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Results for “host:pathogen interactions”

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PubMed2002

Intraspecific variability of Bipolaris sorokiniana isolates determined by random-amplified polymorphic DNA (RAPD).

Isolates of Bipolaris sorokiniana were analyzed by random-amplified polymorphic DNA (RAPD) techniques to determine the amount of intraspecific genetic variability and to study host-pathogen interactions. Ten isolates originated from different regions of Brazil were examined. Plants of the wheat cultivars BR8, BH1146 (original host) and IAC-5 Maringá, classified as resistant, moderately resistant or susceptible to B. sorokiniana, respectively, were inoculated with these 10 isolates. Twenty-seven isolates were recovered from these cultivars and were analyzed by RAPD assay and compared to the RAPD of the original 10 isolates. According to the RAPD profiles there was a high level of genetic variability among the isolates. We detected 69 polymorphic fragments, ranging from 1.6 to 0.54 kb, in the original 10 isolates; 57 fragments with sizes between 1.98 and 0.38 kb from the isolates recovered from BH1146; 47 polymorphic bands, ranging from 1.96-0.54 kb, were detected in the isolates from BR8 and 32 fragments between 1.98 and 0.42 kb in isolates were recovered from IAC-5 Maringá. The number of polymorphic fragments varied, even for the same isolate, when the isolates were recovered from different cultivar hosts.

Ascomycota↗

PubMed2005

The plant's capacity in regulating resource demand.

Regulation of resource allocation in plants is the key to integrate understanding of metabolism and resource flux across the whole plant. The challenge is to understand trade-offs as plants balance allocation between different and conflicting demands, e.g., for staying competitive with neighbours and ensuring defence against parasites. Related hypothesis evaluation can, however, produce equivocal results. Overcoming deficits in understanding underlying mechanisms is achieved through integrated experimentation and modelling the various spatio-temporal scaling levels, from genetic control and cell metabolism towards resource flux at the stand level. An integrated, interdisciplinary research concept on herbaceous and woody plants and its outcome to date are used, while drawing attention to currently available knowledge. This assessment is based on resource allocation as driven through plant-pathogen and plant-mycorrhizosphere interaction, as well as competition with neighbouring plants in stands, conceiving such biotic interactions as a "unity" in the control of allocation. Biotic interaction may diminish or foster effects of abiotic stress on allocation, as changes in allocation do not necessarily result from metabolic re-adjustment but may obey allometric rules during ontogeny. Focus is required on host-pathogen interaction under variable resource supply and disturbance, including effects of competition and mycorrhization. Cost/benefit relationships in balancing resource investments versus gains turned out to be fundamental in quantifying competitiveness when related to the space, which is subject to competitive resource exploitation. A space-related view of defence as a form of prevention of decline in competitiveness may promote conversion of resource turnover across the different kinds of biotic interaction, given their capacity in jointly controlling whole plant resource allocation.

Energy Metabolism↗

PubMed2004

Textmining in support of knowledge discovery for vaccine development.

Complete genome data of infectious microorganisms permit systematic computational sequence-based predictions and experimental testing of candidate vaccine epitopes. Both, predictions and the interpretation of experiments rely on existing information in the literature which is mostly manually extracted and curated. The growing amount of data and literature information has created a major bottleneck for the interpretation of results and maintenance of curated databases. The lack of suitable free-text information extraction, processing, and reporting tools prompted us to develop a knowledge discovery support system that enhances the understanding of immune response and vaccine development. The current prototype system, Gene expression/epitpopes/protein interaction (GEpi), focuses on molecular functions of HIV-infected T-cells and HIV epitope information, using textmining, and interrelation of biomolecular data from domain-specific databases with MEDLINE abstract-inferred information. Results showed that extraction and processing of molecular interaction, disease associations, and gene ontology-derived functional information generate intuitive knowledge reports that aid the interpretation of host-pathogen interaction. In contrast, epitope (word and sequence) information in MEDLINE abstracts is surprisingly sparse and often lacks necessary context information, such as HLA-restriction. Since the majority of epitope information is found in tables, figures, and legends of full-text articles, its extraction may not require sophisticated natural language processing techniques. Support of vaccine development through textmining requires therefore the timely development of domain-specific extraction rules for full-text articles, and a knowledge model for epitope-related information.

