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Results for “host:pathogen interactions”

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PubMed2001

Molecular machinations: chemokine signals in host-pathogen interactions.

Chemokines and their G-protein-coupled receptors represent an ancient and complex system of cellular communication participating in growth, development, homeostasis and immunity. Chemokine production has been detected in virtually every microbial infection examined; however, the precise role of chemokines is still far from clear. In most cases they appear to promote host resistance by mobilizing leukocytes and activating immune functions that kill, expel, or sequester pathogens. In other cases, the chemokine system has been pirated by pathogens, especially protozoa and viruses, which have exploited host chemokine receptors as modes of cellular invasion or developed chemokine mimics and binding proteins that act as antagonists or inappropriate agonists. Understanding microbial mechanisms of chemokine evasion will potentially lead to novel antimicrobial and anti-inflammatory therapeutic agents.

Animals↗
PubMed2003

Exploration of host-pathogen interactions using Listeria monocytogenes and Drosophila melanogaster.

The facultative intracellular bacterial pathogen Listeria monocytogenes is capable of replicating within a broad range of host cell types and host species. We report here the establishment of the fruit fly Drosophila melanogaster as a new model host for the exploration of L. monocytogenes pathogenesis and host response to infection. Listeria monocytogenes was capable of establishing lethal infections in adult fruit flies and larvae with extensive bacterial replication occurring before host death. Bacteria were found in the cytosol of insect phagocytic cells, and were capable of directing host cell actin polymerization. Bacterial gene products necessary for intracellular replication and cell-to-cell spread within mammalian cells were similarly found to be required within insect cells, and although previous work has suggested that L. monocytogenes virulence gene expression requires temperatures above 30 degrees C, bacteria within insect cells were found to express virulence determinants at 25 degrees C. Mutant strains of Drosophila that were compromised for innate immune responses demonstrated increased susceptibility to L. monocytogenes infection. These data indicate L. monocytogenes infection of fruit flies shares numerous features of mammalian infection, and thus that Drosophila has the potential to serve as a genetically tractable host system that will facilitate the analysis of host cellular responses to L. monocytogenes infection.

Actins↗
PubMed2004

The strategies of the Theileria parasite: a new twist in host-pathogen interactions.

Theileria parasites infect and transform cells of the ruminant immune system. Continuous proliferation and survival of Theileria-transformed cells involves the well-orchestrated activation of several host-cell signalling pathways. Constitutive NF-kappa B (nuclear factor kappa B) activation is accomplished by recruiting the IKK (I kappa B kinase) complex, a central regulator of NF-kappa B pathways, to the surface of the transforming schizont, where it becomes permanently activated. Constitutive activation of the PI-3K-PKB [phosphoinositide 3-kinase-(Akt) protein kinase B] pathway is likely to be indirect and is essential for continuous proliferation. Theileria-transformed T cells express a range of anti-apoptotic proteins that can be expected to provide protection against apoptosis induced by death receptors, as well as cellular control mechanisms that are mobilised to eliminate cells that entered a cycle of uncontrolled proliferation.

Animals↗
PubMed2003

[The nematode Caenorhabditis elegans as a model for the study of host-pathogen interactions].

For certain pathogens capable of infecting a broad range of organisms, there exist universal virulence factors, necessary for full pathogenicity regardless of the host. This has been most clearly demonstrated by Ausubel and colleagues for the human opportunistic pathogen Pseudomonas aeruginosa. As a consequence, one can use non-mammalian model systems, including the nematode worm Caenorhabditis elegans, to assay for such virulence factors. A significant number of pathogens of C. elegans, that provoke a range of diseases, are now known, including the opportunistic human pathogen Serratia marcescens. After explaining the practical advantages associated with the use of C. elegans, and briefly reviewing previous studies, the results of a screen for S. marcescens virulence factors will be presented.

Animals↗
PubMed2003

Micromanipulation of the Chlamydia pneumoniae inclusion: implications for cloning and host-pathogen interactions.

The Chlamydia trachomatis inclusion is fragile, rendering it incompatible to micromanipulation. We show that the Chlamydia pneumoniae inclusion differs, being resistant to micromanipulation as shown by direct microinjection of the infected host cytosol or the inclusion itself. We have used micromanipulation to clone C. pneumoniae and to free it from mycoplasma contamination.

Cell Membrane↗
PubMed1975

Host-pathogen interactions in scrapie.

