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Results for “host:pathogen interactions”

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PubMed2004

Isolation of the repertoire of VSG expression site containing telomeres of Trypanosoma brucei 427 using transformation-associated recombination in yeast.

Trypanosoma brucei switches between variant surface glycoproteins (VSGs) allowing immune escape. The active VSG is in one of many telomeric bloodstream form VSG expression sites (BESs), also containing expression site-associated genes (ESAGs) involved in host adaptation. The role of BES sequence diversity in parasite virulence can best be understood through analysis of the full repertoire of BESs from a given T. brucei strain. However, few BESs have been cloned, as telomeres are highly underrepresented in standard libraries. We devised a strategy for isolating the repertoire of T. brucei 427 BES-containing telomeres in Saccaromyces cerevisiae by using transformation-associated recombination (TAR). We isolated 182 T. brucei 427 BES TAR clones, 167 of which could be subdivided into minimally 17 BES groups. This set gives us the first view of the breadth and diversity of BESs from one T. brucei strain. Most BESs ranged between 40 and 70 kb (average, 57 +/- 17 kb) and contained most identified ESAGs. Phylogenetic comparison of the cohort of BES promoter and ESAG6 sequences did not show similar trees, indicating rapid evolution most likely mediated by sequence exchange between BESs. This cloning strategy could be used for any T. brucei strain, facilitating research on the biodiversity of telomeric gene families and host-pathogen interactions.

Animals↗

PubMed2005

Insights on biology and evolution from microbial genome sequencing.

No field of research has embraced and applied genomic technology more than the field of microbiology. Comparative analysis of nearly 300 microbial species has demonstrated that the microbial genome is a dynamic entity shaped by multiple forces. Microbial genomics has provided a foundation for a broad range of applications, from understanding basic biological processes, host-pathogen interactions, and protein-protein interactions, to discovering DNA variations that can be used in genotyping or forensic analyses, the design of novel antimicrobial compounds and vaccines, and the engineering of microbes for industrial applications. Most recently, metagenomics approaches are allowing us to begin to probe complex microbial communities for the first time, and they hold great promise in helping to unravel the relationships between microbial species.

DNA, Bacterial↗

PubMed2006

Genomic islands of differentiation between house mouse subspecies.

Understanding the genes that contribute to reproductive isolation is essential to understanding speciation, but isolating such genes has proven very difficult. In this study I apply a multilocus test statistic to >10,000 SNP markers assayed in wild-derived inbred strains of house mice to identify genomic regions of elevated differentiation between two subspecies of house mice, Mus musculus musculus and M. m. domesticus. Differentiation was high through approximately 90% of the X chromosome. In addition, eight regions of high differentiation were identified on the autosomes, totaling 7.5% of the autosomal genome. Regions of high differentiation were confirmed by direct sequencing of samples collected from the wild. Some regions of elevated differentiation have an overrepresentation of genes with host-pathogen interactions and olfaction. The most strongly differentiated region on the X has previously been shown to fail to introgress across a hybrid zone between the two subspecies. This survey indicates autosomal regions that should also be examined for differential introgression across the hybrid zone, as containing potential genes causing hybrid unfitness.

Animals↗

PubMed1981

Hydroxyproline Enhancement as a Primary Event in the Successful Development of Erysiphe graminis in Wheat.

Host cell wall hydroxyproline enhancement was observed in the successful development of the parasite Erysiphe graminis DC. f. sp. tritici em Marchal (MS-1) on wheat (em Thell). Hydroxyproline enhancement, which was observed only in susceptible hosts, was detected as early as 25 hours after infection. This observation suggests that the increase in cell wall hydroxyproline is a primary event in the host-pathogen interaction of Erysiphe graminis in wheat.

Journal Article↗

PubMed1982

Ethylene Production and Leaflet Abscission of Three Peanut Genotypes Infected with Cercospora arachidicola Hori.

