scholarly journals Mechanisms of maintenance of intestinal homeostasis by autochthonic microbiota and probiotics

2016 ◽  
Vol 72 (10) ◽  
pp. 611-615 ◽  
Author(s):  
Marian Binek ◽  
Magdalena Kizerwetter-Świda ◽  
Agata Anna Cisek ◽  
Magdalena Rzewuska ◽  
Dorota Chrobak-Chmiel ◽  
...  
Keyword(s):  
Intestinal Microbiota ◽  
Competitive Exclusion ◽  
Inflammatory Responses ◽  
Critical Role ◽  
Probiotic Bacteria ◽  
Secretory Iga ◽  
Epithelial Barrier Function ◽  
Intestinal Microbes ◽  
Innate Defense ◽  
Pathogen Colonization

Intestinal microbes are taxonomically diverse and constitute an ecologically dynamic microbiom interactively performing various physiological and physiopathological processes. It has been proposed that normal intestinal microbiotas play a critical role in the host’s metabolic homeostasis and immune tolerance. The modulation of intestinal microbiota populations by prebiotics, probiotics, and synbiotics may be beneficial for the host’s health. Under certain conditions, the intestinal microbiota and the host’s homeostasis can be restored by introducing bacteria that co-mediate anti-inflammatory responses. Commensal microbes and probiotics exert their beneficial effect by at least three mechanisms. These include - the maintenance of the epithelial barrier function and the attenuation of changes in intestinal permeability through effects on tight junction, decreasing paracellular permeability, providing innate defense against pathogens, and enhancing the physical impediment of the mucous layer, - competitive exclusion by the application of probiotic bacteria stabilizing the indigenous microflora, - immunomodulatory capacity, affecting a variety of signaling pathways with modulation of proper immune, inflammatory and allergic responses. The epithelial gut barrier faces important challenges, since its function is to prevent pathogens and harmful elements of the gut lumen from penetrating into the internal environment. Competitive exclusion treatment can increase resistance to pathogen colonization and control intestinal disturbance. The dominance of symbiotic and probiotic bacteria among the gut microbiota favors a tolerogenic immune response. The release of secretory IgA stabilizes tight junctions between cells of the epithelial layer as well as hampers pathogens and symbionts invading deeper layers. The understanding of these vital processes may help to protect the host against infection, prevent chronic inflammation, and maintain mucosal integrity.

scholarly journals Relative Effects of Dietary Administration of a Competitive Exclusion Culture and a Synbiotic Product, Age and Sampling Site on Intestinal Microbiota Maturation in Broiler Chickens

2021 ◽  
Vol 8 (9) ◽  
pp. 187
Author(s):  
Nikoletta Such ◽  
Valéria Farkas ◽  
Gábor Csitári ◽  
László Pál ◽  
Aliz Márton ◽  
...  
Keyword(s):  
Intestinal Microbiota ◽  
Broiler Chickens ◽  
Competitive Exclusion ◽  
Sampling Site ◽  
Probiotic Bacteria ◽  
Production Traits ◽  
Ileal Mucosa ◽  
Genus Lactobacillus ◽  
Continuous Feeding ◽  
Dietary Treatments

In this research, the effects of early post-hatch inoculation of a competitive exclusion product (Br) and the continuous feeding of a synbiotic supplement (Sy) containing probiotic bacteria, yeast, and inulin on the production traits and composition of ileal chymus (IC), ileal mucosa (IM), and caecal chymus (CC) microbiota of broiler chickens were evaluated. The dietary treatments had no significant effects on the pattern of intestinal microbiota or production traits. The digestive tract bacteriota composition was affected mostly by the sampling place and age of birds. The dominant family of IC was Lactobacillaceae, without change with the age. The abundance of the two other major families, Enterococcaceae and Lachnospiraceae decreased with the age of birds. In the IM, Clostridiaceae was the main family in the first three weeks. Its ratio decreased later and Lactobacillaceae became the dominant family. In the CC, Ruminococcaceae and Lachnospiraceae were the main families with decreasing tendency in the age. In IC, Br treatment decreased the abundance of genus Lactobacillus, and both Br and Sy increased the ratio of Enterococcus at day 7. In all gut segments, a negative correlation was found between the IBD antibody titer levels and the ratio of genus Leuconostoc in the first three weeks, and a positive correlation was found in the case of Bifidobacterium, Rombutsia, and Turicibacter between day 21 and 40.

