carbohydrates are key dietary factors that impact how microbes participate in host glucose metabolism. It is possible that micronutrient and microbiota-derived factors also participate in host-microbe responses that tip the balance in the endocrine control of host glucose metabolism. Dietary micronutrients should be considered, tested, and controlled in pre-clinical and clinical studies investigating host-microbe factors in metabolic diseases.

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Pickard, Joseph M., Corinne F. Maurice, Melissa A. Kinnebrew, Michael C. Abt, Dominik Schenten, Tatyana V. Golovkina, Said R. Bogatyrev, et al. "Rapid fucosylation of intestinal epithelium sustains host–commensal symbiosis in sickness." Nature 514, no. 7524 (October 2014): 638–41. http://dx.doi.org/10.1038/nature13823.

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Brown, Eric M., Xiaobo Ke, Daniel Hitchcock, Sarah Jeanfavre, Julian Avila-Pacheco, Toru Nakata, Timothy D. Arthur, et al. "Bacteroides-Derived Sphingolipids Are Critical for Maintaining Intestinal Homeostasis and Symbiosis." Cell Host & Microbe 25, no. 5 (May 2019): 668–80. http://dx.doi.org/10.1016/j.chom.2019.04.002.

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Fehér, János, Illés Kovács, Elena Pacella, and Zsolt Radák. "Microbiota–host symbiosis in the pathophysiology and treatment of irritable bowel, irritable eye and irritable mind syndrome." Orvosi Hetilap 155, no. 37 (September 2014): 1454–60. http://dx.doi.org/10.1556/oh.2014.29987.

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Accumulating clinical evidence supports co-morbidity of irritable bowel, irritable eye and irritable mind symptoms. Furthermore, perturbation of the microbiota–host symbiosis (dysbiosis) is considered a common pathogenic mechanism connecting gastrointestinal, ocular and neuropsychiatric symptoms. Consequently, maintaining or restoring microbiota–host symbiosis represents a new approach to treat these symptoms or to prevent their relapses. Current treatment approach assigned a primary role to live probiotics alone or in combination with prebiotics to enhance colonization of beneficial bacteria and to strengthen the symbiosis. However, several papers showed major benefits of heat-killed probiotics as compared to their live counterparts on both intestinal and systemic symptoms. Recently, in addition to killing probiotics, in a proof of concept study lysates (fragments) of probiotics in combination with vitamins A, B, D and omega 3 fatty acids were successfully tested. These findings suggested a conceptual change in the approach addressed to both the microbiota and host as targets for intervention. Orv. Hetil., 2014, 155(37), 1454–1460.

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Sonnenburg, J. L. "Glycan Foraging in Vivo by an Intestine-Adapted Bacterial Symbiont." Science 307, no. 5717 (March 25, 2005): 1955–59. http://dx.doi.org/10.1126/science.1109051.

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Jovandaric, Miljana Z., Stefan Dugalic, Sandra Babic, Ivana R. Babovic, Srboljub Milicevic, Dejan Mihajlovic, Miljan Culjic, et al. "Programming Factors of Neonatal Intestinal Dysbiosis as a Cause of Disease." International Journal of Molecular Sciences 24, no. 6 (March 17, 2023): 5723. http://dx.doi.org/10.3390/ijms24065723.

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The intestinal microbiota consists of trillions of bacteria, viruses, and fungi that achieve a perfect symbiosis with the host. They perform immunological, metabolic, and endocrine functions in the body. The microbiota is formed intrauterine. Dysbiosis is a microbiome disorder characterized by an imbalance in the composition of the microbiota, as well as changes in their functional and metabolic activities. The causes of dysbiosis include improper nutrition in pregnant women, hormone therapy, the use of drugs, especially antibiotics, and a lack of exposure to the mother’s vaginal microbiota during natural birth. Changes in the intestinal microbiota are increasingly being identified in various diseases, starting in the early neonatal period into the adult period. Conclusions: In recent years, it has become more and more obvious that the components of the intestinal microbiota are crucial for the proper development of the immune system, and its disruption leads to disease.

