PubMed Health⌕ Search

SEARCH · PubMed Health

Results for “Host Microbial Interactions”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 253 records · Page 14Linked to original sources

Comparison of cellular fatty acid profiles of the microbiota in different gut regions of BALB/c and C57BL/6J mice.

The gastrointestinal tracts of developed animals are colonized by an extremely complex and diverse microbial ecosystem. The host and its microbiota are in close interaction with each other, and the host's genetic characteristics have been suggested to have an influence on the composition of fecal bacteria. However, different sections of gastrointestinal tract harbor microbes typical of each particular section and knowledge of the effect of the host's genotype on the microbiota in the different parts of the gastrointestinal tract is limited. In this study, mice from two inbred strains, C57BL/6J and BALB/c, were raised in identical conditions. Bacterial samples were collected from four parts of the gastrointestinal tract and analyzed for bacterial fatty acids using gas-liquid chromatography (GLC). Significant differences between the microbiota in the feces, in the cecum, in the small bowel and in the stomach were observed. Cecal samples produced more diverse bacterial fatty acid profiles than any of the other samples, revealing a higher bacterial density and a higher number of bacterial species. Further, a significant difference between the two strains of mice was observed throughout the gastrointestinal tract. These findings indicate that the host's genotype has an influence on the gastrointestinal microbiota as a whole, and provide further evidence that the cecum is the most species-rich region of the murine gut.

Animals↗

Who controls the crowd? New findings and old questions about the intestinal microflora.

It is probably one of the most complex tasks to understand the mutual relationship between members of the microbial community in the gut and their interaction with the host. Although many animals including humans can live without gut flora, it is beneficial for the growth and protection of the host against pathogens. On the other hand, clinical and experimental intestinal inflammatory reactions have been attributed to immune recognition of the intestinal microflora. This review discusses recent and old findings on function and immunological relevance of the endogenous microflora.

Animals↗

Cleavage of interleukin 1 beta (IL-1 beta) precursor to produce active IL-1 beta by a conserved extracellular cysteine protease from Streptococcus pyogenes.

Streptococcal pyrogenic exotoxin B (SPE B), a conserved extracellular cysteine protease expressed by the human pathogenic bacterium Streptococcus pyogenes, was purified and shown to cleave inactive human interleukin 1 beta precursor (pIL-1 beta) to produce biologically active IL-1 beta. SPE B cleaves pIL-1 beta one residue amino-terminal to the site where a recently characterized endogenous human cysteine protease acts. IL-1 beta resulting from cleavage of pIL-1 beta by SPE B induced nitric oxide synthase activity in vascular smooth muscle cells and killed of the human melanoma A375 line. Two additional naturally occurring SPE B variants cleaved pIL-1 beta in a similar fashion. By demonstrating that SPE B catalyzes the formation of biologically active IL-1 beta from inactive pIL-1 beta, our data add a further dimension to an emerging theme in microbial pathogenesis that bacterial and viral virulence factors act directly on host cytokine pathways. The data also contribute to an enlarging literature demonstrating that microbial extracellular cysteine proteases are important in host-parasite interactions.

Amino Acid Oxidoreductases↗

Oral candidiasis: pathogenesis and host defense.

Oral candidiasis is a common problem, frequently presenting as a chronic recurring infection. Oral infection is a potential reservoir of organisms for severe, spreading, local disease and systemic disease in the compromised host. Nonspecific local oral factors in host defense include the epithelial barrier, flow or saliva, microbial interactions, antimicrobial constituents of saliva, lysozyme, lactoferrin, the lactoperoxidase system, levels of iron, and salivary glycoproteins. Immunoglobins are present in saliva, but their role is poorly understood. The activity of antibody against Candida on oral mucosal surfaces may not be mediated by complement and phagocyte activity. Specific antibodies against Candida may function by aggregating the organisms and preventing mucosal adherence of the fungi.

Animals↗

Three-dimensional tissue assemblies: novel models for the study of Salmonella enterica serovar Typhimurium pathogenesis.

