Human microbiota. Friend? Enemy? Neighbors?

2021 ◽  
Author(s):  
G. V. Zaychenko ◽  
N. O. Karpenko ◽  
T. B. Ravshanov
Keyword(s):  
Pathogenic Bacteria ◽  
Positive Impact ◽  
Inflammatory Diseases ◽  
Eradication Therapy ◽  
Intestinal Barrier ◽  
Intestinal Microbiome ◽  
Intestinal Epithelial ◽  
Epithelial Regeneration ◽  
Normal Microflora

The review is dedicated to the modern ideas about the composition of the human intestinal microbiome, factors that determine the bacterial «landscape» and affect its activity. The main functions of normal microflora have been described, including intestinal motility, protection of intestinal barrier against pathogenic bacteria, parasites, intestinal epithelial regeneration, metabolic and immunological functions, participation in digestive processes, synthesis of amino acids and proteins, antibiotics, vitamins, hormonally active substances, promoting the absorption of minerals and nutrients, preventing the development of pathological conditions. Determination of intestinal microbiota expression of the innate immune system explains the role of microflora in chronic inflammation and diseases such as liver fibrosis, metabolic syndrome, type 2 diabetes mellitus, atherosclerosis, cardiovascular, neurodegeneration and cancer. A promising way is the use of microorganisms with beneficial properties (probiotics), the necessary substrate for them (prebiotics), their metabolites (metabiotics) and complexes of pro‑ and prebiotics (synbiotics) not only to restore and regulate the intestinal microflora, but also as therapeutic agents in some diseases, in particular during eradication therapy of the bacterium Helicobacter pylori. The functions of some species and strains of beneficial bacteria have being discussed, in particular the strain Bacillus causii UBBC‑07, as well as the results of preclinical and clinical trials of its use at antibiotic‑associated diarrhea in the inhibition of Clostridium difficile. The issues of safety and facts of positive impact on human health of probiotic products of Probeez line (Organosyn Ltd.) are considered, which differ in the personification of appointments to certain segments of the population: Probeez®, Probeez® Femina, Probeez® Kids, Probeez® DUO and Probeez® Immuno contain successfully selected live probiotic bacteria. The available range of monocomponent (Probeez® with Kids, Probeez® DUO), multicomponent (Probeez®, Probeez® Femina) and synbiotic (Probeez® Immuno) products allows to choose the best option in specific conditions for their application not only in inflammatory diseases of the gastrointestinal tract, but also in chronic disorders of other systems and organs.  

scholarly journals Arctigenin fromFructus Arctii(Seed of Burdock) Reinforces Intestinal Barrier Function in Caco-2 Cell Monolayers

2015 ◽  
Vol 2015 ◽  
pp. 1-7 ◽  
Author(s):  
Hee Soon Shin ◽  
Sun Young Jung ◽  
Su Yeon Back ◽  
Jeong-Ryong Do ◽  
Dong-Hwa Shon
Keyword(s):  
Barrier Function ◽  
Active Component ◽  
Inflammatory Diseases ◽  
Intestinal Barrier ◽  
Transepithelial Electrical Resistance ◽  
Intestinal Barrier Function ◽  
Intestinal Epithelial ◽  
Traditional Herbal Medicine ◽  
Cell Monolayers ◽  
Basolateral Side

Fructus Arctiiis used as a traditional herbal medicine to treat inflammatory diseases in oriental countries. This study aimed to investigate effect ofF. Arctiiextract on intestinal barrier function in human intestinal epithelial Caco-2 cells and to reveal the active component ofF. Arctii. We measured transepithelial electrical resistance (TEER) value (as an index of barrier function) and ovalbumin (OVA) permeation (as an index of permeability) to observe the changes of intestinal barrier function. The treatment ofF. Arctiiincreased TEER value and decreased OVA influx on Caco-2 cell monolayers. Furthermore, we found that arctigenin as an active component ofF. Arctiiincreased TEER value and reduced permeability of OVA from apical to the basolateral side but not arctiin. In the present study, we revealed thatF. Arctiicould enhance intestinal barrier function, and its active component was an arctigenin on the functionality. We expect that the arctigenin fromF. Arctiicould contribute to prevention of inflammatory, allergic, and infectious diseases by reinforcing intestinal barrier function.

