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 559 records · Page 31Linked to original sources

PubMed1993

The role of transepithelial transport by M cells in microbial invasion and host defense.

Transepithelial transport of antigens by M cells in the epithelium associated with lymphoid follicles in the intestine delivers immunogens directly to organized mucosal lymphoid tissues, the inductive sites for mucosal immune responses. We have exploited M cell transport to generate and characterize specific monoclonal IgA antibodies that can prevent interaction of pathogens with epithelial surfaces. The relative protective capacities of specific monoclonal IgA antibodies have been tested in vivo by generation of hybridoma tumors that result in secretion of monoclonal IgA into the intestine. Using this method, we have established that secretion of IgA antibodies recognizing a single surface epitope on enteric pathogens can provide protection against colonization or invasion of the intestinal mucosa.

Animals↗

PubMed1990

Adherence of a virulent strain of Listeria monocytogenes to the surface of a hepatocarcinoma cell line via lectin-substrate interaction.

Listeria monocytogenes was examined for the presence of surface carbohydrates to ascertain whether surface sugars, if present, would interact with eucaryotic surface carbohydrate receptors. We found that a virulent, but not two avirulent strains had a surface alpha-D-galactose residue as determined by agglutination with Griffonia simplicifolia (GS-I) and other lectins. The virulent strain bound to a human hepatocarcinoma cell line (HepG2), which has a well characterized receptor for alpha-D-galactose. This interaction could be blocked by pretreatment of the HepG2 cells with either alpha-D-galactose or neuraminidase, the latter of which will render the galactose receptor functionally inactive. We propose that the attachment of the virulent Listeria to eucaryotic cells occurs as a result of the interaction of the microbial alpha-D-galactose with that of the eucaryotic galactose receptor. This surface carbohydrate may provide an explanation for the mechanism of attachment and penetration of virulent Listeria into host cells during infection. As such, this may allow for amplification of pathogenesis through intracellular multiplication in nonprofessional phagocytes prior to macrophage involvement.

Agglutination↗

PubMed2005

Links between the innate immune system and sleep.

Sleep is a fundamental physiologic process with unknown functions. It is divided into 2 distinct states: non-rapid-eye-movement sleep and rapid-eye-movement sleep. After acute infection with nonneurotropic agents, there are stereotypic changes in non-rapid-eye-movement sleep, particularly increased time spent in slow-wave sleep, and often a reduction of time spent in rapid-eye-movement sleep. It is now recognized that both infection-associated sleep and spontaneous sleep are regulated, in part, by immune mediators called cytokines. This review provides brief tutorials on the elements of the innate immune system that detect infection, how sleep is characterized in the laboratory, issues regarding the interpretation of sleep effects on immune function, the interaction of sleep with circadian rhythms and stress, and some of the microbial products, cytokines, and neuropeptides associated with sleep regulation. We also summarize our current understanding of the role of sleep in host defense and asthma exacerbation.

Acute-Phase Reaction↗

PubMed2026

Lineage dynamics of invasive Escherichia coli isolates in the Netherlands from 1975 to 2021: a retrospective longitudinal genomic analysis.