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Cao, Ruige, Xing Wu, Hui Guo, Xin Pan, Rong Huang, Gangqiang Wang, and Jikai Liu. "Naringin Exhibited Therapeutic Effects against DSS-Induced Mice Ulcerative Colitis in Intestinal Barrier–Dependent Manner." Molecules 26, no. 21 (October 31, 2021): 6604. http://dx.doi.org/10.3390/molecules26216604.

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Naringin is a kind of multi-source food additive which has been explored broadly for its various biological activities and therapeutic potential. In the present study, the protective effect and mechanism of naringin on dextran sulfate sodium (DSS)-induced ulcerative colitis (UC) in mice were investigated. The results showed that naringin significantly alleviated DSS-induced colitis symptoms, including disease activity index (DAI), colon length shortening, and colon pathological damage. The tissue and serum secretion of inflammatory cytokines, as well as the oxidative stress, were decreased accordingly upon naringin intervention. Naringin also decreased the proteins involved in inflammation and increased the expression of tight junction (TJ) proteins. Moreover, naringin increased the relative abundance of Firmicutes/Bacteroides and reduced the content of Proteobacteria to improve the intestinal flora disorder caused by DSS, which promotes the intestinal health of mice. It was concluded that naringin can significantly ameliorate the pathogenic symptoms of UC through inhibiting inflammatory response and regulating intestinal microbiota, which might be a promising natural therapeutic agent for the dietary treatment of UC and the improvement of intestinal symbiosis.

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Гончар, Н. В., and Н. В. Скрипченко. "PROMISING AREAS OF SCIENTIFIC RESEARCH ON THE PROBLEMS OF INTESTINAL INFECTIONS." Children's medicine of the North-West 11, no. 2 (November 9, 2023): 50–61. http://dx.doi.org/10.56871/cmn-w.2023.46.73.004.

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Решение современных проблем диагностики и лечения кишечных инфекций у детей определяет важнейшие направления научных исследований, в ряду которых стоят молекулярно- генетические и клинические особенности возбудителей вирусных диарей, совершенствование методов терапии острых гастроэнтеритов вирусной этиологии, молекулярная диагностика токсинпродуцирующих бактериальных кишечных патогенов, биологическая безопасность и кишечные инфекции, прогнозирование антибиотик-ассоциированной диареи и подходы к лечению, клиническое значение диареи условно- патогенной бактериальной этиологии у детей, антибиотикорезистентность энтеробактерий и эффективность фаготерапии, персонифицированная симбионтная терапия реконвалесцентов кишечных инфекций. The solution of modern problems of diagnosis and treatment of intestinal infections in children is determined by the most important areas of scientifi c research, among which are the molecular genetics and clinical features of viral diarrhea pathogens, improvement of therapy methods for acute gastroenteritis of viral etiology, molecular diagnostics of toxin- producing bacterial intestinal pathogens, biological safety and intestinal infections, prediction of antibiotic- associated diarrhea and treatment approaches, clinical signifi cance of diarrhea of conditionally pathogenic bacterial etiology in children, antibiotic resistance of Enterobacteriaceae and the eff ectiveness of phage therapy, personalized symbiont therapy of convalescents of intestinal infections.

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Wopereis, Harm, Raish Oozeer, Karen Knipping, Clara Belzer, and Jan Knol. "The first thousand days - intestinal microbiology of early life: establishing a symbiosis." Pediatric Allergy and Immunology 25, no. 5 (June 5, 2014): 428–38. http://dx.doi.org/10.1111/pai.12232.

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Palmer-Young, Evan C., Thomas R. Raffel, and Quinn S. McFrederick. "pH-mediated inhibition of a bumble bee parasite by an intestinal symbiont." Parasitology 146, no. 3 (September 24, 2018): 380–88. http://dx.doi.org/10.1017/s0031182018001555.

