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At least 127 records · Page 7Linked to original sources
PubMed2005

A whole cell BIAcore assay to evaluate P1-mediated adherence of Streptococcus mutans to human salivary agglutinin and inhibition by specific antibodies.

Researchers now recognize the utility of surface plasmon resonance technology to evaluate interactions of microbial pathogens with host components. The surface adhesin and candidate vaccine antigen P1 of Streptococcus mutans, the main causative agent of dental caries, interacts with a high molecular weight glycoprotein called salivary agglutinin, or gp340, in the salivary pellicle. We optimized a BIAcore assay to measure P1-mediated Ca(2+) dependent binding of S. mutans whole cells to this physiological ligand immobilized on a Pioneer F1 sensor chip. Regeneration conditions allowed cells to be eluted from the sensor chip permitting multiple reuse of the agglutinin-coated surface. An isogenic P1-deficient S. mutans mutant did not bind to immobilized agglutinin demonstrating specificity of the detected interaction. Glutaraldehyde-fixation of bacterial cells showed the assay measured a whole cell-ligand interaction and was not an artifact of solubilized or leached proteins. Adherence inhibition assays demonstrated varying degrees of disruption of the S. mutans-agglutinin interaction by anti-P1 monoclonal antibodies recognizing different epitopes, whereas a polyclonal reagent demonstrated more complete inhibition. This report describes an improved method to assess salivary agglutinin-mediated adherence of S. mutans in vitro under physiological-like conditions and to evaluate the effectiveness of antibodies of differing specificities to inhibit binding.

Agglutinins↗
PubMed2002

How Drosophila combats microbial infection: a model to study innate immunity and host-pathogen interactions.

During the past year, dramatic progress has been achieved in our understanding of Drosophila immune reactions. The completion of the Drosophila genome sequencing project, microarray analysis and the use of genetic screens have led to the identification of several new genes required to combat microbial infection, filling in some important gaps in the understanding of innate immunity. At the same time, this insect was used as a model for the study of host-pathogen interactions. The recent major advances on the mechanisms by which this insect defends itself against intrusion of pathogens are discussed in this review.

Animals↗
PubMed2006

Microbial considerations in genetically engineered mouse research.

Microbial infections have long been of concern to scientists using laboratory rodents because of their potential to confound and invalidate research. With the explosion of genetically engineered mice (GEM), new concerns over the impact of microbial agents have emerged because these rodents in many cases are more susceptible to disease than their inbred or outbred counterparts. Moreover, interaction between microbe and host and the resulting manifestation of disease conceivably differ between GEM and their inbred and outbred counterparts. As a result, infections may alter the GEM phenotype and confound interpretation of results and conclusions about mutated gene function. In addition, because GEM are expensive to produce and maintain, contamination by pathogens or opportunists has severe economic consequences. This review addresses how microbial infections may influence phenotype, how immunomodulation of the host as the result of induced mutations may modify host susceptibility to microbial infections, how novel host:microbe interactions have led to the development of new animal models for disease, how phenotype changes have led to the discovery of new pathogens, and new challenges associated with prevention and control of microbial infections in GEM. Although the focus is on naturally occurring infections, extensive literature on the use of GEM in studies of microbial pathogenesis also exists, and the reader is referred to this literature if microbial infection is a suspected culprit in phenotype alteration.

Animals↗
PubMed2004

The behaviour of microbes.

Viruses and bacteria have complex interactions with their hosts, beyond mere replication in them. They range from those that are detrimental, to others that may be non-pathogenic or even beneficial. Molecular techniques can help to unravel these interactions, sometimes revealing phenomena that benefit host as well as microbial populations.

Adaptation, Physiological↗
PubMed2025

Health-associated key gut microbiota drives the variation in community metabolic interactions in non-human primates.

Gut microbiota often undergo metabolic cross-feeding and resource competition. However, our understanding of global variations in these interactions and their implications for host health remain elusive. By analyzing a microbial genome catalog from 841 fecal metagenomes across 53 primate species worldwide, we identified key microbiota assigned to two taxa, i.e., Bacillota_A and Pseudomonadota, which well predicted the trade-off of community-level interaction types between metabolic competition and cooperation. Specifically, Bacillota_A species were inherently competitive and amino acid auxotrophic and typically found in anaerobic habitats. In contrast, members of Pseudomonadota were inherently cooperative, siderophore producers, and more abundant in aerobic conditions. Random forest models successfully distinguished unhealthy gut samples from healthy samples through the key competitive and cooperative microbiota, suggesting potential links between community metabolic interactions and host health. Together, this study enhances our mechanistic understanding of microbial interaction dynamism within complex gut ecosystems, offering new targets for understanding host health.