Animals↗

PubMed2002

Cellular hijacking: a common strategy for microbial infection.

Eukaryotic cells are under constant attack from microbial intruders seeking a selective advantage for survival, propagation and dissemination. Microbial infections can often result in disease and might even be lethal to the host if they are not combatted effectively. Studies of host-pathogen interactions have revealed that virulence often requires the usurpation of existing cell signaling pathways or membrane traffic machinery of the host. Such studies provide a rich source of cell biological data that will probably prove essential for future efforts designed to either thwart these attacks or learn from them.

ADP Ribose Transferases↗

PubMed2003

Transcriptional analysis of the response of poultry species to respiratory pathogens.

Respiratory tract diseases are the single most important cause of economic loss due to infections among poultry populations worldwide. However, the molecular mechanisms of the host response to infections remain unknown. Here, we review the literature and describe the adoption of a conceptually simple approach to understand the genetic and biochemical responses of host cells during infection with respiratory pathogens, such as avian pneumovirus (APV). The strategy that we have adopted integrates the powerful techniques of cDNA subtraction hybridization and microarray analysis for global transcriptional profiling. The results of our investigations identify the specific transcriptional alterations in host-cell gene expression that result from an attempt by the host to combat and limit the spread of the pathogen or by the pathogen to enhance its own survival and ability to reproduce. Our studies suggest that a molecular description of host-pathogen interactions in terms of differential gene expression will provide key insights on the molecular basis of disease pathogenesis, pathogen virulence, and host immunity. In addition, the results suggest that the identification of genes and pathways with a role in host response to infection has considerable practical implications for the future design and development of effective immunomodulators and vaccines.

Animals↗

PubMed2005

Genome-wide RNAi screen for host factors required for intracellular bacterial infection.

Most studies of host-pathogen interactions have focused on pathogen-specific virulence determinants. Here, we report a genome-wide RNA interference screen to identify host factors required for intracellular bacterial pathogenesis. Using Drosophila cells and the cytosolic pathogen Listeria monocytogenes, we identified 305 double-stranded RNAs targeting a wide range of cellular functions that altered L. monocytogenes infection. Comparison to a similar screen with Mycobacterium fortuitum, a vacuolar pathogen, identified host factors that may play a general role in intracellular pathogenesis and factors that specifically affect access to the cytosol by L. monocytogenes.

Animals↗

PubMed2001

Molecular mechanisms of bacteria induced apoptosis.

Interaction of mammalian cells with pathogenic bacteria results in a whole variety of responses in the infected cells including internalization or phagocytosis of the bacterium, release of cytokines, secretion of defensins or production of oxygen radicals. However, recent studies pointed out that many bacteria are able to trigger apoptosis in the host cell. The induction of apoptosis upon infection results from a complex interaction of bacterial proteins with cellular proteins finally mediating apoptosis. Thus, bacteria are able to activate several pro-apoptotic proteins, e.g. caspases, to inactivate anti-apoptotic proteins, e.g. NF(kappa)B or MAP-kinases, or to upregulate endogenous receptor/ligand systems, that induce apoptosis, on the surface of the infected cell. Host cell apoptosis very often serves the bacteria to attack the host and to gain access to the tissue. However, in some infections, apoptosis of mammalian cells significantly contributes to the host defense against the bacteria further indicating the role of apoptosis in host-pathogen interactions.

Animals↗

PubMed1999

A natural variant of the cysteine protease virulence factor of group A Streptococcus with an arginine-glycine-aspartic acid (RGD) motif preferentially binds human integrins alphavbeta3 and alphaIIbbeta3.