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AbstractGut symbionts can augment resistance to pathogens by stimulating host-immune responses, competing for space and nutrients, or producing antimicrobial metabolites. Gut microbiota of social bees, which pollinate many crops and wildflowers, protect hosts against diverse infections and might counteract pathogen-related bee declines. Bumble bee gut microbiota, and specifically abundance ofLactobacillus‘Firm-5’ bacteria, can enhance resistance to the trypanosomatid parasiteCrithidia bombi. However, the mechanism underlying this effect remains unknown. We hypothesized that the Firm-5 bacteriumLactobacillus bombicola, which produces lactic acid, inhibitsC. bombi viapH-mediated effects. Consistent with our hypothesis,L. bombicolaspent medium inhibitedC. bombigrowthviareduction in pH that was both necessary and sufficient for inhibition. Inhibition of all parasite strains occurred within the pH range documented in honey bees, though sensitivity to acidity varied among strains. Spent medium was slightly more potent than HCl,d- andl-lactic acids for a given pH, suggesting that other metabolites also contribute to inhibition. Results implicate symbiont-mediated reduction in gut pH as a key determinant of trypanosomatid infection in bees. Future investigation intoin vivoeffects of gut microbiota on pH and infection intensity would test the relevance of these findings for bees threatened by trypanosomatids.

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Kim, Girak, Yikun Yao, Zuojia Chen, Chuan Wu, and Michael J. Lenardo. "Mucus sialylation determines intestinal host-commensal homeostasis." Journal of Immunology 210, no. 1_Supplement (May 1, 2023): 227.02. http://dx.doi.org/10.4049/jimmunol.210.supp.227.02.

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Abstract Intestinal mucus forms the first line of defense against bacterial invasion while providing nutrition to support microbial symbiosis. How the host controls mucus barrier integrity and commensalism is unclear. We show that terminal sialylation of glycans on intestinal mucus by ST6GALNAC1 (ST6), the dominant sialyltransferase specifically expressed in goblet cells and induced by microbial pathogen-associated molecular patterns, is essential for mucus integrity and protecting against excessive bacterial proteolytic degradation. Glycoproteomic profiling and biochemical analysis of ST6 mutations identified in patients show that decreased sialylation causes defective mucus proteins and congenital inflammatory bowel disease (IBD). Mice harboring a patient ST6 mutation have compromised mucus barriers, dysbiosis, and susceptibility to intestinal inflammation. Based on our understanding of the ST6 regulatory network, we show that treatment with sialylated mucin or a Foxo3 inhibitor can ameliorate IBD. Supported by the Intramural Research Program of the NIAID, NIH, United States and by National Multiple Sclerosis Society Career Transition Award, United States (TA 3059-A-2 to C.W.).

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Madách, Krisztina, Katalin Kristóf, Eszter Tulassay, Zsolt Iványi, Anna Erdei, András Király, János Gál, and Zsuzsa Bajtay. "Mucosal Immunity and the Intestinal Microbiome in the Development of Critical Illness." ISRN Immunology 2011 (November 24, 2011): 1–12. http://dx.doi.org/10.5402/2011/545729.

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The intestinal community, including the commensal microbial flora as well as the host tissues, represents a functional whole in vivo. Under physiological circumstances, this symbiosis brings great benefit for the host; however, critical illness induces profound disturbances in the intestinal ecosystem affecting both procaryotic and eucaryotic members. Today, 25 years after the gut was first described as a motor of multiple organ dysfunction syndrome, the role of the injured splanchnic compartment in the pathomechanism and development of critical illness is still in the first line of research. Multiple mechanisms have been identified by which the stressed gut may affect host homeostasis, and how external intervention might help to rebalance physiology. This paper provides a brief overview of the present of this field.

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Su, Marcia Shu-Wei, Phaik Lyn Oh, Jens Walter, and Michael G. Gänzle. "Intestinal Origin of SourdoughLactobacillus reuteriIsolates as Revealed by Phylogenetic, Genetic, and Physiological Analysis." Applied and Environmental Microbiology 78, no. 18 (July 13, 2012): 6777–80. http://dx.doi.org/10.1128/aem.01678-12.

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ABSTRACTLactobacillus reuteriis both a gut symbiont and a stable member of sourdough microbiota. This study employed multilocus sequence analysis and an analysis of host-specific physiological and genetic traits to assign five sourdough isolates to rodent- or human-specific lineages. Comparative genome hybridization revealed that the model sourdough isolate LTH2584 had a genome content very similar to that of the model rodent isolate 100-23. These results demonstrate that sourdough isolates ofL. reuteriare of intestinal origin.