The lack of readily available experimental systems has limited knowledge pertaining to the development of Salmonella-induced gastroenteritis and diarrheal disease in humans. We used a novel low-shear stress cell culture system developed at the National Aeronautics and Space Administration in conjunction with cultivation of three-dimensional (3-D) aggregates of human intestinal tissue to study the infectivity of Salmonella enterica serovar Typhimurium for human intestinal epithelium. Immunohistochemical characterization and microscopic analysis of 3-D aggregates of the human intestinal epithelial cell line Int-407 revealed that the 3-D cells more accurately modeled human in vivo differentiated tissues than did conventional monolayer cultures of the same cells. Results from infectivity studies showed that Salmonella established infection of the 3-D cells in a much different manner than that observed for monolayers. Following the same time course of infection with Salmonella, 3-D Int-407 cells displayed minimal loss of structural integrity compared to that of Int-407 monolayers. Furthermore, Salmonella exhibited significantly lower abilities to adhere to, invade, and induce apoptosis of 3-D Int-407 cells than it did for infected Int-407 monolayers. Analysis of cytokine expression profiles of 3-D Int-407 cells and monolayers following infection with Salmonella revealed significant differences in expression of interleukin 1alpha (IL-1alpha), IL-1beta, IL-6, IL-1Ra, and tumor necrosis factor alpha mRNAs between the two cultures. In addition, uninfected 3-D Int-407 cells constitutively expressed higher levels of transforming growth factor beta1 mRNA and prostaglandin E2 than did uninfected Int-407 monolayers. By more accurately modeling many aspects of human in vivo tissues, the 3-D intestinal cell model generated in this study offers a novel approach for studying microbial infectivity from the perspective of the host-pathogen interaction.

Apoptosis↗

Clinical and genomic features of mitis group streptococcal bacteremia in patients with febrile neutropenia.

BACKGROUND: Viridans group streptococci (VGS) can cause the life-threatening viridans streptococcal shock syndrome (VSSS) in patients with febrile neutropenia (FN). The Mitis group, a major subgroup of VGS, is frequently implicated in these severe infections, but its specific clinical and genomic characteristics remain incompletely characterized, particularly in patients with FN. This study aimed to systematically describe these features in this population. METHODS: In this single-center retrospective study, we compared the clinical data and whole-genome sequencing (WGS) results of Mitis group streptococcal isolates from patients with and without FN. Virulence-associated and antimicrobial resistance genes were initially screened using a reference-based approach, followed by assembly-based reanalysis and manual sequence validation. RESULTS: Compared with the non-FN cohort (n = 34), the FN cohort (n = 61) was significantly younger, had a higher prevalence of hematologic malignancy, and more frequently presented with primary bacteremia. VSSS occurred exclusively in the FN group (11.5%) and was associated with high mortality (14-day mortality, 42.9%), which did not correlate with in vitro antimicrobial susceptibility. Genomic analyses revealed marked diversity among isolates. Initial screening suggested variable detection of several virulence-associated loci, including pavA, slrA, and rfb-related loci; however, subsequent assembly-based analyses indicated that many apparent absences were attributable to extreme allelic divergence rather than true gene loss. No single virulence determinant clearly segregated with clinical severity. CONCLUSIONS: Mitis group bacteremia in patients with FN appears to be characterized by distinct clinical features and marked genomic diversity. Our findings suggest that the development of severe disease, including VSSS, may not be explained by microbial factors alone and potentially reflects complex host-pathogen interactions. CLINICAL TRIAL: Not applicable.

Humans↗

Recognition and response in the plant immune system.

Molecular communication between plants and potential pathogens determines the ultimate outcome of their interaction. The directed delivery of microbial molecules into and around the host cell, and the subsequent perception of these by the invaded plant tissue (or lack thereof), determines the difference between disease and disease resistance. In theory, any foreign molecule produced by an invading pathogen could act as an elicitor of the broad physiological and transcriptional re-programming indicative of a plant defense response. The diversity of elicitors recognized by plants seems to support this hypothesis. Additionally, these elicitors are often virulence factors from the pathogen recognized by the host. This recognition, though genetically as simple as a ligand-receptor interaction, may require additional host proteins that are the nominal targets of virulence factor action. Transduction of recognition probably requires regulated protein degradation and results in massive changes in cellular homeostasis, including a programmed cell death known as the hypersensitive response that indicates a successful, if perhaps over-zealous, disease resistance response.