The human pathogenic bacterium group A Streptococcus produces an extracellular cysteine protease [streptococcal pyrogenic exotoxin B (SpeB)] that is a critical virulence factor for invasive disease episodes. Sequence analysis of the speB gene from 200 group A Streptococcus isolates collected worldwide identified three main mature SpeB (mSpeB) variants. One of these variants (mSpeB2) contains an Arg-Gly-Asp (RGD) sequence, a tripeptide motif that is commonly recognized by integrin receptors. mSpeB2 is made by all isolates of the unusually virulent serotype M1 and several other geographically widespread clones that frequently cause invasive infections. Only the mSpeB2 variant bound to transfected cells expressing integrin alphavbeta3 (also known as the vitronectin receptor) or alphaIIbbeta3 (platelet glycoprotein IIb-IIIa), and binding was blocked by a mAb that recognizes the streptococcal protease RGD motif region. In addition, mSpeB2 bound purified platelet integrin alphaIIbbeta3. Defined beta3 mutants that are altered for fibrinogen binding were defective for SpeB binding. Synthetic peptides with the mSpeB2 RGD motif, but not the RSD sequence present in other mSpeB variants, blocked binding of mSpeB2 to transfected cells expressing alphavbeta3 and caused detachment of cultured human umbilical vein endothelial cells. The results (i) identify a Gram-positive virulence factor that directly binds integrins, (ii) identify naturally occurring variants of a documented Gram-positive virulence factor with biomedically relevant differences in their interactions with host cells, and (iii) add to the theme that subtle natural variation in microbial virulence factor structure alters the character of host-pathogen interactions.

Alleles↗

PubMed1998

Supernumerary chromosomes in filamentous fungi.

Within a fungal species, a subset of individuals may have more than the minimal complement of chromosomes. If the extra chromosomes are composed primarily of DNA not found in all representatives of the species, they are most appropriately referred to as supernumerary chromosomes. The patterns of repeated DNA sequences on certain supernumerary chromosomes suggest that they have a different evolutionary history from the essential chromosomes in the same genome. Supernumerary chromosomes can carry functional genes and, in at least two fungal species, genes on such chromosomes play important roles in host-pathogen interactions. Supernumerary chromosomes that confer an adaptive advantage in certain habitats, such as the ability to cause disease on a specific host, may be referred to as "conditionally dispensable" chromosomes in order to reflect their importance in some, but not all, growth conditions. In addition to describing the structural and functional characteristics of known supernumerary chromosomes in fungi, this review discusses the relative merits of the terms that have been used to describe them, and establishes experimental criteria for their identification.

Chromosomes, Fungal↗

PubMed2006

Staphylococcal colonization and infection: homeostasis versus disbalance of human (innate) immunity and bacterial virulence.

PURPOSE OF REVIEW: This review identifies trends in the study of interactions between Staphylococcus aureus and humans. When nasal colonization is in the neutral state, infection clearly represents a state of host-pathogen disbalance. The features leading from apparent homeostatic colonization to pathogenesis are identified at an increasing rate. RECENT FINDINGS: Persistent carriage of S. aureus predisposes to infection but limits bacteraemia-associated mortality. Intermittent carriage is usually imposed and of lesser clinical relevance. The nature and function of several staphylococcal virulence factors have been elucidated and near complete gene catalogues have been established. There does not seem to be a difference in virulence, however, between methicillin-susceptible and resistant S. aureus. Biological selection takes place in the nose and innate immune features relevant to colonization have been discovered. Acquired immunity remains underexposed, but the host factors involved in the host-pathogen interaction have been identified. SUMMARY: Virulence assessment of S. aureus has been facilitated by novel technology: genome-wide inventories of virulence potential can be made and new pathogenic mechanisms have been presumptively identified. These involve invasion procedures but also (innate) immune evasion strategies. These cross-fertilizing developments shed light on the feasibility of novel prophylactic or therapeutic strategies for combating staphylococcal carriage and disease.

Antibodies, Bacterial↗

PubMed2006

Mos1 mutagenesis reveals a diversity of mechanisms affecting response of Caenorhabditis elegans to the bacterial pathogen Microbacterium nematophilum.

A specific host-pathogen interaction exists between Caenorhabditis elegans and the gram-positive bacterium Microbacterium nematophilum. This bacterium is able to colonize the rectum of susceptible worms and induces a defensive tail-swelling response in the host. Previous mutant screens have identified multiple loci that affect this interaction. Some of these loci correspond to known genes, but many bus genes [those with a bacterially unswollen (Bus) mutant phenotype] have yet to be cloned. We employed Mos1 transposon mutagenesis as a means of more rapidly cloning bus genes and identifying new mutants with altered pathogen response. This approach revealed new infection-related roles for two well-characterized and much-studied genes, egl-8 and tax-4. It also allowed the cloning of a known bus gene, bus-17, which encodes a predicted galactosyltransferase, and of a new bus gene, bus-19, which encodes a novel, albeit ancient, protein. The results illustrate advantages and disadvantages of Mos1 transposon mutagenesis in this system.