scholarly journals Curcumin and Intestinal Inflammatory Diseases: Molecular Mechanisms of Protection

2019 ◽  
Vol 20 (8) ◽  
pp. 1912 ◽  
Author(s):  
Kathryn Burge ◽  
Aarthi Gunasekaran ◽  
Jeffrey Eckert ◽  
Hala Chaaban
Keyword(s):  
Molecular Mechanisms ◽  
Intestinal Inflammation ◽  
Inflammatory Diseases ◽  
Intestinal Barrier ◽  
Immunological Response ◽  
Intestinal Microbiome ◽  
Intestinal Barrier Function ◽  
Dietary Antigens ◽  
Inflammatory Bowel ◽  
Intestinal Inflammatory Disease

Intestinal inflammatory diseases, such as Crohn’s disease, ulcerative colitis, and necrotizing enterocolitis, are becoming increasingly prevalent. While knowledge of the pathogenesis of these related diseases is currently incomplete, each of these conditions is thought to involve a dysfunctional, or overstated, host immunological response to both bacteria and dietary antigens, resulting in unchecked intestinal inflammation and, often, alterations in the intestinal microbiome. This inflammation can result in an impaired intestinal barrier allowing for bacterial translocation, potentially resulting in systemic inflammation and, in severe cases, sepsis. Chronic inflammation of this nature, in the case of inflammatory bowel disease, can even spur cancer growth in the longer-term. Recent research has indicated certain natural products with anti-inflammatory properties, such as curcumin, can help tame the inflammation involved in intestinal inflammatory diseases, thus improving intestinal barrier function, and potentially, clinical outcomes. In this review, we explore the potential therapeutic properties of curcumin on intestinal inflammatory diseases, including its antimicrobial and immunomodulatory properties, as well as its potential to alter the intestinal microbiome. Curcumin may play a significant role in intestinal inflammatory disease treatment in the future, particularly as an adjuvant therapy.

scholarly journals Regnase-1 controls colon epithelial regeneration via regulation of mTOR and purine metabolism

2018 ◽  
Vol 115 (43) ◽  
pp. 11036-11041 ◽  
Author(s):  
Yasuharu Nagahama ◽  
Mayuko Shimoda ◽  
Guoliang Mao ◽  
Shailendra Kumar Singh ◽  
Yuuki Kozakai ◽  
...  
Keyword(s):  
Acute Inflammation ◽  
Intestinal Inflammation ◽  
Intestinal Barrier ◽  
Body Weight Loss ◽  
Purine Metabolism ◽  
Intestinal Epithelial ◽  
Beneficial Effects ◽  
Epithelial Regeneration ◽  
Mtorc1 Signaling ◽  
Inflammatory Bowel

Damage to intestinal epithelial cell (IEC) layers during intestinal inflammation is associated with inflammatory bowel disease. Here we show that the endoribonuclease Regnase-1 controls colon epithelial regeneration by regulating protein kinase mTOR (the mechanistic target of rapamycin kinase) and purine metabolism. During dextran sulfate sodium-induced intestinal epithelial injury and acute colitis, Regnase-1∆IEC mice, which lack Regnase-1 specifically in the intestinal epithelium, were resistant to body weight loss, maintained an intact intestinal barrier, and showed increased cell proliferation and decreased epithelial apoptosis. Chronic colitis and tumor progression were also attenuated in Regnase-1∆IEC mice. Regnase-1 predominantly regulates mTORC1 signaling. Metabolic analysis revealed that Regnase-1 participates in purine metabolism and energy metabolism during inflammation. Furthermore, increased expression of ectonucleotidases contributed to the resolution of acute inflammation in Regnase-1∆IEC mice. These findings provide evidence that Regnase-1 deficiency has beneficial effects on the prevention and/or blocking of intestinal inflammatory disorders.

scholarly journals Kaempferol Alleviates Murine Experimental Colitis by Restoring Gut Microbiota and Inhibiting the LPS-TLR4-NF-κB Axis