BACKGROUND: Escherichia coli is a common cause of invasive infections such as bloodstream and cerebrospinal fluid infections in neonates. Strains positive for the K1 capsule are considered the most common cause of such neonatal invasive infections. This assumption of K1 dominance, and indeed the population genomics of E coli causing invasive infections in general is largely unstudied. We aimed to provide a comprehensive characterisation of this pathogen population using a longitudinal isolate collection. METHODS: In this analysis we report the findings of the SENTINEL study, a longitudinal genomic analysis of 1790 invasive E coli isolates collected mainly from newborns in the Netherlands between 1975 and 2021 by the Netherlands Reference Laboratory for Bacterial Meningitis, Amsterdam University Medical Centre, Amsterdam, Netherlands. The dataset included all bacterial strains cultured from cerebrospinal fluid or blood in cases of (clinical) bacterial meningitis (1976 to 1980). In 1981 the criteria were expanded to include neonates (aged ≤4 weeks) with E coli sepsis, and from July, 2016 all infants younger than 1 year with E coli sepsis were included. All isolates were sequenced using either the HiSeq 2500 or HiSeq 4000 platforms (Illumina, San Diego, CA, USA). We confirmed species and identified sequence types (STs), detected antimicrobial resistance genes, virulence genes, and the presence of K1 capsule, and characterised the dynamics of these factors over time. FINDINGS: Our data show a highly dynamic bacterial population that is entirely unaffected by antimicrobial resistance determinants. Key pathogen population fluctuations include the complete disappearance of the dominant lineage ST567 and the swapping of dominant ST95 clones from a single serotype O18:H7 clone to two distinct serotype O1:H7 clones, with changes in virulence factors including major fimbrial adhesins. These findings, combined with only 58·8% (1053 of 1790) prevalence in K1-expressing isolates in the entire study population, point to host-pathogen interaction and immune selection pressures as key drivers of bacterial population dynamics in this largely antimicrobial-naive population. INTERPRETATION: Our data show the vital need for ongoing genomic surveillance of microbial pathogen populations to guide appropriate intervention strategies. Additionally, genomic insights of a pathogen population from one specific disease syndrome or patient population cannot always be generalised across other cohorts. FUNDING: Wellcome Antimicrobial and Antimicrobial Resistance Doctoral Training Programme and the National Institute for Health and Care Research Birmingham Biomedical Research Centre.

Netherlands↗

PubMed1996

Neuroendocrine changes in systemic lupus erythematosus and Sjögren's syndrome.

It has become clear that the neuroendocrine and immune systems are closely linked and interdependent. The exact mechanisms of this interaction are only beginning to be unravelled. The complexity of these connections may partly explain why the aetiopathogenesis of autoimmune diseases remains obscure and why genetic, hormonal, microbial, environmental, as well as a host of other factors, have all been put forward as explanations. What has become clear is that a number of neuroendocrine and hormonal factors have important immunomodulatory roles in health and disease.

Animals↗

PubMed2003

Outer membrane protein A deficient Escherichia coli activates neutrophils to produce superoxide and shows increased susceptibility to antibacterial peptides.

The outer membrane protein A (OmpA) of Gram-negative bacteria has been ascribed multiple functions including maintenance of structural membrane integrity and porin activity. OmpA has also been implicated in various host defense processes in that it contributes to bacterial serum resistance and activates certain immune cells. Recently, OmpA was shown to be the molecular target for neutrophil elastase (NE), and Escherichia coli mutants lacking OmpA were resistant to the bactericidal effects of NE. In addition to NE, neutrophils use a variety of other antibacterial effector molecules such as oxygen radicals and bactericidal peptides or proteins. The aim of this study was to investigate the role of E. coli OmpA regarding susceptibility to other neutrophil-derived defense systems. We found that OmpA-deficient (OmpA(-)), but not wild-type isogenic, E. coli activated human neutrophils to produce oxygen radicals intracellularly. This activation was found to require an intact neutrophil cytoskeleton but was independent of bacterial phagocytosis. Furthermore, we found that the OmpA(-) strain was more susceptible to membrane-acting bactericidal peptides than the wild-type strain, although the susceptibility to different oxygen radicals was independent of the presence of OmpA. Taken together, these data suggest an important role for OmpA in the context of bacteria vs. host interactions.

Anti-Bacterial Agents↗

PubMedDate not supplied

Enzymes associated with the survival and virulence of gram-negative anaerobes.

gram -negative anaerobic bacteria constitute a major portion of the indigenous microflora of humans. Enzymes produced by these bacteria provide nutrients for growth, participate in the pathogenesis of infections involving these bacteria, modify the local environment so that it is suitable for growth, and alter nonnutrients in the immediate vicinity of the bacterial cell. Metabolism of compounds in the gastrointestinal tract by enzymes produced by gram-negative anaerobes may have appreciable effects on the absorption, distribution, and excretion of these compounds as well as on their biologic properties. Knowledge of the enzymes produced by anaerobes is important for understanding and possibly modulating interactions between these bacteria and the host.

Bacteroides↗

PubMed2004

D(-)-lactic acid-producing probiotics, D(-)-lactic acidosis and infants.