scholarly journals A35 MICROBIAL PROTEOLYTIC SIGNATURE IN ULCERATIVE COLITIS INDUCES AN INFLAMMATORY SIGNATURE IN MICROBIOTA-HUMANIZED MICE

2020 ◽  
Vol 3 (Supplement_1) ◽  
pp. 42-43
Author(s):  
H J Galipeau ◽  
W Turpin ◽  
A Caminero Fernandez ◽  
A Santiago ◽  
J Libertucci ◽  
...  
Keyword(s):  
Ulcerative Colitis ◽  
At Risk ◽  
Proteolytic Activity ◽  
Intestinal Microbiota ◽  
Inflammatory Responses ◽  
Critical Role ◽  
Low Grade ◽  
Polymorphonuclear Cells ◽  
Fecal Samples ◽  
Patients At Risk

Abstract Background Altered gut microbiota composition has been associated with inflammatory bowel diseases (IBD) including ulcerative colitis (UC), but causality and bacterially-driven mechanisms, are unclear. Proteases within the gastrointestinal tract play a critical role in maintaining homeostasis and are tightly regulated by anti-proteases. Host-derived proteolytic imbalances have been described in IBD, including UC, however, the role of intestinal microbiota as a source of proteases and anti-proteases has largely been ignored. Aims To study microbial proteolytic activity and intestinal microbiota profiles in a cohort of individuals at-risk for IBD, and in those individuals that develop UC at follow-up. Methods Fecal samples were collected from healthy individuals at-risk for IBD and who went on to develop UC (pre-UC; n=14) and again after UC diagnosis (post-UC, n=10). Fecal samples from matched at-risk individuals that did not develop UC were used as healthy controls (n=52). Overall fecal proteolytic and elastolytic activity was measured. We performed metagenomics sequencing in 4 UC subjects (pre and post) and 4 matched HC using Illumina Hi-Seq from stool DNA. To investigate bacterial origin and functional significance, pregnant germ-free (GF) mice were colonized with a fecal sample from a selected UC subject (pre and post) and a matched HC. Naturally colonized litters were followed for 12 weeks, after which proteolytic activities and signs of inflammation were measured. Results Fecal proteolytic and elastase activity was increased in pre- and post-UC samples compared to HCs. Metagenomics revealed over 20k genes were significantly different between HC and pre-UC samples, and of these, 440 related to proteases and peptidases. Increased fecal proteolytic activity, higher lipocalin levels, and increased colonic polymorphonuclear cells in colonic H&E sections was observed in pre- and post-UC colonized mice compared to HC colonized mice. Mice colonized with pre-UC microbiota showed increased mRNA expression of genes linked to immunological disease, antimicrobial and inflammatory responses (ie. Tlr2, Tlr5, Nod2, and Il1b) as compared to HC colonized mice. Conclusions These results suggest increased fecal proteolytic activity is observed prior to the onset and clinical diagnosis of UC in patients at-risk for IBD, and upon transfer to mice born from colonized GF dams, low-grade inflammation develops. These pathways could be developed as novel non-invasive biomarkers to monitor at-risk populations. Submitted on behalf of the CCC-GEM Project consortium. Supported by CCC GIA to EF Verdu Funding Agencies CCC

scholarly journals Intestinal microbiota as part of normal physiology of the host

