Browse
Submit Data
Databases
API
Help

Dataset Information

7 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Host Protective Mechanisms to Intestinal Amebiasis.

ABSTRACT: The protozoan parasite Entamoeba histolytica is the causative agent of amebiasis, an infection that manifests as colitis and, in some cases, liver abscess. A better understanding of host protective factors is key to developing an effective remedy. Recently, significant advances have been made in understanding the mechanisms of MUC2 production by goblet cells upon amebic infection, regulation of antimicrobial peptide production by Paneth cells, the interaction of commensal microbiota with immune stimulation, and host genetics in conferring protection from amebiasis. In addition to host pathways that may serve as potential therapeutic targets, significant progress has also been made with respect to development of a vaccine against amebiasis. Here, we aim to highlight the current understanding and knowledge gaps critically.

SUBMITTER: Uddin MJ

PROVIDER: S-EPMC7840892 | biostudies-literature | 2021 Feb

REPOSITORIES: biostudies-literature

ACCESS DATA

Json Xml

Publications

Host Protective Mechanisms to Intestinal Amebiasis.

Uddin Md Jashim MJ Leslie Jhansi L JL Petri William A WA

Trends in parasitology 20201023 2

The protozoan parasite Entamoeba histolytica is the causative agent of amebiasis, an infection that manifests as colitis and, in some cases, liver abscess. A better understanding of host protective factors is key to developing an effective remedy. Recently, significant advances have been made in understanding the mechanisms of MUC2 production by goblet cells upon amebic infection, regulation of antimicrobial peptide production by Paneth cells, the interaction of commensal microbiota with immune ...[more]

PMID: 33502317

Similar Datasets

Intestinal amebiasis: a concerning cause of acute gastroenteritis among hospitalized lebanese children.

Project description:BackgroundIntestinal amebiasis is an important public health problem worldwide. More severe disease is associated with young age, malnutrition and immunosuppression.AimThe aim of this study is to evaluate the prevalence and characteristic nature of intestinal amebiasis among pediatric population, and compare it with other causes of gastroenteritis.Materials and methodsThis is a retrospective comparative study conducted at Makassed General Hospital between January 2008 and December 2012, including all pediatric patients between birth and 15 years of age, who presented with symptoms of acute gastroenteritis.ResultsOne thousand three hundred ninety-five patients were included in the study, and were divided into four groups: Group I (Entameba histolytica group = 311 cases, 22.3%), group II (Rotavirus group = 427 cases, 30.6%), group III (bacterial group = 107 cases, 7.7%), group IV (unidentified group = 550 cases, 39.4%). Significant leukocytosis, neutrophilia and positive C-reactive protein were found among more than 50% of admitted Entemaba histolytica cases with a picture of severe invasive disease in young infants.ConclusionEntameba histolytica can be an emerging serious infection, especially when it finds suitable environmental conditions and host factors, so we should be ready to face it with effective preventive measures.

| S-EPMC3877530 | biostudies-literature

Molecular epidemiology of amebiasis.

Project description:Entamoeba histolytica, the causative agent of human amebiasis, remains a significant cause of morbidity and mortality in developing countries and is responsible for up to 100,000 deaths worldwide each year. Entamoeba dispar, morphologically indistinguishable from E. histolytica, is more common in humans in many parts of the world. Similarly Entamoeba moshkovskii, which was long considered to be a free-living ameba, is also morphologically identical to E. histolytica and E. dispar, and is highly prevalent in some E. histolytica endemic countries. However, the only species to cause disease in humans is E. histolytica. Most old epidemiological data on E. histolytica are unusable as the techniques employed do not differentiate between the above three Entamoeba species. Molecular tools are now available not only to diagnose these species accurately but also to study intra-species genetic diversity. Recent studies suggest that only a minority of all E. histolytica infections progress to the development of clinical symptoms in the host and there exist population level differences between the E. histolytica strains isolated from the asymptomatic and symptomatic individuals. Nevertheless the underlying factors responsible for variable clinical outcome of infection by E. histolytica remain largely unknown. We anticipate that the recently completed E. histolytica genome sequence and new molecular techniques will rapidly advance our understanding of the epidemiology and pathogenicity of amebiasis.