Ethylene can induce abscission of leaves and other plant organs. Increased ethylene production by plant tissues can occur after invasion by microorganisms. The fungus Cercospora arachidicola Hori, attacks peanut leaflets and causes defoliation. Our objective was to determine if ethylene was involved in this defoliation. Leaves of three peanut, Arachis sp., genotypes were inoculated with C. arachidicola. Two genotypes, ;Tamnut 74' and PI 109839, produced ethylene and were defoliated. The third genotype, PI 276233, a wild species, did not produce ethylene above control levels and was not defoliated. Increase in ethylene production by Tamnut 74 and PI 109839 coincided with appearance of disease symptoms. Tamnut 74 produced the most ethylene, but PI 109839 was equally defoliated. Thus, less overall ethylene production did not necessarily indicate a more resistant genotype in this system unless ethylene production remained at control levels, as it did for PI 276233. Ethylene sufficient to initiate abscission could have been produced by the seventh day after inoculation when it was similar for both Tamnut 74 and PI 109839, but 3 to 4 times control amounts. This occurred before the rapid increase in ethylene production and before disease symptoms were visible. Silver ion, a potent inhibitor of ethylene action, was sprayed at three concentrations on intact Tamnut 74 plants. All rates reduced abscission and 150 mg/liter Ag(I) decreased abscission to below 10%. The data indicate that ethylene produced by peanut leaves in response to C. arachidicola infection initiates abscission and that ethylene action can be blocked by Ag(I) in such a host-pathogen interaction.

Journal Article↗

PubMed1984

Ethylene-Induced Chlorosis in the Pathogenesis of Bipolaris sorokiniana Leaf Spot of Poa pratensis.

Endogenous ethylene of Poa pratensis leaves infected by Bipolaris sorokiniana was evaluated as a factor in leaf chlorosis during pathogenesis. Detectable increases in endogenous ethylene of leaves of intact plants under normal ambient pressure occurred 12 hours after inoculation and was maximum at 48 hours; from 48 to 96 hours the ethylene progressively decreased. Necrotic lesions surrounded by chlorotic halos occurred on infected leaves between 24 and 48 hours. Midvein chlorosis interconnecting individual lesions and complete chlorosis of all tissues not directly affected by the lesions occurred between 72 and 96 hours, after maximum production of ethylene at 48 hours. The chlorophyll loss in infected leaves by 96 hours was 44% compared with controls.Subjecting inoculated leaves of intact plants to a controlled atmospheric-environmental system with an atmospheric pressure of 233 millibars and O(2) and CO(2) partial pressures adjusted to approximately that of normal ambient pressure during infection and disease development prevented most midvein chlorosis and complete chlorosis, but did not prevent necrotic lesion or chlorotic halo development. Under the hypobaric conditions, chlorophyll loss during disease development was reduced to 22% compared with controls at 96 hours. The observations suggest that ethylene may function late in pathogenesis of this host-pathogen interaction and is responsible for much of the chlorophyll loss after its maximum production at 48 hours.

Journal Article↗

PubMed2006

Genome sequences of the honey bee pathogens Paenibacillus larvae and Ascosphaera apis.

Genome sequences offer a broad view of host-pathogen interactions at the systems biology level. With the completion of the sequence of the honey bee, interest in the relevant pathogens is heightened. Here we report the genome sequences of two of the major pathogens of honey bees, the bacterium Paenibacillus larvae (causative agent for American foulbrood disease) and the fungus Ascosphaera apis. (causative agent for chalkbrood disease). Ongoing efforts to characterize the genomes of these species can be used to understand and mitigate the effects of two important pathogens, and will provide a contrast with pathogenic, benign and freeliving relatives.

Animals↗

PubMed2004

Quorum sensing and signal interference: diverse implications.

Quorum sensing (QS) is a community genetic regulation mechanism that controls microbiological functions of medical, agricultural and industrial importance. Discovery of microbial QS signals and the signalling mechanisms led to identification of numerous enzymatic and non-enzymatic signal interference mechanisms that quench microbial QS signalling. Evidence is accumulating that such signal interference mechanisms can be developed as promising approaches to control microbial infection and biofilm formation. In addition, these mechanisms exist not only in microorganisms but also in the host organisms of bacterial pathogens, highlighting their potential implications in microbial ecology and in host-pathogen interactions. Investigation of QS and signal interference mechanisms might significantly broaden the scope of research in microbiology.