2016 ◽  
Vol 72 (9) ◽  
pp. 536-541
Author(s):  
Marian Binek ◽  
Magdalena Rzewuska ◽  
Magdalena Kizerwetter-Świda ◽  
Dorota Chrobak-Chmiel ◽  
Małgorzata Gieryńska ◽  
...  
Keyword(s):  
Microbial Community ◽  
Pathogenic Bacteria ◽  
Inflammatory Responses ◽  
Intestinal Barrier ◽  
Well Being ◽  
Secretory Iga ◽  
Lectin Receptors ◽  
Epithelial Barrier Function ◽  
Susceptibility To Infection ◽  
Peptide Secretion

The gastrointestinal tract in humans and animals contains a very large number of highly diverse microorganisms. This microbiota plays a major role in the host’s physiology, homeostasis, and well-being. It forms a barrier against infection, helps to develop and mature the immune system, and participates in the extraction of nutrients and energy from food. Various members of microbial community maintain the integrity of the intestinal barrier and promote epithelial repair after injury. The intestinal barrier defenses consist of the mucous layer, antimicrobial peptides, secretory IgA, and the epithelial barrier function by junctional adhesion complex. A healthy host exists in a state of balance with its microorganisms. A disruption of the microbial community increases the host’s susceptibility to infection. Although the immune response is necessary for the host to eliminate the invading pathogen, certain aspects of the host’s response may work to the pathogen’s advantage. Certain components of the microbiota have been shown to drive inflammatory response, which, if uncontrolled, has the potential to induce a pathological response, whereas others enhance or promote anti-inflammatory responses. The effector microbial molecules are usually detected via receptor-signaling pathways including Toll-like receptors, NOD-like receptors, and C-type lectin receptors. These pattern-recognition receptors (PRRs) interact with and identify microbe-associated molecular patterns (MAMPs) of both commensal and pathogenic bacteria. PRRs signaling, once thought to exclusively yield pro-inflammatory activation by pathogenic bacteria, is now known to be differentially activated by commensal and probiotic bacteria to induce pathways involved in gut homeostasis, cytoprotection, epithelial cell proliferation, regulation of tight junctions, and antimicrobial peptide secretion. The microbial-epithelial cross-talk is fundamental in appreciating how the developing intestine achieves tolerance to bacteria and how dysregulation of this process may predispose the gut to inflammation and disease.

Chicken intestinal microbiota function with a special emphasis on the role of probiotic bacteria

2014 ◽  
Vol 17 (2) ◽  
pp. 385-394 ◽  
Author(s):  
A.A. Cisek ◽  
M. Binek
Keyword(s):  
Intestinal Microbiota ◽  
Broiler Chickens ◽  
Bacterial Colonization ◽  
Well Being ◽  
Nutrient Utilization ◽  
Probiotic Bacteria ◽  
Gut Health ◽  
Intestinal Microbes ◽  
Beneficial Effects ◽  
Metabolic Functions

AbstractBacterial colonization of the chicken gut by environmental microbes begins immediately after hatching. Composition of the intestinal microbiota is dependent on the surrounding environment, diet variation, pathological conditions, antibiotic therapy, and others. The genomes of all these intestinal microbes form a microbiome which by far outnumbers the host’s genome. As a consequence, the microbiome provides additional metabolic functions to the host, including nutrient utilization and absorption, fermentation of non-digestible dietary fiber, synthesis of some vitamins, biotransformation of bile acids, and the well-being of their chicken host. Microorganisms can also directly interact with the lining of the gastrointestinal tract, which may alter the physiology and immunological status of the bird. Since newly hatched broiler chickens demonstrate delayed commensal colonization and low bacterial diversity, the most effective and harmless method available to control the development and composition of the intestinal microbiota is a competitive exclusion treatment by applying probiotic bacteria. Additionally, recent research has shown that probiotic bacteria have a variety of beneficial effects, including counteraction of dysbiosis, promotion of gut health and homeostasis, enhancement of immune defenses and antagonization of infectious agents

scholarly journals Histatin-1 Attenuates LPS-Induced Inflammatory Signaling in RAW264.7 Macrophages