Animals↗
PubMed2003

Interactions between M proteins of Streptococcus pyogenes and glycosaminoglycans promote bacterial adhesion to host cells.

Several microbial pathogens have been reported to interact with glycosaminoglycans (GAGs) on cell surfaces and in the extracellular matrix. Here we demonstrate that M protein, a major surface-expressed virulence factor of the human bacterial pathogen, Streptococcus pyogenes, mediates binding to various forms of GAGs. Hence, S. pyogenes strains expressing a large number of different types of M proteins bound to dermatan sulfate (DS), highly sulfated fractions of heparan sulfate (HS) and heparin, whereas strains deficient in M protein surface expression failed to interact with these GAGs. Soluble M protein bound DS directly and could also inhibit the interaction between DS and S. pyogenes. Experiments with M protein fragments and with streptococci expressing deletion constructs of M protein, showed that determinants located in the NH2-terminal part as well as in the C-repeat region of the streptococcal proteins are required for full binding to GAGs. Treatment with ABC-chondroitinase and HS lyase that specifically remove DS and HS chains from cell surfaces, resulted in significantly reduced adhesion of S. pyogenes bacteria to human epithelial cells and skin fibroblasts. Together with the finding that exogenous DS and HS could inhibit streptococcal adhesion, these data suggest that GAGs function as receptors in M protein-mediated adhesion of S. pyogenes.

Bacterial Adhesion↗
PubMed1997

Shared themes of antigenic variation and virulence in bacterial, protozoal, and fungal infections.

Pathogenic microbes have evolved highly sophisticated mechanisms for colonizing host tissues and evading or deflecting assault by the immune response. The ability of these microbes to avoid clearance prolongs infection, thereby promoting their long-term survival within individual hosts and, through transmission, between hosts. Many pathogens are capable of extensive antigenic changes in the face of the multiple constitutive and dynamic components of host immune defenses. As a result, highly diverse populations that have widely different virulence properties can arise from a single infecting organism (clone). In this review, we consider the molecular and genetic features of antigenic variation and corresponding host-parasite interactions of different pathogenic bacterial, fungal, and protozoan microorganisms. The host and microbial molecules involved in these interactions often determine the adhesive, invasive, and antigenic properties of the infecting organisms and can dramatically affect the virulence and pathobiology of individual infections. Pathogens capable of such antigenic variation exhibit mechanisms of rapid mutability in confined chromosomal regions containing specialized genes designated contingency genes. The mechanisms of hypermutability of contingency genes are common to a variety of bacterial and eukaryotic pathogens and include promoter alterations, reading-frame shifts, gene conversion events, genomic rearrangements, and point mutations.

Animals↗
PubMed2025

Impact of RNA extraction on respiratory microbiome analysis using third-generation sequencing.

BACKGROUND: The respiratory microbiome, which comprises bacteria, fungi, and viruses, plays a crucial role in respiratory health and disease. However, its study is limited by the low microbial biomass in respiratory samples and the dominance of host RNA. Metatranscriptomics offers comprehensive insights into active microbial communities and their interactions with the host but requires optimized RNA extraction protocols for robust and unbiased analysis. This study evaluated two RNA extraction kits&#x2014;one employing chemical lysis (CL) and another combining chemical and mechanical lysis (CML)&#x2014;to determine their effectiveness for metatranscriptomic analysis of respiratory samples. RESULTS: The CML protocol significantly increased double-stranded DNA (dsDNA) library yields, leading to higher sequencing read counts for both sample types (p&#x2009;<&#x2009;0.0001). The read length was unaffected by the lysis protocol for the BAL and NPS samples. Taxonomic profiling revealed that CML enhanced the detection of robust microorganisms, such as gram-positive bacteria and fungi, without compromising viral detection. CONCLUSIONS: The CML protocol demonstrated superior recovery of genetic material, particularly for fungi and gram-positive bacteria, making it better suited for comprehensive metatranscriptomic analyses. These findings underscore the need for tailored RNA extraction strategies on the basis of sample type and research objectives. Optimized metatranscriptomic protocols are pivotal for advancing our understanding of the respiratory microbiome and its role in health and disease.

Microbiota↗
PubMed1998

Molecular basis of host-pathogen interaction in septic shock.