| S-EPMC2577599 | biostudies-literature

New insights into amebiasis using a human 3D-intestinal model

Project description:Entamoeba histolytica, the agent of amebiasis, colonizes the human colon and can invade the lining of the colon to disseminate in the deep layers of the intestine. Amebiasis mainly affects poor people in developing countries, where the barriers between human feces and food or water are inadequate. Humans are the only reservoir of E. histolytica and are the sole target organism of the development of the disease, which limits our knowledge of the crosstalk between the colon and the parasite, especially during the acute phase of amebiasis. In the present work, we constructed a three-Dimensional (3D)-intestinal model capable of reproducing important features of the human intestine. Using this model and leading-edge technologies, including tissue and cell imaging, transcriptomics, and proteomics, as well as ELISA-based immune response inspection, the early stages of amebic infection have been studied. The data obtained highlight the importance of several virulence markers already shown in patients or experimental models, but also underscore the involvement of other factors that appear to be key regulators of gene expression or important in the secretome of the infected tissue. In addition, we characterized the cellular stress responses against amebiasis and novel regulatory mechanisms utilized by this parasite to modulate the immune response and survive within the human intestine.

2020-03-24 | PXD015312 | Pride

Protective effects and potential mechanisms of fermented egg-milk peptides on the damaged intestinal barrier.

Project description:IntroductionFermented egg-milk peptides (FEMPs) could enhance the colon-intestinal barrier and upgrade the expression of zonula occludens-1 and mucin 2. Besides, the underlying biological mechanism and the targets FEMPs could regulate were analyzed in our study.MethodsHerein, the immunofluorescence technique and western blot were utilized to evaluate the repair of the intestinal barrier. Network pharmacology analysis and bioinformatics methods were performed to investigate the targets and pathways affected by FEMPs.Results and discussionAnimal experiments showed that FEMPs could restore intestinal damage and enhance the expression of two key proteins. The pharmacological results revealed that FEMPs could regulate targets related to kinase activity, such as AKT, CASP, RAF, and GSK. The above targets could interact with each other. GO analysis indicated that the targets regulated by FEMPs could participate in the kinase activity of the metabolic process. KEGG enrichment revealed that the core targets were enriched in pathways related to cell apoptosis and other important procedures. Molecular docking demonstrated that FEMPs could bind to the key target AKT via hydrogen bond interactions. Our study combined the experiment in vivo with the method in silico and investigated the interaction between peptides and targets in a pattern of multi-targets and multi-pathways, which offered a new perspective on the functional validation and potential application of bioactive peptides.

| S-EPMC9767966 | biostudies-literature

Human amebiasis: breaking the paradigm?

Project description:For over 30 years it has been established that the Entamoeba histolytica protozoan included two biologically and genetically different species, one with a pathogenic phenotype called E. histolytica and the other with a non-pathogenic phenotype called Entamoeba dispar. Both of these amoebae species can infect humans. E. histolytica has been considered as a potential pathogen that can cause serious damage to the large intestine (colitis, dysentery) and other extraintestinal organs, mainly the liver (amebic liver abscess), whereas E. dispar is a species that interacts with humans in a commensal relationship, causing no symptoms or any tissue damage. This paradigm, however, should be reconsidered or re-evaluated. In the present work, we report the detection and genotyping of E. dispar sequences of DNA obtained from patients with amebic liver abscesses, including the genotyping of an isolate obtained from a Brazilian patient with a clinical diagnosis of intestinal amebiasis that was previously characterized as an E. dispar species. The genetic diversity and phylogenetic analysis performed by our group has shown the existence of several different genotypes of E. dispar that can be associated to, or be potentiality responsible for intestinal or liver tissue damage, similar to that observed with E. histolytica.

| S-EPMC2872301 | biostudies-literature

A protective mechanism of probiotic Lactobacillus against hepatic steatosis via reducing host intestinal fatty acid absorption.

Project description:The gut microbiome has been known to contribute up to ~30% of the energy absorption of the host. Although various beneficial mechanisms of probiotics have been suggested for non-alcoholic fatty liver disease (NAFLD), whether and which probiotics impact the host's intestinal energy absorption have not yet been quantitatively studied. Here, we suggest a novel mechanism of probiotics against NAFLD, in which Lactobacillus rhamnosus GG, the most common probiotic, shares intestinal fatty acids and prevents the development of diet-induced hepatic steatosis. By using quantitative methods (radioactive tracers and LC-MS) under both in vitro and in vivo conditions, we found that bacteria and hosts competed for fatty acid absorption in the intestine, resulting in decreased weight gain, body fat mass, and hepatic lipid accumulation without differences in calorie intake and excretion in mice fed the probiotic bacteria.

| S-EPMC6802638 | biostudies-literature

Mechanisms of cross-talk between the diet, the intestinal microbiome, and the undernourished host.