2021 ◽  
Vol 22 (15) ◽  
pp. 7856
Author(s):  
Sang Min Lee ◽  
Kyung-No Son ◽  
Dhara Shah ◽  
Marwan Ali ◽  
Arun Balasubramaniam ◽  
...  
Keyword(s):  
Molecular Mechanisms ◽  
Cytokine Production ◽  
Inflammatory Responses ◽  
Critical Role ◽  
Mapk Signaling ◽  
Response To Treatment ◽  
No Production ◽  
Inflammatory Signaling ◽  
Raw264.7 Macrophages ◽  
Inflammatory Mediator Production

Macrophages play a critical role in the inflammatory response to environmental triggers, such as lipopolysaccharide (LPS). Inflammatory signaling through macrophages and the innate immune system are increasingly recognized as important contributors to multiple acute and chronic disease processes. Nitric oxide (NO) is a free radical that plays an important role in immune and inflammatory responses as an important intercellular messenger. In addition, NO has an important role in inflammatory responses in mucosal environments such as the ocular surface. Histatin peptides are well-established antimicrobial and wound healing agents. These peptides are important in multiple biological systems, playing roles in responses to the environment and immunomodulation. Given the importance of macrophages in responses to environmental triggers and pathogens, we investigated the effect of histatin-1 (Hst1) on LPS-induced inflammatory responses and the underlying molecular mechanisms in RAW264.7 (RAW) macrophages. LPS-induced inflammatory signaling, NO production and cytokine production in macrophages were tested in response to treatment with Hst1. Hst1 application significantly reduced LPS-induced NO production, inflammatory cytokine production, and inflammatory signaling through the JNK and NF-kB pathways in RAW cells. These results demonstrate that Hst1 can inhibit LPS-induced inflammatory mediator production and MAPK signaling pathways in macrophages.

scholarly journals Reversal of the Inflammatory Responses in Fabry Patient iPSC-Derived Cardiovascular Endothelial Cells by CRISPR/Cas9-Corrected Mutation

2021 ◽  
Vol 22 (5) ◽  
pp. 2381
Author(s):  
Hui-Yung Song ◽  
Yi-Ping Yang ◽  
Yueh Chien ◽  
Wei-Yi Lai ◽  
Yi-Ying Lin ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Inflammatory Responses ◽  
Late Onset ◽  
Critical Role ◽  
Vascular Complications ◽  
Digital Pcr ◽  
Mapk Signaling ◽  
Autophagic Flux ◽  
Fabry Patient ◽  
Genomic Editing

The late-onset type of Fabry disease (FD) with GLA IVS4 + 919G > A mutation has been shown to lead to cardiovascular dysfunctions. In order to eliminate variations in other aspects of the genetic background, we established the isogenic control of induced pluripotent stem cells (iPSCs) for the identification of the pathogenetic factors for FD phenotypes through CRISPR/Cas9 genomic editing. We adopted droplet digital PCR (ddPCR) to efficiently capture mutational events, thus enabling isolation of the corrected FD from FD-iPSCs. Both of these exhibited the characteristics of pluripotency and phenotypic plasticity, and they can be differentiated into endothelial cells (ECs). We demonstrated the phenotypic abnormalities in FD iPSC-derived ECs (FD-ECs), including intracellular Gb3 accumulation, autophagic flux impairment, and reactive oxygen species (ROS) production, and these abnormalities were rescued in isogenic control iPSC-derived ECs (corrected FD-ECs). Microarray profiling revealed that corrected FD-derived endothelial cells reversed the enrichment of genes in the pro-inflammatory pathway and validated the downregulation of NF-κB and the MAPK signaling pathway. Our findings highlighted the critical role of ECs in FD-associated vascular dysfunctions by establishing a reliable isogenic control and providing information on potential cellular targets to reduce the morbidity and mortality of FD patients with vascular complications.

scholarly journals Signaling pathways in intestinal homeostasis and colorectal cancer: KRAS at centre stage

2021 ◽  
Vol 19 (1) ◽  
Author(s):  
Camille Ternet ◽  
Christina Kiel
Keyword(s):  
Colorectal Cancer ◽  
Signaling Pathways ◽  
Intestinal Microbiota ◽  
Critical Role ◽  
Neuroendocrine Cells ◽  
Cell Junction ◽  
Intestinal Cell ◽  
Intestinal Homeostasis ◽  
Cell Functions ◽  
The Impact