There are many strains of the agent which causes scrapie and these can be used singly or given as mixed infections to investigate the ways in which agent and host control mechanisms interact during the pathogenesis of the disease. Two genes in mice are described; one only affects the kinetics of the disease when extraneural injections are used, the other acts irrespective of the route of injection and it is suggested that it determines the structure of a multimeric agent-replication site, the number of such subcellular sites in the body being strictly limited.--Different agent strain/host genotype combinations give such a wide range of results that conventional quantitative analysis can yield little of predictive genetical value unless the major biological variables in host and agent can be specified.

Alleles↗
PubMed2000

Growth of Legionella pneumophila in Dictyostelium discoideum: a novel system for genetic analysis of host-pathogen interactions.

Legionella pneumophila, the Gram-negative bacterium that causes Legionnaires' disease, can be cultured in the laboratory in a variety of fresh-water amoebae and macrophage-like cell lines. None of these hosts, however, is amenable to genetic analysis, which has limited the ability of researchers to analyse the host factors essential for L. pneumophila growth. In this article, we describe a novel method in which L. pneumophila is grown within the soil amoeba Dictyostelium discoideum and how D. discoideum genetics is being used to analyse the host cell factors involved in L. pneumophila pathogenesis.

Animals↗
PubMed1997

Host-pathogen interactions in the immunopathogenesis of Lyme disease.

The immunopathogenesis of Lyme disease is complicated and requires a thorough understanding of the interaction among the causative organism, Borrelia burgdorferi, its tick vector, and its mammalian hosts. In vitro, animal and human studies have shown that the organism is capable of adapting to and utilizing elements from its environment to establish infection and persist despite a inducing a strong immune response. Indeed, the immune response may be responsible for many of the symptoms associated with Lyme disease. It appears that humoral immunity plays the greatest role in clearance of the organism. Cytokines released by Th 1 or Th 2 subsets of CD4+ cells have been shown to play an important role in determining outcome of the disease in animal models possibly through their effects on immunoglobulin class switching. In the small percentage of patients who have treatment resistant chronic Lyme disease, autoimmune mechanisms may play a role in persistent disease.

Animals↗
PubMed2002

Caenorhabditis elegans as a host for the study of host-pathogen interactions.

Recently, pathogenicity models that involve the killing of the genetically tractable nematode Caenorhabditis elegans by human pathogens have been developed. From the perspective of the pathogen, the advantage of these models is that thousands of mutagenized bacterial clones can be individually screened for avirulent mutants on separate petri plates seeded with C. elegans. The advantages of using C. elegans to study host responses to pathogen attack are the extensive genetic and genomic resources available and the relative ease of identifying C. elegans mutants that exhibit altered susceptibility to pathogen attack. The use of Caenorhabditis elegans as the host for a variety of human pathogens is discussed.

Actinomycetales↗
PubMed2005

Subcellular proteomic analysis of host-pathogen interactions using human monocytes exposed to Yersinia pestis and Yersinia pseudotuberculosis.

Yersinia pestis, the etiological agent of plague, is of concern to human health both from an infectious disease and a biodefense perspective. While Y. pestis and Yersinia pseudotuberculosis share more than 90% DNA homology, they have significantly different clinical manifestations. Plague is often fatal if untreated, yet Y. pseudotuberculosis causes severe intestinal distress but is rarely fatal. A better understanding of host response to these closely related pathogens may help explain the different mechanisms of virulence and pathogenesis that result in such different clinical outcomes. The aim of this study was to characterize host protein expression changes in human monocyte U937 cells after exposure to Y. pestis and Y. pseudotuberculosis. In order to gain global proteomic coverage of host response, proteins from cytoplasmic, nuclear and membrane fractions of host cells were studied by two-dimensional differential gel electrophoresis and relative protein expression differences were quantitated. Differentially expressed proteins, with at least 1.5-fold expression changes and p values of 0.01 or less, were identified by mass spectrometry including matrix-assisted laser desorption/ionization-MS or liquid chromatography tandem mass spectrometry. With these criteria, differential expression was detected in 16 human proteins after Y. pestis exposure and 13 human proteins after Y. pseudotuberculosis exposure, of which only two of the differentially expressed proteins identified were shared between the two exposures. Proteins identified in this study are reported to be involved in a wide spectrum of cellular functions and host defense mechanisms including apoptosis, cytoskeletal rearrangement, protein synthesis and degradation, DNA replication and transcription, metabolism, protein folding, and cell signaling. Notably, the differential expression patterns observed can distinguish the two pathogen exposures from each other and from unexposed host cells. The functions of the differentially expressed proteins identified provide insight on the different virulence and pathogenic mechanisms of Y. pestis and Y. pseudotuberculosis.