There is mounting evidence that ingestion of selected probiotics can modify disease morbidity for specific conditions affecting humans, and there is growing interest in the amelioration or prevention of disease with probiotics. Modulation in gene expression of the cellular elements of the intestinal mucosa and interbacterial interactions are leading theories as to the mechanism whereby probiotics can effect benefit for the host. Furthermore, gene-environmental interactions are considered to be important in the development of disease in those at genetic risk. With the intestinal tract harbouring large numbers of bacteria, alteration of the microbial environment with probiotic microbes is being considered as a controllable factor that may limit disease expression for those at genetic risk. This reasoning has led to interest in the administration of probiotics to infants. However, there are significant developmental changes occurring in many organ systems from the time of parturition and during the first months of life. Because there is little in the published scientific medical literature regarding the effects of long-term administration of probiotics to infants, potential problems must be considered; one such issue is that of administration of D(-)-lactate-producing probiotics. An appraisal of the current knowledge of this potential adverse effect is the subject of this communication.

Acidosis, Lactic↗

PubMed2002

Molecular determinants and regulation of Leishmania virulence.

A Leishmania model to explain microbial virulence in chronic infectious diseases is proposed. All these diseases progress from infection to symptomatic phase to host death or recovery. The outcome of each phase is depicted to result from the interactions of a distinct group of parasite molecules with a specific host immune compartment. The first group consists of invasive/evasive determinants, which are largely parasite cell surface and secreted molecules. Their activities help parasites establish infection by overcoming host immunologic and non-immunologic barriers. These determinants do not cause disease per se, but are indispensable for infection necessary for the development of a disease-state. The second group of parasite molecules consists of "pathoantigenic" determinants - unique parasite epitopes present often within otherwise highly conserved cytoplasmic molecules. Immune response against these determinants is thought to result in immunopathology manifested as clinical signs or symptoms, namely the virulent phenotype. The third group of parasite molecules is hypothetically perceived as vaccine determinants. Their interactions with the host immune system lead to the elimination or reduction of parasites to effect a clinical cure. Differential expression of these determinants alone by parasites may alter their interactions with the hosts. Virulent phenotype is consequently presented as a spectrum of manifestations from asymptomatic infection to fatality. A secondary level of regulation lies in host genetic and environmental factors. The model suggests that different parasite determinants may be targeted by different strategies to achieve more effective control of leishmaniasis and other similar diseases.

Journal Article↗

PubMed2002

The development of gut immune responses and gut microbiota: effects of probiotics in prevention and treatment of allergic disease.

The infant's immature intestinal immune system develops as it comes into contact with dietary and microbial antigens in the gut. The evolving indigenous intestinal microbiota have a significant impact on the developing immune system and there is accumulating evidence indicating that an intimate interaction between gut microbiota and host defence mechanisms is mandatory for the development and maintenance of a balance between tolerance to innocuous antigens and capability of mounting an inflammatory response towards potential pathogens. Disturbances in the mucosal immune system are reflected in the composition of the gut microbiota and vice versa. Distinctive alterations in the composition of the gut microbiota appear to precede the manifestation of atopic disease, which suggests a role for the interaction between the intestinal immune system and specific strains of the microbiota in the pathogenesis of allergic disorders. The administration of probiotics, strains of bacteria from the healthy human gut microbiota, have been shown to stimulate antiinflammatory, tolerogenic immune responses, the lack of which has been implied in the development of atopic disorders. Thus probiotics may prove beneficial in the prevention and alleviation of allergic disease.

Food Hypersensitivity↗

PubMed1982

Isolation and ultrastructural examination of conidial wall components of Coccidioides and Aspergillus.

The role of the propagule in the initiation of fungal disease is not fully appreciated. Knowledge of the nature of early interactions between infectious propagules and host tissue during onset of respiratory mycoses is particularly scanty. This stems partly from lack of sufficient data on the structure, chemical composition and immunological activity of the microbial surface. In this study, a technique is described for isolation and subsequent ultrastructural examination of the surface wall components of infectious propagules (conidia) produced by the respiratory fungal pathogens, Coccidioides immitis and Aspergillus fumigatus. The SEM has proved very useful in monitoring the cell shearing procedure employed for isolation of the outer conidial wall fractions.

Aspergillus fumigatus↗

PubMed1998

Antibiotic-selective environments.