AbstractThe intestinal epithelium acts as a physical barrier that separates the intestinal microbiota from the host and is critical for preserving intestinal homeostasis. The barrier is formed by tightly linked intestinal epithelial cells (IECs) (i.e. enterocytes, goblet cells, neuroendocrine cells, tuft cells, Paneth cells, and M cells), which constantly self-renew and shed. IECs also communicate with microbiota, coordinate innate and adaptive effector cell functions. In this review, we summarize the signaling pathways contributing to intestinal cell fates and homeostasis functions. We focus especially on intestinal stem cell proliferation, cell junction formation, remodelling, hypoxia, the impact of intestinal microbiota, the immune system, inflammation, and metabolism. Recognizing the critical role of KRAS mutants in colorectal cancer, we highlight the connections of KRAS signaling pathways in coordinating these functions. Furthermore, we review the impact of KRAS colorectal cancer mutants on pathway rewiring associated with disruption and dysfunction of the normal intestinal homeostasis. Given that KRAS is still considered undruggable and the development of treatments that directly target KRAS are unlikely, we discuss the suitability of targeting pathways downstream of KRAS as well as alterations of cell extrinsic/microenvironmental factors as possible targets for modulating signaling pathways in colorectal cancer.

scholarly journals The Inflammatory Role of Pro-Resolving Mediators in Endometriosis: An Integrative Review

2021 ◽  
Vol 22 (9) ◽  
pp. 4370
Author(s):  
Cássia de Fáveri ◽  
Paula M. Poeta Fermino ◽  
Anna P. Piovezan ◽  
Lia K. Volpato
Keyword(s):  
Intracellular Signaling ◽  
Inflammatory Responses ◽  
Therapeutic Potential ◽  
Critical Role ◽  
Integrative Review ◽  
Inflammatory Factors ◽  
Resolvin D1 ◽  
Endogenous Factors

The pathogenesis of endometriosis is still controversial, although it is known that the inflammatory immune response plays a critical role in this process. The resolution of inflammation is an active process where the activation of endogenous factors allows the host tissue to maintain homeostasis. The mechanisms by which pro-resolving mediators (PRM) act in endometriosis are still little explored. Thus, this integrative review aims to synthesize the available content regarding the role of PRM in endometriosis. Experimental and in vitro studies with Lipoxin A4 demonstrate a potential inhibitory effect on endometrial lesions’ progression, attenuating pro-inflammatory and angiogenic signals, inhibiting proliferative and invasive action suppressing intracellular signaling induced by cytokines and estradiol, mainly through the FPR2/ALX. Investigations with Resolvin D1 demonstrated the inhibition of endometrial lesions and decreased pro-inflammatory factors. Annexin A1 is expressed in the endometrium and is specifically present in women with endometriosis, although the available studies are still inconsistent. Thus, we believe there is a gap in knowledge regarding the PRM pathways in patients with endometriosis. It is important to note that these substances’ therapeutic potential is evident since the immune and abnormal inflammatory responses play an essential role in endometriosis development and progression.

scholarly journals Study of the effect exerted by fructo-oligosaccharides from yacon (Smallanthus sonchifolius) root flour in an intestinal infection model with Salmonella Typhimurium

2012 ◽  
Vol 109 (11) ◽  
pp. 1971-1979 ◽  
Author(s):  
Eva Velez ◽  
Natalia Castillo ◽  
Oscar Mesón ◽  
Alfredo Grau ◽  
María E. Bibas Bonet ◽  
...  
Keyword(s):  
Mouse Model ◽  
Protective Effect ◽  
Salmonella Enteritidis ◽  
Inflammatory Responses ◽  
Intestinal Barrier ◽  
Secretory Iga ◽  
Infection Model ◽  
Enteric Infection ◽  
Smallanthus Sonchifolius ◽  
Iga Production