Gene Expression Regulation, Plant↗

Adherence of oral microorganisms to human parotid salivary proteins.

Bacterial colonisation of oral surfaces by microorganisms may be dependent on their interaction with specific host receptor molecules. Primary oral colonisers are known to remove specific proteins from parotid saliva. The aim of this study was to determine whether these interactions facilitate microbial attachment to a surface and hence identify specific salivary components as putative host receptor molecules. Parotid saliva was resolved by sodium dodecyl sulphate-polyacrylamide gel electrophoresis (SDS-PAGE) and then electroblotted onto nitrocellulose membranes. Suspensions of fluorescently labelled microorganisms were incubated with the blots and salivary components with adherent bacteria identified as fluorescent bands under ultraviolet (UV) transillumination. Species of streptococci known to be early colonisers of the clean tooth surface were found to adhere specifically to certain salivary proteins, especially to basic proline-rich proteins (PRPs). Polymorphic variations in these patterns could form the basis of differences in oral microflora, susceptibility to oral infections and consequent disease.

Bacterial Adhesion↗

Penicillium melinii promotes root growth through subtle host reprogramming across model and crop species.

Root development is highly responsive to microbial interactions, yet the mechanisms by which beneficial fungi promote root growth remain incompletely understood. Here, we identified Penicillium melinii 'isolate 2' through a screen of endophytic fungi isolated from Arabidopsis and characterized it as a promoter of root development in both Arabidopsis and crop species. We combined phenotyping in vitro, rhizotron, greenhouse and field assays with reporter and mutant analyses, transcriptomics, phytohormone profiling and sequencing and annotation of the fungal genome to investigate the basis of this interaction. P. melinii consistently stimulated root growth and modified root architecture across experimental systems and host species. These effects were associated with subtle but reproducible host transcriptional reprogramming, supporting a model in which the fungus fine-tunes endogenous developmental programmes rather than broadly perturbing stress or growth pathways. Genetic and reporter analyses further suggested that this interaction modulates root branching through localized developmental reprogramming. Genomic analysis provided a framework for understanding the fungal traits associated with this beneficial interaction. The conservation of the response across model and crop species supports the relevance of P. melinii as both a useful experimental system to study beneficial plant-fungus interactions and a promising candidate for improving root traits and crop performance.

Penicillium melinii↗

Phage display in the study of infectious diseases.

Microbial infections are dependent on the panoply of interactions between pathogen and host and identifying the molecular basis of such interactions is necessary to understand and control infection. Phage display is a simple functional genomic methodology for screening and identifying protein-ligand interactions and is widely used in epitope mapping, antibody engineering and screening for receptor agonists or antagonists. Phage display is also used widely in various forms, including the use of fragment libraries of whole microbial genomes, to identify peptide-ligand and protein-ligand interactions that are of importance in infection. In particular, this technique has proved successful in identifying microbial adhesins that are vital for colonization.

Adhesins, Bacterial↗

Development and application of in vivo expression technology (IVET) for analysing microbial gene expression in complex environments.

Establishing the mechanisms by which microbes interact with their environment, including eukaryotic hosts, is a major challenge that is essential for the economic utilisation of microbes and their products. Techniques for determining global gene expression profiles of microbes, such as microarray analyses, are often hampered by methodological restraints, particularly the recovery of bacterial transcripts (RNA) from complex mixtures and rapid degradation of RNA. A pioneering technology that avoids this problem is In Vivo Expression Technology (IVET). IVET is a 'promoter-trapping' methodology that can be used to capture nearly all bacterial promoters (genes) upregulated during a microbe-environment interaction. IVET is especially useful because there is virtually no limit to the type of environment used (examples to date include soil, oomycete, a host plant or animal) to select for active microbial promoters. Furthermore, IVET provides a powerful method to identify genes that are often overlooked during genomic annotation, and has proven to be a flexible technology that can provide even more information than identification of gene expression profiles. A derivative of IVET, termed resolvase-IVET (RIVET), can be used to provide spatio-temporal information about environment-specific gene expression. More recently, niche-specific genes captured during an IVET screen have been exploited to identify the regulatory mechanisms controlling their expression. Overall, IVET and its various spin-offs have proven to be a valuable and robust set of tools for analysing microbial gene expression in complex environments and providing new targets for biotechnological development.