Project description:Undernutrition remains one of the most pressing global health challenges today, contributing to nearly half of all deaths in children under five years of age. Although insufficient dietary intake and environmental enteric dysfunction are often inciting factors, evidence now suggests that unhealthy gut microbial populations perpetuate the vicious cycle of pathophysiology that results in persistent growth impairment in children. The metagenomics era has facilitated new research identifying an altered microbiome in undernourished hosts and has provided insight into a number of mechanisms by which these alterations may affect growth. This article summarizes a range of observational studies that highlight differences in the composition and function of gut microbiota between undernourished and healthy children; discusses dietary, environmental and host factors that shape this altered microbiome; examines the consequences of these changes on host physiology; and considers opportunities for microbiome-targeting therapies to combat the global challenge of child undernutrition.

| S-EPMC5390823 | biostudies-literature

Gut microbiome communication with the bone marrow regulates intestinal inflammation and susceptibility to amebiasis.

Project description:We discovered that colonization of the gut with the human bile acid 7'-dehydroxylating bacteria Clostridia scindens provided immunity to the parasite E. histolytica in a murine model, increased granulocyte monocyte progenitors, and that adoptive marrow transplant from C. scindens colonized mice into naive mice could recapitualte this protection.

2020-08-10 | GSE121503 | GEO

Toxoplasma gondii soluble tachyzoite antigen triggers protective mechanisms against fatal intestinal pathology in oral infection of C57BL/6 mice.

Project description:Toxoplasma gondii induces a potent IL-12 response early in infection that results in IFN-?-dependent control of parasite growth. It was previously shown that T. gondii soluble tachyzoite antigen (STAg) injected 48 hr before intraperitoneal infection reduces lipoxin A4 and 5-lipoxygenase (5-LO)-dependent systemic IL-12 and IFN-? production as well as hepatic immunopathology. This study investigated the ability of STAg-pretreatment to control the fatal intestinal pathology that develops in C57BL/6 mice orally infected with 100 T. gondii cysts. STAg-pretreatment prolonged the animals' survival by decreasing tissue parasitism and pathology, mainly in the ilea. Protection was associated with decreases in the systemic IFN-? levels and IFN-? and TNF message levels in the ilea and with increased TGF-? production in this tissue, but protection was independent of 5-LO and IL-4. STAg-pretreatment decreased CD4(+) T cell, NK cell, CD11b(+) monocyte and CD11b(+)CD11c(+) dendritic cell numbers in the lamina propria and increased CD8(+) T cells in the intestinal epithelial compartment. In parallel, decreases were observed in iNOS and IL-17 expression in this organ. These results demonstrate that pretreatment with STAg can induce the recruitment of protective CD8(+) T cells to the intraepithelial compartment and decrease proinflammatory immune mechanisms that promote intestinal pathology in T. gondii infection.

| S-EPMC3782460 | biostudies-literature

Challenges and opportunities targeting mechanisms of epithelial injury and recovery in acute intestinal graft-versus-host disease.

Project description:Despite advances in immunosuppressive prophylaxis and overall supportive care, gastrointestinal (GI) graft-versus-host disease (GVHD) remains a major, lethal side effect after allogeneic hematopoietic stem cell transplantation (allo-HSCT). It has become increasingly clear that the intestinal epithelium, in addition to being a target of transplant-related toxicity and GVHD, plays an important role in the onset of GVHD. Over the last two decades, increased understanding of the epithelial constituents and their microenvironment has led to the development of novel prophylactic and therapeutic interventions, with the potential to protect the intestinal epithelium from GVHD-associated damage and promote its recovery following insult. In this review, we will discuss intestinal epithelial injury and the role of the intestinal epithelium in GVHD pathogenesis. In addition, we will highlight possible approaches to protect the GI tract from damage posttransplant and to stimulate epithelial regeneration, in order to promote intestinal recovery. Combined treatment modalities integrating immunomodulation, epithelial protection, and induction of regeneration may hold the key to unlocking mucosal recovery and optimizing therapy for acute intestinal GVHD.

| S-EPMC9259481 | biostudies-literature

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data