Specific mechanisms of recognition of microbial products have been developed by host cells. Among these mechanisms, recognition of lipopolysaccharide of Gram-negative bacteria by CD14, a glycoprotein expressed at the surface of myelomonocytic cells, plays a major role. There is increasing evidence that CD14 also serves as a receptor for other microbial products including peptidoglycan of Gram-positive bacteria. A common theme is that CD14 represents a key molecule in innate immunity. Recognition of microbial products by host cells leads to cell activation and production of a large array of mediators that are necessary for the development of controlled inflammatory processes. When the activation process is out of control, such as in septic shock, these mediators can be detrimental to the host.

Animals↗
PubMed2004

Frontal and stealth attack strategies in microbial pathogenesis.

Interactions between microbes and human hosts can range from a benign, even symbiotic collaboration to a competition that may turn fatal--resulting in death of the host, the microbe or both. Despite advances that have been made over the past decades in understanding microbial pathogens, more people worldwide still die every year from infectious disease than from any other cause. This highlights the relevance of continuing to probe the mechanisms used by microorganisms to cause disease, and emphasizes the need for new model systems to advance our understanding of host-pathogen interactions.

Bartonella↗
PubMed1999

Structure-function relationships of bacterial endotoxins. Contribution to microbial sepsis.

A substantial body of knowledge has emerged over the past several decades concerning the primary and tertiary, and quaternary structure of endotoxic LPS and their contribution to the pathogenesis of gram-negative sepsis; however, important questions remain. Among them are the precise three-dimensional configuration of the LPS macromolecule and the contribution of the quaternary structure to the ability of these potent microbial factors to interact with host humoral and cellular inflammatory mediator systems. Also remaining to be sufficiently addressed is the relative contribution of endotoxin interactions with the host to the overall manifestation of disease and conditions under which such contributions serve as the pivotal event in determining outcome. The answers to these questions can be expected to provide valuable insights into potential novel therapeutic intervention strategies and approaches that will ultimately reduce both morbidity and mortality in infection from gram-negative microbes.

Animals↗
PubMed2003

Mpi recombinase globally modulates the surface architecture of a human commensal bacterium.

The mammalian gut represents a complex and diverse ecosystem, consisting of unique interactions between the host and microbial residents. Bacterial surfaces serve as an interface that promotes and responds to this dynamic exchange, a process essential to the biology of both symbionts. The human intestinal microorganism, Bacteroides fragilis, is able to extensively modulate its surface. Analysis of the B. fragilis genomic sequence, together with genetic conservation analyses, cross-species cloning experiments, and mutational studies, revealed that this organism utilizes an endogenous DNA inversion factor to globally modulate the expression of its surface structures. This DNA invertase is necessary for the inversion of at least 13 regions located throughout the genome, including the promoter regions for seven of the capsular polysaccharide biosynthesis loci, an accessory polysaccharide biosynthesis locus, and five other regions containing consensus promoter sequences. Bacterial DNA invertases of the serine site-specific recombinase family are typically encoded by imported elements such as phage and plasmids, and act locally on a single region of the imported element. In contrast, the conservation and unique global regulatory nature of the process in B. fragilis suggest an evolutionarily ancient mechanism for surface adaptation to the changing intestinal milieu during commensalism.

Bacterial Capsules↗
PubMed2002

Suppression of NF-kappaB activation by infection with Toxoplasma gondii.

The interaction of host cells with microbial products or their invasion by pathogens frequently results in activation of the NF-kappaB family of transcription factors. The studies presented here reveal that in vivo, infection with Toxoplasma gondii results in the activation of NF-kappaB. To determine whether host cells could activate NF-kappaB in response to invasion by T. gondii, Western blots, immunofluorescence, and electrophoretic mobility shift assays were used to assess the response of host cells to infection. In these studies, infection of macrophages or fibroblasts with T. gondii did not result in the activation of NF-kappaB. In addition, the ability of lipopolysaccharide to activate NF-kappaB was impaired in cultures of macrophages infected with T. gondii. Together, these data demonstrate that invasion of cells by T. gondii does not lead to the activation of NF-kappaB and suggest that the parasite may actively interfere with the pathways that lead to NF-kappaB activation.

Active Transport, Cell Nucleus↗
PubMed2005

Bacterial peptidoglycan-associated lipoprotein: a naturally occurring toll-like receptor 2 agonist that is shed into serum and has synergy with lipopolysaccharide.