Anti-Bacterial Agents↗

A novel Alteromonas phage with tail fiber containing six potential iron-binding domains.

Viruses play a vital role in regulating microbial communities, contributing to biogeochemical cycles of carbon, nitrogen, and essential metals. Alteromonas is widespread and plays an essential role in marine microbial ecology. However, there is limited knowledge about the interactions of Alteromonas and its viruses (alterophages). This study isolated a novel podovirus, vB_AmeP-R22Y (R22Y), which infects Alteromonas marina SW-47 (T). Phylogenetic analysis suggested that R22Y represented a novel viral genus within the Schitoviridae family. R22Y exhibited a broad host range and a relatively large burst size, exerting an important impact on the adaptability and dynamics of host populations. Two auxiliary metabolic genes, encoding Acyl carrier protein and AAA domain-containing protein, were predicted in R22Y, which may potentially assist in host fatty acid metabolism and VB12 biosynthesis, respectively. Remarkably, the prediction of the R22Y tail fiber structure revealed six conserved histidine residues (HxH motifs) that could potentially bind iron ions, suggesting that alterophages may function as organic iron-binding ligands in the marine environment. Our isolation and characterization of R22Y complements the Trojan Horse hypothesis, proposes the possible role of alterophages for marine iron biogeochemical cycling, and provides new insights into phage-host interactions in the iron-limited ocean.IMPORTANCEIron (Fe), as an essential micronutrient, is often a limiting factor for microbial growth in marine ecosystems. The Trojan Horse hypothesis suggests that iron in the phage tail fibers is recognized by the host's siderophore-bound iron receptor, enabling the phage to attach and initiate infection. The potential role of phages as iron-binding ligands has significant implications for oceanic trace metal biogeochemistry. In this study, we isolated a new phage R22Y with the potential to bind iron ions, using Alteromonas, a major siderophore producer, as the host. The tail fiber structure of R22Y exhibits six conserved HxH motifs, suggesting that each phage could potentially bind up to 36 iron ions. R22Y may contribute to colloidal organically complexed dissolved iron in the marine environment. This finding provides further insights into the Trojan Horse hypothesis, suggesting that alterophages may act as natural iron-binding ligands in the marine environment.

Bacteriophages↗

The gut microflora and intestinal epithelial cells: a continuing dialogue.

The mammalian intestinal epithelium effectively performs its physiological functions in a microbe-rich environment, while the prokaryotic population thrives amidst efficient cellular defenses. Recent delineation of the mechanisms by which bacteria communicate with their eukaryotic hosts and the cellular sites that microbial signals act in may shed light on these complex interactions.

Bacterial Physiological Phenomena↗

Bacterial strategies for overcoming host innate and adaptive immune responses.

In higher organisms a variety of host defense mechanisms control the resident microflora and, in most cases, effectively prevent invasive microbial disease. However, it appears that microbial organisms have coevolved with their hosts to overcome protective host barriers and, in selected cases, actually take advantage of innate host responses. Many microbial pathogens avoid host recognition or dampen the subsequent immune activation through sophisticated interactions with host responses, but some pathogens benefit from the stimulation of inflammatory reactions. This review will describe the spectrum of strategies used by microbes to avoid or provoke activation of the host's immune response as well as our current understanding of the role this immunomodulatory interference plays during microbial pathogenesis.

Animals↗

Multiparameter analysis of immunogenetic mechanisms in clinical diagnosis and management of inflammatory bowel disease.