2021 ◽  
Vol 12 ◽  
Author(s):  
Yifan Qu ◽  
Xinyi Li ◽  
Fengying Xu ◽  
Shimin Zhao ◽  
Xuemei Wu ◽  
...  
Keyword(s):  
Gut Microbiota ◽  
Fecal Microbiota Transplantation ◽  
Inflammatory Diseases ◽  
Intestinal Barrier ◽  
Fluorescein Isothiocyanate ◽  
Experimental Colitis ◽  
Intestinal Microbiome ◽  
Attractive Alternative ◽  
Protective Effects ◽  
Linear Discriminant

Intestinal microbiota dysbiosis is an established characteristic of ulcerative colitis (UC). Regulating the gut microbiota is an attractive alternative UC treatment strategy, considering the potential adverse effects of synthetic drugs used to treat UC. Kaempferol (Kae) is an anti-inflammatory and antioxidant flavonoid derived from a variety of medicinal plants. In this study, we determined the efficacy and mechanism of action of Kae as an anti-UC agent in dextran sulfate sodium (DSS)-induced colitis mice. DSS challenge in a mouse model of UC led to weight loss, diarrhea accompanied by mucous and blood, histological abnormalities, and shortening of the colon, all of which were significantly alleviated by pretreatment with Kae. In addition, intestinal permeability was shown to improve using fluorescein isothiocyanate (FITC)–dextran administration. DSS-induced destruction of the intestinal barrier was also significantly prevented by Kae administration via increases in the levels of ZO-1, occludin, and claudin-1. Furthermore, Kae pretreatment decreased the levels of IL-1β, IL-6, and TNF-α and downregulated transcription of an array of inflammatory signaling molecules, while it increased IL-10 mRNA expression. Notably, Kae reshaped the intestinal microbiome by elevating the Firmicutes to Bacteroidetes ratio; increasing the linear discriminant analysis scores of beneficial bacteria, such as Prevotellaceae and Ruminococcaceae; and reducing the richness of Proteobacteria in DSS-challenged mice. There was also an evident shift in the profile of fecal metabolites in the Kae treatment group. Serum LPS levels and downstream TLR4-NF-κB signaling were downregulated by Kae supplementation. Moreover, fecal microbiota transplantation from Kae-treated mice to the DSS-induced mice confirmed the effects of Kae on modulating the gut microbiota to alleviate UC. Therefore, Kae may exert protective effects against colitis mice through regulating the gut microbiota and TLR4-related signaling pathways. This study demonstrates the anti-UC effects of Kae and its potential therapeutic mechanisms, and offers novel insights into the prevention of inflammatory diseases using natural products.

The importance of prebiotics in the regulation of metabolic syndrome disorders

2021 ◽  
Author(s):  
O. S. Nyankovska ◽  
S. L. Nyankovskyy ◽  
M. S. Yatsula ◽  
M. I. Horodylovska
Keyword(s):  
Metabolic Syndrome ◽  
Well Being ◽  
Short Chain Fatty Acids ◽  
Intestinal Microbiome ◽  
Intestinal Epithelial ◽  
Beneficial Effects ◽  
Interleukin 22 ◽  
Positive Effects ◽  
Normal Microflora ◽  
Good Nutrition

The products of functional foods differ from other meals by their ability to improve health and well‑being or to reduce the risk of diseases and not only to provide the good nutrition. The composition of such products includes oligosaccharides of the fructan type such as inulin. Inulin is a soluble dietary fiber, consisting of a group of natural polysaccharides that are not digested in the intestine and instead fermented into short‑chain fatty acids associated with multiple metabolic processes, including glucose homeostasis and insulin resistance. Besides, inulin affects the lipid exchange regulation and improvement of lipid profile. Inulin is a mixture of linear fructose polymers or fructans with 2 — 60 units, each of them is connected by unique β (2‑1) bonds with a glucose unit. In contrary to typical carbohydrate, these β (2‑1) connections cannot be hydrolyzed by enzymes of saliva or pancreas, that’s why inulin has a reduced energetic value as well as dietary prebiotic effects.Functional food is an important component of the change in the lifestyle to control obesity and related risks for health. Obesity and dyslipidemia are important aspects of metabolic syndrome, associated with changes in the gut microbiome. The most important direction in the modern preventive and therapeutic medicine presents the use of prebiotics, that provide positive effects on the normal microflora and cause a whole cascade of secondary beneficial effects for humans (metabolic, anticarcinogenic, immunostimulating, antitoxic, etc.). Prebiotic Inulin promotes the restoration of intestinal microbiome by means of increasing production of intestinal epithelial cells and recovering interleukin‑22 expression.On the domestic market inulin presented as an Inulin‑NEO preparation, available in a form of tablets and sachet, which makes it easy to use.