The evolution and spread of antibiotic resistance depends on the antibiotic pressure exerted in the microbial environment. Selective effects occur in selective compartments, where particular antibiotic concentrations result in a differential growth rate of resistant bacterial variants. This may happen even at very low antibiotic concentrations able to select low-level-resistant bacteria. When more than one antibiotic is present in the environment, the multiple and fluctuating pressure produces the selection of bacterial variants that use multiple or multipurpose mechanisms or optimize a single mechanism of resistance to survive under the variable environmental conditions. Host factors such as immunity contribute to the selective process. Antibiotics themselves may promote bacterial diversity, either mediated by the random drift effect or triggering the increase of mutational events under bacterial stress. Analysis of selective environment-related antibiotic-host-bacteria interactions is essential to understanding the biology of antibiotic resistance.

Adaptation, Physiological↗

PubMed2001

Symbiotic fungal endophytes control insect host-parasite interaction webs.

Symbiotic microorganisms that live intimately associated with terrestrial plants affect both the quantity and quality of resources, and thus the energy supply to consumer populations at higher levels in the food chain. Empirical evidence on resource limitation of food webs points to primary productivity as a major determinant of consumer abundance and trophic structure. Prey quality plays a critical role in community regulation. Plants infected by endophytic fungi are known to be chemically protected against herbivore consumption. However, the influence of this microbe-plant association on multi-trophic interactions remains largely unexplored. Here we present the effects of fungal endophytes on insect food webs that reflect limited energy transfer to consumers as a result of low plant quality, rather than low productivity. Herbivore-parasite webs on endophyte-free grasses show enhanced insect abundance at alternate trophic levels, higher rates of parasitism, and increased dominance by a few trophic links. These results mirror predicted effects of increased productivity on food-web dynamics. Thus 'hidden' microbial symbionts can have community-wide impacts on the pattern and strength of resource-consumer interactions.

Animals↗

PubMed2007

Rat model of polymicrobial infection, immunity, and alveolar bone resorption in periodontal disease.

One of the predominant polymicrobial infections of humans is expressed clinically as periodontal disease. Porphyromonas gingivalis, Treponema denticola, and Tannerella forsythia have been strongly implicated as members of a pathogenic consortium in the etiology of adult periodontitis. In this study we hypothesized that P. gingivalis, T. denticola, and T. forsythia are synergistic in terms of virulence potential and induce chronic periodontal inflammation that leads to alveolar bone resorption in a polymicrobial infection in rats. Groups of rats were infected with either P. gingivalis, T. denticola, or T. forsythia in monomicrobial infections or with all three species in polymicrobial oral infections with or without Fusobacterium nucleatum. PCR analyses of oral microbial samples demonstrated that rats infected with one bacterium were orally colonized by each of the bacteria during the study interval, and increased serum immunoglobulin G (IgG) antibody levels substantiated the interaction of the host with the infecting bacteria. PCR analyses of the rats with polymicrobial infections demonstrated that most rats were infected with P. gingivalis, T. denticola, and T. forsythia as a consortium. Furthermore, all rats exhibited a significant increase in the level of IgG antibody to the polymicrobial consortium. Radiographic measurement of alveolar bone resorption showed that rats infected with the polymicrobial consortium with or without F. nucleatum exhibited significantly increased alveolar bone resorption compared to the resorption in uninfected control rats, as well as the resorption in rats infected with one of the microbes. These results documented that P. gingivalis, T. denticola, and T. forsythia not only exist as a consortium that is associated with chronic periodontitis but also exhibit synergistic virulence resulting in the immunoinflammatory bone resorption characteristic of periodontitis.

Alveolar Bone Loss↗

PubMed2026

Expanding vaginal microbiome pangenomes via a custom MIDAS database reveals Lactobacillus crispatus accessory genes associated with cervical dysplasia.