Beneficial effects of prebiotics like inulin and fructo-oligosaccharides (FOS) have been proven in health and nutrition. Yacon (Smallanthus sonchifolius), an Andean crop, contains FOS (50–70 % of its dry weight) and, therefore, is considered a prebiotic. Commercial FOS can up-regulate total secretory IgA (S-IgA) in infant mice, prevent infection with Salmonella in swine or enhance immune response for Salmonella vaccine in a mouse model. Previously, we found that administration of yacon root flour regulates gut microbiota balance and has immunomodulatory effects without inflammatory responses. The aim of the present paper is to analyse if yacon prevents enteric infection caused by a strain of Salmonella enteritidis serovar Typhimurium (S. Typhimurium) in a mouse model. BALB/c mice were supplemented with yacon flour (45 d), challenged with S. Typhimurium and killed to study pathogen translocation, total and specific IgA production by ELISA, presence of IgA and other cytokines and Toll-like receptor 4 (TLR4) and clustor of differentiation 206 (CD206) receptors positive cells by immunofluorescence and histological changes. Yacon flour administration had a protective effect from 15 to 30 d of treatment. We found a peak of total S-IgA production without translocation of the pathogen for these periods. At 30 d, there was an increase in IL-6 and macrophage inflammatory proteins-1α+ cells and expression of the receptors CD206 and TLR4. Yacon flour did not have incidence in pathogen-specific S-IgA production. Longer periods (45 d) of administration had no protective effect. Therefore, yacon can prevent enteric infection caused by S. Typhimurium when given up to 30 d; this effect would be mediated by enhancing non-specific immunity, such as total S-IgA, that improves the immunological intestinal barrier.

scholarly journals Dysbiosis of intestinal microbiota in early life aggravates high-fat diet induced dysmetabolism in adult mice

2021 ◽  
Vol 21 (1) ◽  
Author(s):  
Z. H. Miao ◽  
W. X. Zhou ◽  
R. Y. Cheng ◽  
H. J. Liang ◽  
F. L. Jiang ◽  
...  
Keyword(s):  
Intestinal Microbiota ◽  
High Fat Diet ◽  
Early Life ◽  
Fasting Blood Glucose ◽  
Fecal Microbiota ◽  
Long Term Effects ◽  
High Fat ◽  
Host Animal ◽  
Intestinal Microbes ◽  
Lipid Metabolism Disorders

Abstract Background Accumulating evidence have shown that the intestinal microbiota plays an important role in prevention of host obesity and metabolism disorders. Recent studies also demonstrate that early life is the key time for the colonization of intestinal microbes in host. However, there are few studies focusing on possible association between intestinal microbiota in the early life and metabolism in adulthood. Therefore the present study was conducted to examine whether the short term antibiotic and/or probiotic exposure in early life could affect intestinal microbes and their possible long term effects on host metabolism. Results A high-fat diet resulted in glucose and lipid metabolism disorders with higher levels of visceral fat rate, insulin-resistance indices, and leptin. Exposure to ceftriaxone in early life aggravated the negative influences of a high-fat diet on mouse physiology. Orally fed TMC3115 protected mice, especially those who had received treatment throughout the whole study, from damage due to a high-fat diet, such as increases in levels of fasting blood glucose and serum levels of insulin, leptin, and IR indices. Exposure to ceftriaxone during the first 2 weeks of life was linked to dysbiosis of the fecal microbiota with a significant decrease in the species richness and diversity. However, the influence of orally fed ceftriaxone on the fecal microbiota was limited to 12 weeks after the termination of treatment. Of note, at week 12 there were still some differences in the composition of intestinal microbiota between mice provided with high fat diet and antibiotic exposure and those only fed a high fat diet. Conclusions These results indicated that exposure to antibiotics, such as ceftriaxone, in early life may aggravate the negative influences of a high-fat diet on the physiology of the host animal. These results also suggest that the crosstalk between the host and their intestinal microbiota in early life may be more important than that in adulthood, even though the same intestinal microbes are present in adulthood.

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