scholarly journals Apoptosis, Necrosis, and Necroptosis in the Gut and Intestinal Homeostasis

2015 ◽  
Vol 2015 ◽  
pp. 1-10 ◽  
Author(s):  
Anna Negroni ◽  
Salvatore Cucchiara ◽  
Laura Stronati
Keyword(s):  
Cell Death ◽  
Immune Responses ◽  
Intestinal Epithelial Cells ◽  
Inflammatory Diseases ◽  
Intestinal Barrier ◽  
Intestinal Lumen ◽  
Intestinal Epithelial ◽  
Commensal Microbiota ◽  
Adaptive Immune ◽  
Epithelial Cell Death

Intestinal epithelial cells (IECs) form a physiochemical barrier that separates the intestinal lumen from the host’s internal milieu and is critical for electrolyte passage, nutrient absorption, and interaction with commensal microbiota. Moreover, IECs are strongly involved in the intestinal mucosal inflammatory response as well as in mucosal innate and adaptive immune responses. Cell death in the intestinal barrier is finely controlled, since alterations may lead to severe disorders, including inflammatory diseases. The emerging picture indicates that intestinal epithelial cell death is strictly related to the maintenance of tissue homeostasis. This review is focused on previous reports on different forms of cell death in intestinal epithelium.

scholarly journals Bacillus thuringiensistargets the host intestinal epithelial junctions for successful infection ofCaenorhabditis elegans

2018 ◽  
Author(s):  
Liting Wan ◽  
Jian Lin ◽  
Hongwen Du ◽  
Alejandra Bravo ◽  
Mario Soberón ◽  
...  
Keyword(s):  
Virulence Factors ◽  
Pathogenic Bacteria ◽  
Intestinal Barrier ◽  
Infection Process ◽  
Intestinal Epithelial ◽  
Cry Toxins ◽  
Early Stages ◽  
Successful Infection ◽  
Epithelial Junctions ◽  
Sporulation Phase

ABSTRACTPathogenic bacteria use different strategies to infect their hosts including the simultaneous production of pore forming toxins and several virulence factors that help to synergize their pathogenic effects. However, how the pathogenic bacteria are able to complete their life cycle and break out the host intestinal barrier is poorly understood. The infectious cycle ofBacillus thuringiensis(Bt) bacterium inCaenorhabditis elegansis a powerful model system to study the early stages of the infection process. Bt produces Cry pore-forming toxins during the sporulation phase that are key virulence factors involved in Bt pathogenesis. Here we show that during the early stages of infection, the Cry toxins disrupt the midgut epithelial tissue allowing the germination of spores. The vegetative Bt cells then trigger a quorum sensing response that is activated by PlcR regulator resulting in production of different virulence factors, such as the metalloproteinases ColB and Bmp1, that besides Cry toxins are necessary to disrupt the nematode epithelial junctions causing efficient bacterial host infection and dead of the nematode. Overall our work describes a novel mechanism for Bt infection, targeting the epithelial junctions of its host midgut cells.Author summaryThe entomopathogenic bacteriaBacillus thuringiensis(Bt) are used worldwide as biopesticides due to their insecticidal properties. Crystal proteins (Cry) produced by Bt during the sporulation phase of growth are mainly responsible for their insecticidal properties. The infection process of Bt includes three successive steps, virulence, necrotrophic, and sporulation processes. During the virulence process, after ingestion by the susceptible hosts, the Cry toxins form pores in the apical membrane of intestinal cells, inducing favorable conditions for bacterial spore germination. Vegetative bacteria multiply in the host and coordinate their behavior by using the quorum sensor regulator PlcR, which leads to the production of virulence factors allowing the bacteria to kill the host. However, how the bacteria are able to disrupt the host intestinal barrier during the early stages of infection remains unknown. Here we show that Bt employs the nematicidal Cry toxins and additional virulence factors controlled by the PlcR regulon to disrupt the intestinal epithelial junctions ofC. elegansat the early stages of infection allowing that Bt bacteria complete its life cycle in the worms. Our work provides new insights into the pathogenesis of Bt, and highlights the importance of breaking down host epithelial junctions for a successful infection, a similar mechanism could be used by other pathogens-host interactions since epithelial junctions are conserved structures from insects to mammals.