Actinomycetales↗

PubMed2006

Characterizing plasma membrane H+-ATPase in two varieties of coffee leaf (Coffea arabica L.) and its interaction with an elicitor fraction from the orange rust fungus (H. vastatrix Berk and Br.) race II.

Early intercellular signaling in Coffea arabica L.-Hemileia vastatrix host-pathogen interaction was studied, using inside-out plasma membrane from two varieties of coffee leaf and a fungal fraction to determine the plant's biochemical responses. Microsomal pellets (100,000 x g) from the susceptible (Caturra) and resistant (Colombia) coffee leaf varieties were purified by partitioning in two-polymer DEX (6.3% w/w) and PEG (6.3% w/w) system aqueous phase. Fungal material was obtained from orange rust Hemileia vastatrix Berk and Br. race II urediospore germ tubes. Plasma membrane vesicles were preferentially localized to PEG phase, as indicated by its enzyme marker distribution. Both H(+)-ATPase activities displayed similar kinetic and biochemical characteristics, comparable to those described for P-type ATPases. Several enzymes may play pivotal roles in plants regarding early interaction with fungal elicitors. Studies of fungal fractions' effects on H(+)-ATPase and both varieties' proton pumping activities were thus carried out. Concentration as low as 0.1 Gluc eq. ml(-1) fungal fraction induced specific inhibition of H(+)-ATPase and the resistant variety's proton pumping activities. The present work describes characterizing the H(+)-ATPase plasma membrane from two Coffea arabica L. varieties (Caturra and Colombia) for the first time and the race specific inhibitory effect of a crude fungal fraction on both H(+)-ATPase and the resistant variety's proton pumping activities.

Cell Membrane↗

PubMed2006

Early cytokine profiles in the joint define pathogen clearance and severity of arthritis in Chlamydia-induced arthritis in rats.

OBJECTIVE: Although Chlamydia trachomatis-induced arthritis is among the most common rheumatic diseases having an identified infectious trigger, the pathogenesis of this arthritis is not well defined. We sought to investigate the host-microbe interactions that contribute to the severity of arthritis initiated by chlamydial infection. METHODS: We established an experimental rat model of C. trachomatis-induced arthritis that recapitulates many pathologic features of the clinical disease. The severity of the arthritis was defined using an established histopathologic scoring system. Host clearance of the pathogen and local cytokine production were examined by enzyme-linked immunosorbent assays. RESULTS: Lewis rats were susceptible to C. trachomatis-induced arthritis, whereas BN rats were relatively resistant to this disease. Significant differences in the histopathologic severity of arthritis were originally observed on day 21, and this prompted an examination of the acute phase of the arthritis. As early as day 5 after the onset of the arthritis, pathologic changes in Lewis rats were more severe than those in BN rats. An evaluation of the role of complement using cobra venom factor treatment excluded complement as being the key to differential sensitivity, because decomplementation did not eliminate the differences in arthritis severity between Lewis and BN rats. Host clearance, in contrast, was significantly different between the rat strains, with BN rats showing more prompt and effective clearance of the pathogen from both synovial tissues and spleen compared with Lewis rats. Local cytokine profiles demonstrated that host resistance was characterized by enhanced synovial expression of tumor necrosis factor alpha, interferon-gamma (IFNgamma), and interleukin-4. CONCLUSION: These studies demonstrated that cytokines thought to be proinflammatory in nature can play an important role in host defense in infection-triggered arthritis and serve to highlight the dynamic cytokine relationships that constitute effective host-pathogen interactions.

Animals↗

PubMed2005

Application of microbial genomic science to advanced therapeutics.

Since the publication of the first complete microbial genome sequence of Haemophilus influenzae in 1995, more than 200 additional microbial genome sequences have become available in the public domain. Approximately 40% of these represent important human pathogens. Comparative in silico methods, along with large-scale approaches such as transcriptomics and proteomics, are beginning to reveal insights into new virulence genes, pathogen-host interactions, and the molecular basis of host specificity. Sequence data are also starting to accumulate from multiple isolates or strains of a single pathogen, and this type of data has proven to be quite valuable in providing new insights into the genetic variability that is present in a particular species as well as in facilitating correlations between genotype and phenotype. Ultimately, a major goal of genome-enabled infectious disease research is the development of novel diagnostics, therapeutics, and vaccines.