Electrophoresis, Gel, Two-Dimensional↗
PubMed1995

Therapeutic approaches to HIV infection based on virus structure and the host pathogen interaction.

The HIV-1 infection of central nervous system, with attendant neuropathy and dementia, poses a unique challenge for antiviral therapy. For practical considerations, it is important to define carefully the precise therapeutic objectives. (1) Is it necessary to inhibit spreading HIV-1 infection in the central nervous system? (2) What is the role of inflammatory responses in central nervous system disease during HIV-1 infection? (3) Is there a correlation between pathology and dementia? (4) Are virions or virus gene products toxic in the central nervous system? (5) Is there a role for immune suppression and opportunistic pathogens in AIDS dementia? The development of therapeutic agents for HIV-1 infection is guided by our knowledge of virus structure, the function of viral proteins, the interactions with host components, and detailed features of the virus life cycle. In each case, unique features of the virus can be identified and established as targets for unique antiviral compounds. Drugs acting as inhibitors of virus enzymatic functions are plagued by the rapid development in vivo of drug-resistant virus variants, although combination or alternating chemotherapeutic regimens may obviate some of these concerns. Novel approaches to inhibiting virus are flourishing. In vitro studies show the value of agents as diverse as molecular decoys for tat activity to efforts to mutagenize integrated proviruses by modified oligonucleotides that form triple helices with chromosomal genes. As each particular clinical situation is better defined, the design and application of these agents can be refined to inhibit HIV-1 replication and reduce the associated morbidity.

Antiviral Agents↗
PubMed2006

Altered host:pathogen interactions conferred by the Blau syndrome mutation of NOD2.

Blau syndrome (BS) is a rare familial granulomatous disease manifested by uveitis, arthritis and skin rash. BS has recently been found to be associated with a distinctive mutation in NOD2, which encodes an intracellular toll-like receptor. We have compared host cell interaction with bacterial challenge in U937 cells expressing wild type human NOD2 (NOD2(wt)), mutant NOD2 (NOD2(Blau)), or a vector control (VC). The cells were incubated with Salmonella typhimurium. Intracellular uptake was assessed by harvesting the cells at different time points following invasion and quantitating the CFU, recovered after gentamicin treatment to kill extracellular organisms. Expression of TNF-alpha, TLR2 and TLR4 was determined by semi-quantitative RT-PCR under resting conditions and after stimulation by bacteria. Invasion of target cells with S. typhimurium was diminished in the presence of NOD2(Blau). Expression of TNF-alpha mRNA was enhanced following bacterial invasion in all cell lines but NOD2(Blau) was associated with a more rapid decline in TNF-alpha expression. Kinetics of intracellular clearance of bacteria indicated a relative defect in NOD2(Blau) compared to controls. This clearance defect may be related to the lack of sustained TNF-alpha seen in the early stages. These events were not related to differential TLR2 or TLR4 expression since there were no significant differences seen between the cell lines after bacterial stimulation. Our findings indicate that the NOD2 mutation associated with this syndrome alters host:microbial interaction, and this may have relevance to triggering factors in the ocular and joint inflammation seen in BS.

Arthritis↗
PubMed1997

Host-pathogen interactions during entry and actin-based movement of Listeria monocytogenes.

Listeria monocytogenes is a pathogenic bacterium that induces its own uptake into mammalian cells, and spreads from one cell to another by an actin-based motility process. Entry into host cells involves the bacterial surface proteins InlA (internalin) and InlB. The receptor for InlA is the cell adhesion molecule E-cadherin. InlB-mediated entry requires activation of the host protein phosphoinositide (PI) 3-kinase, probably in response to engagement of a receptor. Actin-based movement of L. monocytogenes is mediated by the bacterial surface protein ActA. The N-terminal region of this protein is necessary and sufficient for polymerization of host cell actin. Other host proteins involved in bacterial motility include profilin, Vasodilator-Stimulated Phosphoprotein (VASP), the Arp2/Arp3 complex, and cofilin. Studies of entry and intracellular movement of L. monocytogenes could lead to a better understanding of receptor-ligand signaling and dynamics of actin polymerization in mammalian cells.

Actins↗