Animals↗

PubMed2005

Human fibrinogen bound to Streptococcus pyogenes M protein inhibits complement deposition via the classical pathway.

Human fibrinogen (Fg) binds to surface proteins expressed by many pathogenic bacteria and has been implicated in different host-pathogen interactions, but the role of bound Fg remains unclear. Here, we analyse the role of Fg bound to Streptococcus pyogenes M protein, a major virulence factor that confers resistance to phagocytosis. Studies of the M5 system showed that a chromosomal mutant lacking the Fg-binding region was completely unable to resist phagocytosis, indicating that bound Fg plays a key role in virulence. Deposition of complement on S. pyogenes occurred via the classical pathway even under non-immune conditions, but was blocked by M5-bound Fg, which reduced the amount of classical pathway C3 convertase on the bacterial surface. This property of M protein-bound Fg may explain its role in phagocytosis resistance. Previous studies have shown that many M proteins do not bind Fg, but interfere with complement deposition and phagocytosis by recruiting human C4b-binding protein (C4BP), an inhibitor of the classical pathway. Thus, all M proteins may share ability to recruit a human plasma protein, Fg or C4BP, which inhibits complement deposition via the classical pathway. Our data identify a novel function for surface-bound Fg and allow us to propose a unifying mechanism by which M proteins interfere with innate immunity.

Antigens, Bacterial↗

PubMed2005

A glutamate-alanine-leucine (EAL) domain protein of Salmonella controls bacterial survival in mice, antioxidant defence and killing of macrophages: role of cyclic diGMP.

Signature-tagged transposon mutagenesis of Salmonella with differential recovery from wild-type and immunodeficient mice revealed that the gene here named cdgR[for c-diguanylate (c-diGMP) regulator] is required for the bacterium to resist host phagocyte oxidase in vivo. CdgR consists solely of a glutamate-alanine-leucine (EAL) domain, a predicted cyclic diGMP (c-diGMP) phosphodiesterase. Disruption of cdgR decreased bacterial resistance to hydrogen peroxide and accelerated bacterial killing of macrophages. An ultrasensitive assay revealed c-diGMP in wild-type Salmonella with increased levels in the CdgR-deficient mutant. Thus, besides its known role in regulating cellulose synthesis and biofilm formation, bacterial c-diGMP also regulates host-pathogen interactions involving antioxidant defence and cytotoxicity.

Amino Acid Sequence↗

PubMed2006

Antibody responses to Ascaris-derived proteins and glycolipids: the role of phosphorylcholine.

In addition to proteins, glycolipids can be targets of antibody responses and contribute to host-pathogen interaction. Following the structural analysis of Ascaris lumbricoides-derived glycolipids, the antibody responses of a group of children with no, light and heavy infections were analysed. The role of the phosphorylcholine moiety, present on Ascaris glycoproteins and glycolipids, in antibody reactivity of these infected individuals was determined. Children carrying heavy infections showed highest IgG reactivity to glycolipids compared to lightly or non-infected children. Substantial IgG antibody reactivity to both (glyco)proteins and glycolipids was found to be directed to the phosphorylcholine moiety as determined by either removal of this group or a competition assay. This was most pronounced for glycolipids, where removal of the phosphorylcholine moieties by hydrofluoric acid treatment abrogated IgG antibody reactivity. Measurement of IgG4 and IgE isotypes showed no IgG4 reactivity to Ascaris glycolipids, but raised IgE responses were detected in subjects with light or no Ascaris infections, suggesting that IgE responses to glycolipids may play a role in controlling parasite burden. Differences found in antibody profiles to glycolipids and (glyco)proteins, indicate that these different classes of compounds may have distinct roles in shaping of and interacting with humoral immune responses.

Animals↗

PubMed2004

Prospects for new tuberculosis treatment in Africa.