Animals↗

PubMed1991

Genetics of prion infections.

Although the infectious prions causing scrapie and several human transmissible neurodegenerative diseases resemble viruses in many respects, molecular and genetic analyses indicate that prions are fundamentally different from viruses in their structure and the mechanisms by which they cause disease. The only macromolecule that has been identified in infectious prion preparations is a disease-specific isoform of the prion protein, which is encoded by a host gene. A growing body of data supports the contention that prion infections represent a novel host-pathogen interaction.

Animals↗

PubMedDate not supplied

How Mannheimia haemolytica defeats host defence through a kiss of death mechanism.

Mannheimia haemolytica induced pneumonias are only observed in goats, sheep and cattle. The bacterium produces several virulence factors,whose principal ones are lipopolysaccharide and leukotoxin. The latter is cytotoxic only for ruminant leukocytes, a phenomenon that is correlated with its ability to bind and interact with the ruminant beta2-integrin Lymphocyte Function-associated Antigen 1. This paper globally reviews all the information available on host-pathogen interactions underlying respiratory mannheimiosis (formerly pasteurellosis), from the stable and the Petri dish to the biochemical cascade of events triggered by the leukotoxin inside ruminant leukocytes. One conclusion can be made: the most widespread cattle respiratory disease with the most important impact on beef production worldwide, is probably due to a tiny ruminant-specific focal variation in the CD18- and/or CD11a-expressing genes.

Animals↗

PubMed1980

Ultrastructural observations on cellular and subcellular aspects of experimental Mycoplasma pneumoniae disease.

The ultrastructural organization of Mycoplasma pneumoniae membranes and spatial relationships of this pathogen to epithelial cells in tracheal organ cultures were examined ultrastructurally by freeze-fracture techniques. Areas of morphologically distinct cell membrane variability characterized by membrane blebs and altered distributions of membrane associated particles were observed in replicas of M. pneumoniae cells. Inspection of the host tracheal epithelium demonstrated the alignment of M. pneumoniae to the epithelium with an accompanying deterioration in the integrity of the lumenal surface membranes and subsequent loss of the epithelial cell cytosol. Ciliary dysfunction was suggested by the observation of ciliary lesions and of disorganized epithelial cell cilia. The methodology used in these studies has permitted a new perspective of host-pathogen interactions at both the cellular and subcellular levels in tracheal organ cultures. These studies may also illustrate ultrastructural correlates of the alteration of host macromolecular synthesis in experimental M. pneumoniae infection.

Animals↗

PubMed2006

Directed delivery of heat-labile enterotoxin by enterotoxigenic Escherichia coli.

Enterotoxigenic Escherichia coli (ETEC), leading causes of diarrhoeal morbidity and mortality in developing countries, are heterogenous pathogens that elaborate heat-labile (LT) and/or heat-stable (ST) enterotoxins which elicit watery, cholera-like diarrhoea. The molecular events permitting efficient delivery of LT remain undefined. Here, we characterize the role of host-pathogen interaction as it relates to the delivery of LT by ETEC. Separation of bacteria from target intestinal epithelial monolayers by semipermeable filters prevented activation of adenylate cyclase suggesting that pathogen-host cell contact is required for efficient toxin delivery. Likewise, a non-motile strain bearing a mutation in the flagellar fliD gene was deficient in delivery of LT relative to the ETEC (H10407) prototype. Although LT secretion via the type II secretion system (T2SS) was responsive to a variety of environmental factors, neither toxin release nor delivery depended on transcriptional activation of genes encoding LT or the T2SS. Fusions of green fluorescent protein to GspM (a component of the T2SS system for LT) and to LT demonstrated that both T2SS and toxin are distributed at one pole of the ETEC bacterium. Optimal LT delivery may occur in a polarized fashion with transfer of preformed toxin upon close interaction with host cells, preventing neutralization of LT.

Caco-2 Cells↗