The vaginal microbiome plays a central role in reproductive health. Vaginal microbiome dysbiosis is associated with many adverse reproductive health outcomes, but most studies have focused on associations at the species level. The potential contribution of intraspecies microbial variation, especially gene content differences across bacterial strains, remains underexplored in reproductive health contexts. The Metagenomic Intra-Species Diversity Analysis (MIDAS) framework enables such analyses, but depends on comprehensive reference databases. We constructed a MIDAS-compatible pangenome database from over 18,000 genomes in the Vaginal Microbiome Genome Collection (VMGC). Compared to the Genome Taxonomy Database (GTDB)-derived reference, the VMGC-derived database expanded the pangenomes of prevalent vaginal species, better capturing vaginal-specific intraspecies diversity. Applying this database to vaginal samples from a cervical dysplasia cohort, we identified 13 Lactobacillus crispatus accessory genes significantly associated with cervical dysplasia, including a HicAB toxin-antitoxin system, three transcriptional regulators, and three phage-derived genes. These findings highlight the utility of body site-specific reference resources and shotgun metagenomic sequencing for uncovering intraspecies microbial variation relevant to reproductive health.IMPORTANCEThe vaginal microbiome plays a critical role in reproductive health, and different bacteria from the same species can carry different genes that influence how the strains interact with the host and other microbes. These strain-level differences are often overlooked when microbiomes are analyzed only at the species level. Existing genomic reference databases are heavily biased toward gut and environmental bacteria, leaving the genetic diversity of vaginal microbes understudied. We built a specialized reference database from over 18,000 vaginal bacterial genomes that better reflects this diversity. We then applied this resource to quantify gene-level variation in vaginal samples from a cervical dysplasia cohort. Focusing on Lactobacillus crispatus, a prevalent and often beneficial vaginal species, we identified 13 genes that were more common in women with cervical dysplasia than in controls. This work demonstrates that body site-specific genomic resources are essential for uncovering strain-level bacterial differences relevant to reproductive health.

Lactobacillus crispatus↗

PubMed1994

Systemic infection with Herpes bovis virus 2 evokes a biphasic immune response in the mouse.

We evaluated the effects of systemic infection by Herpes bovis virus 2 (HBV-2) on a murine experimental system. We provide evidence that such infection is lethal for the immunocompromised but not for the immunocompetent mouse in which a biphasic immune response is elicited. In particular, 1 day post-infection, we observed a rapid transient depression induced by the virus, as documented by a decrease in peripheral leukocyte counts, mitogenic spleen cell response and resistance to a secondary microbial challenge. Later, HBV-2 infection boosted cytokine secretion and enhanced antimicrobial and antitumoral activities by the splenic district. In conclusion, our experimental model discloses some immunological aspects underlying the complex host-virus interaction.

Animals↗

PubMed1997

Of microbes, macrophages and nitric oxide.

One of the most prominent functions of nitric oxide (NO) is its participation in antimicrobial and antiviral defense. This paper summarizes the evidence for this function and compiles the infectious agents which are currently thought to be controlled via high out-put generation of NO as it occurs in activated macrophages and other cells expressing the inducible isoform of NO-synthase (iNOS, NOS-2). Several less appreciated forms of interaction between NO and microbes will also be reviewed, including the role of NO as an immunosuppressive or tissue-destructive molecule during the course of infections, the regulation of microbial antioxidant systems by host cell-derived NO, the contribution of NO to parasite stage conversion, the induction or suppression of macrophage iNOS by microbial products, and the existence of endogenous NO synthase pathways in certain bacteria and parasites.

Animals↗

PubMed2004

Candida albicans and Saccharomyces cerevisiae induce interleukin-8 production from intestinal epithelial-like Caco-2 cells in the presence of butyric acid.

Intestinal epithelial cells (IEC) are important in initiation and regulation of immune responses against numerous foreign substances including food, microorganisms and their metabolites in the intestine. Since the responses of IEC against yeasts have not yet been well understood, we investigated the effects of Candida albicans, Saccharomyces cerevisiae, and their cell wall components on interleukin-8 (IL-8) secretion by the IEC-like Caco-2 cells. Live cells of both yeast species stimulated Caco-2 cells to produce IL-8 only in the presence of butyric acid, which is a metabolite produced by intestinal bacteria. S. cerevisiae zymosan and glucan also enhanced IL-8 secretion. Treatment of Caco-2 cells with butyric acid increased the expression of mRNAs coding for Toll-like receptor 1 (TLR1), TLR6 and dectin-1, which recognize zymosan. C. albicans induced more IL-8 secretion and also decreased transepithelial electrical resistance more rapidly than S. cerevisiae. These results suggest that both yeasts in the intestine stimulate the host's mucosal immune systems by interacting with IEC.

Butyric Acid↗