Health services in Africa are being overburdened by a continuous increase of cases of tuberculosis (TB), largely resulting from the large pool of infected individuals becoming co-infected with HIV. To help deal with the situation, TB treatment schedules need to be shorter and simpler, with minimal contact between the patient and the service provider required, if the problems of non-compliance and of ineffective service provision are to be overcome. Various drugs not marketed for use in the treatment of TB are currently under investigation for their potential roles in the simplification or shortening of treatment schedules. These mainly include the long-acting rifamycins and the fluoroquinolones. Furthermore, new drug development is focused on an understanding of the host-pathogen interaction leading to infection, latency and disease. Of these, latency is least understood. The use of molecular diversity and combinatorial chemistry, proteomics, and the use of the whole genome to discover drug targets are expected to produce new lead compounds for turning into drugs to treat active, latent and multi-drug-resistant TB more effectively in the foreseeable future.

Africa↗

PubMed2004

Natural killer cell receptors for major histocompatibility complex class I and related molecules in cytomegalovirus infection.

Downmodulation of major histocompatibility complex (MHC) class I molecules by cytomegalovirus (CMV) impairs the engagement of specific leucocyte-inhibitory receptors, rendering infected cells vulnerable to natural killer (NK) cells. Members of the murine Ly49 and human KIR families, CD85j (ILT2 or leucocyte Ig-like receptor-1), as well as the CD94/NKG2A-inhibitory killer lectin-like receptor (KLR) fulfil this surveillance role. On the other hand, NK-activating receptors specific to ligands expressed on virus-infected cells may overcome the control by inhibitory receptors. In this regard, NKG2D and Ly49H lectin-like molecules trigger NK-cell functions recognizing, respectively class I-related stress-inducible molecules and the m157 murine CMV glycoprotein. Among a variety of immune evasion strategies, CMV promotes the synthesis of class I surrogates and selectively preserves the expression of some class I molecules in infected cells; moreover, CMV interferes with the expression of ligands for NKG2D. We herein review these aspects of the host-pathogen interaction, discussing a number of open issues.

Animals↗

PubMed1998

Virulence factors of Streptococcus uberis isolated from cows with mastitis.

For intramammary infections (IMI) to occur, mechanisms associated with avoidance of phagocytic defenses, rapid growth of bacteria, adherence of bacteria to epithelial cells, and/or bacterial colonization of mammary tissue are probably present. During the last decade, several potential virulence factors of Streptococcus uberis have been identified. Some of these factors are cell-associated while other factors are extracellular. Proposed antiphagocytic factors of S. uberis include capsule, neutrophil toxin, M-like protein and R-like protein. Activation of plasminogen by S. uberis has been proposed as an important mechanism for this organism to obtain nutrients for optimal bacterial growth. Potential virulence factors produced by S. uberis and released extracellularly include hyaluronic acid capsule, hyaluronidase and uberis factor. Streptococcus uberis isolated from bovine IMI adhere to and invade mammary epithelial cells. Involvement of intact microfilaments and de novo eukaryotic protein synthesis are required for bacterial invasion of mammary epithelial cells; a process that appeared to occur by a receptor-mediated endocytosis mechanism. De novo bacterial protein synthesis was also required for invasion of S. uberis into mammary epithelial cells. Furthermore, S. uberis survived within mammary epithelial cells for extended periods of time without losing viability or damaging the eukaryotic cell. Further research directed towards characterization of host-pathogen interactions that take place during the early stages of S. uberis intramammary infection are needed to enhance our understanding of pathogenesis and thus contribute to development of methods to minimize production losses associated with S. uberis mastitis in dairy cows.

Animals↗

PubMed2005

Immune responses to dsRNA: implications for gene silencing technologies.

Nucleic acid-induced gene silencing, such as RNA interference (RNAi), induces a multitude of responses in addition to the knockdown of a gene. This is best understood in the context of the antiviral immune response, from which the processes of RNAi are thought to be derived. Viral challenge of a vertebrate host leads to an intricate series of responses that orchestrate antiviral immunity. The success of this multifaceted system in overcoming viral encounters hinges on complex pathogen-host interactions. One aspect of these interactions, the nucleic acid-based immune response, is key to the successful resolution of a viral challenge. In particular, dsRNA, a nucleic acid associated with viral replication, is involved in numerous interactions contributing to induction, activation and regulation of antiviral mechanisms. Specifically, dsRNA is responsible for stimulating important protective responses, such as the activation of dicer-related antiviral pathways, induction of type 1 IFN, and stimulation of dsRNA-activated protein kinase and oligoadenylate synthetase. Furthermore, the modulation and shaping of this overall immune response is facilitated through nucleic acid interactions with pattern recognition receptors such as toll-like receptor 3. These diverse dsRNA-induced antiviral responses have implications for biotechnologies that use dsRNA to harness one arm of the host antiviral machinery for silencing a specific target gene. The interlinked nature of these response elements means that it may be difficult to completely isolate one element from the other arms of the antiviral response program of an organism. Thus, it is beneficial to understand all aspects of the immune response to dsRNA in order to manipulate these systems and minimize unwanted non-specific effects.