The integrity of the intestinal mucosa depends on a functional coordination of the epithelium, lumenal microorganisms, and the local immune system. The mammalian immune system is superbly organized for innate and adaptive recognition of microbial antigens, a defensive capacity that must be balanced against the tissue damage produced by immune activity to preserve normal intestinal function. Inflammatory bowel disease (IBD) is generally thought to reflect an impairment in this balance, due to a combination of host genetic traits that shift the balance of immune and epithelial function to commensal microbiota, and perhaps the composition or activity of certain microbial elements as well. There has been much progress defining the fundamental disorders of these host traits, immunologic processes, and microbial targets in inflammatory bowel disease. Other fields of clinical and geologic microbiology are teaching us about the dynamic interaction of commensal bacteria with their host environment. These lines of investigation have revealed not only important insights about inflammatory bowel disease (IBD) pathogenesis, but also defined technologies and tools useful for its diagnosis and clinical management. This review focuses on these advances at the translational interface. We will first consider the innate anti-microbial response, centering on the utility of NOD2 genotyping for predicting disease susceptibility, prognosis, and therapeutic response profile. We will then turn to the adaptive anti-microbial response, focusing on the application of antibodies to fungal and bacterial species and products for Crohn's disease (CD) diagnosis and prognosis, and immunogenetics of T cell immunosuppression management. Finally, we will describe autoimmune mechanisms in IBD, with particular attention to autoantibodies in IBD diagnosis and infliximab responsiveness. We will conclude with the concept of multiparameter analysis of patients, to refine patient characterization and stratification in diagnosis and clinical management.

Animals↗

In vivo VL-targeted activation-induced apoptotic supraclonal deletion by a microbial B cell toxin.

To interfere with host immune responses, some microbial pathogens produce proteins with the properties of superantigens, which can interact via conserved V region framework subdomains of the Ag receptors of lymphocytes rather than the complementarity-determining region involved in the binding of conventional Ags. In recent studies, we have elucidated how a model B cell superantigen affects the host immune system by targeting a conserved V(H) site on the Ag receptors of B lymphocytes. To determine whether these findings represent a general paradigm, we investigated the in vivo immunobiologic properties of protein L of Peptostreptococcus magnus (PpL), a microbial Ig-binding protein specific for a V region site on Ig L chains. Our studies confirmed that PpL binding is restricted to a subset of murine Vkappa-expressing B cells, and found that B cells with stronger PpL-binding activity are associated with certain B cell subsets: splenic marginal zone (CD21(high) CD23(low)), splenic CD1(+), peritoneal B-1a (IgD(low) CD5(+)), and CD21(high) CD24(high) B cells in peripheral lymph nodes, mesenteric lymph nodes, and Peyer's patches. Infusion of PpL triggered a sequence of events in B cell receptor (BCR)-targeted B cells, with rapid down-regulation of BCR, the induction of an activation phenotype, and limited rounds of proliferation. Apoptosis followed through a process heralded by the dissipation of mitochondrial membrane potential, the induction of the caspase pathway, DNA fragmentation, and the deposition of B cell apoptotic bodies. These studies define a common pathway by which microbial toxins that target V region-associated BCR sites induce programmed cell death.

Adoptive Transfer↗

Role of fibronectin-binding MSCRAMMs in bacterial adherence and entry into mammalian cells.

Most bacterial infections are initiated by the adherence of microorganisms to host tissues. This process involves the interaction of specific bacterial surface structures, called adhesins, with host components. In this review, we discuss a group of microbial adhesins known as Microbial Surface Components Recognizing Adhesive Matrix Molecules (MSCRAMMs) which recognize and bind FN. The interaction of bacteria with FN is believed to contribute significantly to the virulence of a number of microorganisms, including staphylococci and streptococci. Several FN-binding MSCRAMMs of staphylococci and streptococci exhibit a similar structural organization and mechanism of ligand recognition. The ligand-binding domain consists of tandem repeats of a approximately 45 amino acid long unit which bind to the 29-kDa N-terminal region of FN. The binding mechanism is unusual in that the repeat units are unstructured and appear to undergo a conformational change upon ligand binding. Apart from supporting bacterial adherence, FN is also involved in bacterial entry into non-phagocytic mammalian cells. A sandwich model has been proposed in which FN forms a molecular bridge between MSCRAMMs on the bacterial surface and integrins on the host cell. However, the precise mechanism of bacterial invasion and the roles of FN and integrins in this process have yet to be fully elucidated.

Adhesins, Bacterial↗