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Results for “host:pathogen interactions”

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PubMed1998

Host response to Mycobacterium tuberculosis.

Critical to the complete expression of the virulence of M. tuberculosis and thereby its pathogenesis in human infection, is the ability of this pathogen to interact with the host in a specific manner. To date, cytokine circuits during tuberculosis and M. tuberculosis infection have been studied most intensely. With this regard, both the whole M. tuberculosis and its protein and non-protein moieties appear to be influential on the in situ cytokine profile, and consequently, to the final outcome of infection. The interplay and final balance of macrophage activating and immuno-enhancing cytokines versus macrophage deactivating and immunosuppressive cytokines most likely determines the final expression of M. tuberculosis infection. Further, cytokine circuits also underlie the immunopathology of tuberculosis. Modulation of the in vivo cytokine milieu may allow the development of more effective vaccines to prevent M. tuberculosis infection, and adjunctive immunotherapy to improve treatment of tuberculosis.

Animals↗

PubMed2002

Infectomics: genomics and proteomics of microbial infections.

The completion of genomic sequences is the greatest triumph of molecular reductionism since the discovery of the DNA double helix in 1953. However, the utility of reductionism is becoming limited and holistic approaches, including theories and techniques, are desperately needed in the postgenomic era. In the field of infectious diseases there is an urgent need for global approaches that can efficiently, precisely and integratively study structural and functional genomics and proteomics of microbial infections (infectomics). The combination of new (e.g. DNA and protein microarrays) and traditional approaches (e.g. cloning, PCR, gene knockout and knockin, and antisense) will help overcome the challenges we are facing today. We assume that the global phenotypic changes (infectomes) in microbes and their host during infections are encoded by the genomes of microbial pathogens and their hosts, expressed in certain environmental conditions devoted to specific microbe-host interactions. Global drug responses (pharmacomes) in microbes and their host can be detected by genomic and proteomic approaches. Genome-wide approaches to genotyping and phenotyping or expression profiling will eventually lead to global dissection of microbial pathogenesis, efficient and rapid diagnosis of infectious diseases, and the development of novel strategies to control infections. The key fundamental issue of infectious diseases is how to globally and integratively understand the interactions between microbial pathogens and their hosts by using infectomics. In this review, we focus on the events that are considered important in infectomics.

Animals↗

PubMed1996

Differential gene expression by Pseudomonas aeruginosa during interaction with respiratory mucus.

Pseudomonas aeruginosa is a common respiratory tract pathogen that causes serious infections in patients with cystic fibrosis. A number of putative virulence factors have been characterized in several laboratories, and some have been implicated in human infections, based on criteria such as the phenotype of isolates from infected patients, an immune response to a particular antigenic factor, and the effect of a virulence factor on infectivity in an animal model. We have developed a series of genetic tools to study the selective regulation of expression of P. aeruginosa genes during interactions of the pathogen with host tissues. These tools are based on direct enrichment of bacteria, when a particular promoter is induced or repressed. We have found that interaction of bacteria with mucus from patients with cystic fibrosis results in marked induction of expression of several genes, including one that encodes a lipopolysaccharide biosynthetic enzyme, a gene for a protein responsible for uptake of the ferric pyochelin siderophore, and a new gene homologous with a class of iron-responsive repressors. The tools described here are useful for identification of induced or repressed genes in various animal models of infection or in controlled laboratory conditions that mimic natural infections of humans. Such genes might not be detectable when bacteria are cultured in laboratory conditions, and these tools are therefore useful for general probing of a bacterial genome for genes regulated during different stages of infection.

Animals↗

PubMed2002

Bacterial strategies for overcoming host innate and adaptive immune responses.

In higher organisms a variety of host defense mechanisms control the resident microflora and, in most cases, effectively prevent invasive microbial disease. However, it appears that microbial organisms have coevolved with their hosts to overcome protective host barriers and, in selected cases, actually take advantage of innate host responses. Many microbial pathogens avoid host recognition or dampen the subsequent immune activation through sophisticated interactions with host responses, but some pathogens benefit from the stimulation of inflammatory reactions. This review will describe the spectrum of strategies used by microbes to avoid or provoke activation of the host's immune response as well as our current understanding of the role this immunomodulatory interference plays during microbial pathogenesis.

Animals↗

PubMed2006

MNN5 encodes an iron-regulated alpha-1,2-mannosyltransferase important for protein glycosylation, cell wall integrity, morphogenesis, and virulence in Candida albicans.