Animals↗

PubMed2005

Caenorhabditis elegans as a model for innate immunity to pathogens.

The amenability of the nematode Caenorhabditis elegans for genetic analysis and other experimentation provides a powerful tool for studying host-pathogen interactions. Our current understanding of how C. elegans responds to pathogen challenges is in its infancy, but the discovery that the worm has inducible defence responses, which to some extent parallel those of other organisms, demonstrates the potential of this model organism for the study of innate immunity. Most progress in dissecting the C. elegans antimicrobial response has focused around signal transduction pathways and the expression of genes activated by the worm in response to microbial infections.

Animals↗

PubMed2006

Dictyostelium transcriptional host cell response upon infection with Legionella.

Differential gene expression of Dictyostelium discoideum after infection with Legionella pneumophila was investigated using DNA microarrays. Investigation of a 48 h time course of infection revealed several clusters of co-regulated genes, an enrichment of preferentially up- or downregulated genes in distinct functional categories and also showed that most of the transcriptional changes occurred 24 h after infection. A detailed analysis of the 24 h time point post infection was performed in comparison to three controls, uninfected cells and co-incubation with Legionella hackeliae and L. pneumophilaDeltadotA. One hundred and thirty-one differentially expressed D. discoideum genes were identified as common to all three experiments and are thought to be involved in the pathogenic response. Functional annotation of the differentially regulated genes revealed that apart from triggering a stress response Legionella apparently not only interferes with intracellular vesicle fusion and destination but also profoundly influences and exploits the metabolism of its host. For some of the identified genes, e.g. rtoA involvement in the host response has been demonstrated in a recent study, for others such a role appears plausible. The results provide the basis for a better understanding of the complex host-pathogen interactions and for further studies on the Dictyostelium response to Legionella infection.

Animals↗

PubMed2007

Global analysis of community-associated methicillin-resistant Staphylococcus aureus exoproteins reveals molecules produced in vitro and during infection.

Community-associated methicillin-resistant Staphylococcus aureus (CA-MRSA) is a threat to human health worldwide. Although progress has been made, mechanisms of CA-MRSA pathogenesis are poorly understood and a comprehensive analysis of CA-MRSA exoproteins has not been conducted. To address that deficiency, we used proteomics to identify exoproteins made by MW2 (USA400) and LAC (USA300) during growth in vitro. Two hundred and fifty unique exoproteins were identified by 2-dimensional gel electrophoresis coupled with automated direct infusion-tandem mass spectrometry (ADI-MS/MS) analysis. Eleven known virulence-related exoproteins differed in abundance between the strains, including alpha-haemolysin (Hla), collagen adhesin (Cna), staphylokinase (Sak), coagulase (Coa), lipase (Lip), enterotoxin C3 (Sec3), enterotoxin Q (Seq), V8 protease (SspA) and cysteine protease (SspB). Mice infected with MW2 or LAC produced antibodies specific for known or putative virulence factors, such as autolysin (Atl), Cna, Ear, ferritin (Ftn), Lip, 1-phosphatidylinositol phosphodiesterase (Plc), Sak, Sec3 and SspB, indicating the exoproteins are made during infection in vivo. We used confocal microscopy to demonstrate aureolysin (Aur), Hla, SspA and SspB are produced following phagocytosis by human neutrophils, thereby linking exoprotein production in vitro with that during host-pathogen interaction. We conclude that the exoproteins identified herein likely account in part for the success of CA-MRSA as a human pathogen.

Anti-Bacterial Agents↗