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Borghi, Monica, Matteo Puccetti, Marilena Pariano, Giorgia Renga, Claudia Stincardini, Maurizio Ricci, Stefano Giovagnoli, Claudio Costantini, and Luigina Romani. "Tryptophan as a Central Hub for Host/Microbial Symbiosis." International Journal of Tryptophan Research 13 (January 2020): 117864692091975. http://dx.doi.org/10.1177/1178646920919755.

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Amino acid catabolism occurs during inflammation and regulates innate and adaptive immunity. The role of commensal bacteria in amino acid catabolism and the production of metabolites able to regulate the development and function of the innate immune system is increasingly being recognized. Therefore, commensal bacteria are key players in the maintenance of immune homeostasis. However, the intestinal microbiota also contributes to susceptibility and response to infectious diseases. This is self-evident for fungal infections known to occur as a consequence of weakened immune system and broad-spectrum antibiotic use or abuse. Thus, diseases caused by opportunistic fungi can no longer be viewed as dependent only on a weakened host but also on a disrupted microbiota. Based on these premises, the present review focuses on the role of amino acid metabolic pathways in the dialogue between the mammalian host and its microbiota and the potential implications in fungal commensalism and infectivity.

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Neish, Andrew S., and Rheinallt M. Jones. "Redox signaling mediates symbiosis between the gut microbiota and the intestine." Gut Microbes 5, no. 2 (January 23, 2014): 250–53. http://dx.doi.org/10.4161/gmic.27917.

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Hooper, Lora V., Lynn Bry, Per G. Falk, and Jeffrey I. Gordon. "Host-microbial symbiosis in the mammalian intestine: exploring an internal ecosystem." BioEssays 20, no. 4 (December 6, 1998): 336–43. http://dx.doi.org/10.1002/(sici)1521-1878(199804)20:4<336::aid-bies10>3.0.co;2-3.

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Escobar Arrieta, Sandra Noemí, Verónica Mercedes Cando Brito, Hugo Javier Sánchez-Moreno, Yolanda VerónicaBuenaño Suárez Buenaño Suárez, Jhoana Lamiña Cali, Breidy Lamiña Cali, and Andrea Nataly Donoso Barba. "Prevalence of parasitosis and its influence on the intestinal microbiota of school children from rural communities in the province of Chimborazo, Ecuador." Salud, Ciencia y Tecnología - Serie de Conferencias 2 (December 27, 2023): 836. http://dx.doi.org/10.56294/sctconf2023636.

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Abstract:

Introduction: Parasitosis is an infectious disease that puts the life of patients at risk, with higher prevalence in vulnerable groups, such as the infant population. Objective: For this reason, the present research aims to indicate the influence of parasites in the intestinal microbiota of Ecuadorian infants. Methods: The sample population consisted of 264 boys and girls, aged 5 to 10 years, belonging to rural communities of Chimborazo, Ecuador. Stool samples were collected for analysis by the coproparasitic examination technique, and for confirmation of results, 8% of the total samples were analyzed by the Willis flotation concentration method. For the determination of microbiota, massively parallel NGS sequencing was performed, and statistical analysis was performed by chi-square to determine risk factors.Results: The prevalence of parasitosis in children was 44.32%, the most prevalent species being: Entamoeba coli (58.86%), Entamoeba histolytica (17.72%), and Giardia lamblia (10.13%). The presence of Trichuris trichiura eggs was identified by the Willis flotation method. The risk factors for intestinal parasitosis in the study population were: contact with pets, decay in the sanitary service infrastructure, lack of hygienic habits and garbage collection. The most prevalent bacterial population of the intestinal microbiota are: Prevotellaceae (55%), Proteobacteria (47%), Firmicutes (27%), and Treponema (17%). Conclusion: There is a significant relationship between predisposing factors and intestinal parasitosis, and it directly affects intestinal symbiosis.

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Journal articles on the topic 'Symbiose intestinale'

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