Sepsis is initiated by interactions between microbial products and host inflammatory cells. Toll-like receptors (TLRs) are central innate immune mediators of sepsis that recognize different components of microorganisms. Peptidoglycan-associated lipoprotein (PAL) is a ubiquitous gram-negative bacterial outer-membrane protein that is shed by bacteria into the circulation of septic animals. We explored the inflammatory effects of purified PAL and of a naturally occurring form of PAL that is shed into serum. PAL is released into human serum by Escherichia coli bacteria in a form that induces cytokine production by macrophages and is tightly associated with lipopolysaccharide (LPS). PAL activates inflammation through TLR2. PAL and LPS synergistically activate macrophages. These data suggest that PAL may play an important role in the pathogenesis of sepsis and imply that physiologically relevant PAL and LPS are shed into serum and act in concert to initiate inflammation in sepsis.

Animals↗
PubMedDate not supplied

Microbiology of toxic shock syndrome: overview.

The discovery of TSST-1 production by TSS-associated strains of S. aureus provided the first major breakthrough in the understanding of the pathogenesis of TSS. Soon, associations between TSST-1 production and other phenotypic and genotypic characteristics of S. aureus became apparent. In the end, appreciation of the microbiology and molecular genetics of TSST-1 and TSS-associated S. aureus has not only enhanced our knowledge of the pathogenesis of TSS, it will undoubtedly bring new concepts and insights into the possible mechanisms and host-parasite interactions in other microbial infections or intoxications as well.

Bacterial Toxins↗
PubMed2006

Cytosolic entry controls CD8+-T-cell potency during bacterial infection.

Interaction with host immunoreceptors during microbial infection directly impacts the magnitude of the ensuing innate immune response. How these signals affect the quality of the adaptive T-cell response remains poorly understood. Utilizing an engineered strain of the intracellular pathogen Listeria monocytogenes that infects cells but fails to escape from the phagosome, we demonstrate the induction of long-lived memory T cells that are capable of secondary expansion and effector function but are incapable of providing protective immunity. We demonstrate that microbial invasion of the cytosol is required for dendritic cell activation and integration of CD40 signaling, ultimately determining the ability of the elicited CD8+-T-cell pool to protect against lethal wild-type L. monocytogenes challenge. These results reveal a crucial role for phagosomal escape, not for delivery of antigen to the class I major histocompatibility complex pathway but for establishing the appropriate cellular context during CD8+-T-cell priming.

Animals↗
PubMed1999

Association of a vitamin D receptor gene polymorphism with localized early-onset periodontal diseases.

BACKGROUND: Early-onset periodontal diseases (EOP) are caused by interactions between host factors, specific microbial pathogens, and environmental factors. It is, therefore, of interest to investigate the nature of host factors as they may provide useful risk markers and reveal important information regarding the disease pathogenesis. Genetic polymorphisms in the vitamin D receptor (VDR) gene are associated with parameters of bone homeostasis and with diseases in which bone loss is a cardinal sign, in particular osteoporosis. Rapidly progressive bone loss is one feature of EOP. We, therefore, sought to determine whether EOP is associated with a polymorphism in the VDR gene. METHODS: A restriction fragment length polymorphism (RFLP) for Taq I in exon nine of the VDR gene was analyzed by PCR, followed by restriction digestion with Taq I and gel electrophoresis. We analyzed the genotypes of 69 EOP patients, including 20 patients with unequivocal evidence of localized disease (L-EOP), and 72 controls with no history of EOP. RESULTS: The genotype distribution in the L-EOP patient group was 7 (35%), 5 (25%) and 8 (40%) and in the control group 31 (43.1%), 36 (50.0%) and 5 (6.9%) for TT, Tt and tt respectively (where t and T represent the alleles with and without the Taq I RFLP respectively). Chi2 analysis indicated that the distribution of the genotypes between these two groups was highly significantly different (P = 0.001). Allele frequencies were 47.5% and 52.5% for T and t in the L-EOP group; 68.1% and 31.9% in the control group, showing a significant association between the prevalence of the less frequent allele (t) and L-EOP (P = 0.017). There was no significant difference in the genotype distribution or the allele frequencies between the control samples and the larger EOP patient group (n = 69) which included patients with generalized and localized disease. CONCLUSIONS: These data indicate that carriage of the less frequent allele of the Taq I RFLP (t) in the VDR gene significantly increases the risk of developing L-EOP. However, VDR genotype may not affect the incidence of all cases of EOP. These findings contribute to our understanding of the genetic basis for periodontal disease and may help define sub-groups of this disease which share common pathogenic factors.

Adolescent↗