scholarly journals IKKα controls ATG16L1 degradation to prevent ER stress during inflammation

2017 ◽  
Vol 214 (2) ◽  
pp. 423-437 ◽  
Author(s):  
Michaela A. Diamanti ◽  
Jalaj Gupta ◽  
Moritz Bennecke ◽  
Tiago De Oliveira ◽  
Mallika Ramakrishnan ◽  
...  
Keyword(s):  
Intestinal Inflammation ◽  
Inflammatory Diseases ◽  
Intestinal Epithelial ◽  
Unfolded Protein ◽  
Epithelial Regeneration ◽  
Iκb Kinase ◽  
Bowel Diseases ◽  
Inflammatory Bowel ◽  
Protein Response ◽  
Oligomerization Domain

Inhibition of the IκB kinase complex (IKK) has been implicated in the therapy of several chronic inflammatory diseases including inflammatory bowel diseases. In this study, using mice with an inactivatable IKKα kinase (IkkαAA/AA), we show that loss of IKKα function markedly impairs epithelial regeneration in a model of acute colitis. Mechanistically, this is caused by compromised secretion of cytoprotective IL-18 from IKKα-mutant intestinal epithelial cells because of elevated caspase 12 activation during an enhanced unfolded protein response (UPR). Induction of the UPR is linked to decreased ATG16L1 stabilization in IkkαAA/AA mice. We demonstrate that both TNF-R and nucleotide-binding oligomerization domain stimulation promote ATG16L1 stabilization via IKKα-dependent phosphorylation of ATG16L1 at Ser278. Thus, we propose IKKα as a central mediator sensing both cytokine and microbial stimulation to suppress endoplasmic reticulum stress, thereby assuring antiinflammatory function during acute intestinal inflammation.

Iron and Malaria: Absorption, Efficacy and Safety

2010 ◽  
Vol 80 (45) ◽  
pp. 279-292 ◽  
Author(s):  
Richard Hurrell
Keyword(s):  
Pathogenic Bacteria ◽  
Intestinal Barrier ◽  
Systemic Circulation ◽  
Malarial Parasite ◽  
Asymptomatic Malaria ◽  
Iron Supplements ◽  
Fortified Food ◽  
Care Giving ◽  
Single Meal ◽  
Women And Children

Febrile malaria and asymptomatic malaria parasitemia substantially decrease iron absorption in single-meal, stable isotope studies in women and children, but to date there is no evidence of decreased efficacy of iron-fortified foods in malaria-endemic regions. Without inadequate malarial surveillance or health care, giving iron supplements to children in areas of high transmission could increase morbidity and mortality. The most likely explanation is the appearance of non-transferrin-bound iron (NTBI) in the plasma. NTBI forms when the rate of iron influx into the plasma exceeds the rate of iron binding to transferrin. Two studies in women have reported substantially increased NTBI with the ingestion of iron supplements. Our studies confirm this, but found no significant increase in NTBI on consumption of iron-fortified food. It seems likely that the malarial parasite in hepatocytes can utilize NTBI, but it cannot do so in infected erythrocytes. NTBI however may increase the sequestration of parasite-infected erythrocytes in capillaries. Bacteremia is common in children with severe malaria and sequestration in villi capillaries could lead to a breaching of the intestinal barrier, allowing the passage of pathogenic bacteria into the systemic circulation. This is especially important as frequent high iron doses increase the number of pathogens in the intestine at the expense of the barrier bacteria.

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