The cell walls of microbial pathogens mediate physical interactions with host cells and hence play a key role in infection. Mannosyltransferases have been shown to determine the cell wall properties and virulence of the pathogenic fungus Candida albicans. We previously identified a C. albicans alpha-1,2-mannosyltransferase, Mnn5, for its novel ability to enhance iron usage in Saccharomyces cerevisiae. Here we have studied the enzymatic properties of purified Mnn5 and characterized its function in its natural host. Mnn5 catalyzes the transfer of mannose to both alpha-1,2- and alpha-1,6-mannobiose, and this activity requires Mn2+ as a cofactor and is regulated by the Fe2+ concentration. An mnn5Delta mutant showed a lowered ability to extend O-linked, and possibly also N-linked, mannans, hypersensitivity to cell wall-damaging agents, and a reduction of cell wall mannosylphosphate content, phenotypes typical of many fungal mannosyltransferase mutants. The mnn5Delta mutant also exhibited some unique defects, such as impaired hyphal growth on solid media and attenuated virulence in mice. An unanticipated phenotype was the mnn5Delta mutant's resistance to killing by the iron-chelating protein lactoferrin, rendering it the first protein found that mediates lactoferrin killing of C. albicans. In summary, MNN5 deletion impairs a wide range of cellular events, most likely due to its broad substrate specificity. Of particular interest was the observed role of iron in regulating the enzymatic activity, suggesting an underlying relationship between Mnn5 activity and cellular iron homeostasis.

Alcian Blue↗

PubMed2005

Macrophage cell death due to Salmonella enterica serovar Typhi and its acid stress protein has features of apoptosis.

Salmonella spp. have been shown to cause apoptosis of various host cell types as a part of their infection process. However, the induction of apoptosis remains to be looked into under the different host environments including acidic stress experienced by the pathogen. In order to simulate the in vivo acidic conditions, we studied the potential of S. typhi and its protein expressed under in vitro acidic conditions to induce apoptosis in macrophages. Murine macrophages were isolated and interacted with serovar Typhi and its acid stress protein for different time periods. The assessment of nucleosomal DNA, and nuclear staining with H-33342 dye and flow cytometry indicated the occurrence of characteristic features of apoptosis. Analysis of data revealed that S. typhi caused apoptotic cell death in 61% of macrophages whereas stress-induced protein alone accounted for apoptotic cell death in 45% of macrophages. The present study, for the first time demonstrates the potential of stress-induced outermembrane component of S. typhi to induce apoptosis. Identification of such factors may offer new insights for understanding the pathophysiology of the disease during the host-pathogen interactions.

Animals↗

PubMed2006

Host-pathogen systems biology.

Unlike traditional biological research that focuses on a small set of components, systems biology studies the complex interactions between a large number of genes, proteins and other elements of biological networks and systems. Host-pathogen systems biology examines the interactions between the components of two distinct organisms, either a microbial or viral pathogen and its animal host or two different microbial species in a community. With the availability of complete genomic sequences of various hosts and pathogens, together with breakthroughs in proteomics, metabolomics and other experimental areas, the investigation of host-pathogen systems on a multitude of levels of detail has come within reach.

Animals↗

PubMed1996

Antimicrobial approaches to therapy for pneumonia.

Pneumonia remains a serious illness with significant associated morbidity and mortality. Parallelling our increased understanding of the etiology, epidemiology, and pathogenesis of pneumonia and the development of new antibiotics has been the frightening increase in the rate and extent of bacterial resistance. The prevalence of resistance has reached unprecedented levels in many countries, and we are facing the specter of infection by pathogens for which we have no effective treatment. To better understand some of the newer developments in this field, the discussion centers around the interactive triad of the host, pathogen, and drug. Pertinent developments relevant to each of these three areas are considered, along with a discussion of their clinical impact.

Anti-Bacterial Agents↗

PubMed2006

High yield and rapid growth of Neoparamoeba pemaquidensis in co-culture with a rainbow trout gill-derived cell line RTgill-W1.

Neoparamoeba pemaquidensis is an ubiquitous amphizoic marine protozoan and has been implicated as the causative agent for several diseases in marine organisms, most notably amoebic gill disease (AGD) in Atlantic salmon. Despite several reports on the pathology of AGD, relatively little is known about the protozoan and its relationship to host cells. In this study, an in vitro approach using monolayers of a rainbow trout gill cell line (RTgill-W1, ATCC CRL-2523) was used to rapidly grow large numbers of N. pemaquidensis (ATCC 50172) and investigate cell-pathogen interactions. Established cell lines derived from other tissues of rainbow trout and other fish species were also evaluated for amoeba growth support. The amoebae showed preference and highest yield when grown with RTgill-W1 over nine other tested fish cell lines. Amoeba yields could reach as high as 5 x 10(5) cells mL(-1) within 3 days of growth on the gill cell monolayers. The amoebae caused visible focal lesions in RTgill-W1 monolayers within 24 h of exposure and rapidly proliferated and spread with cytopathic effects destroying the neighbouring pavement-like cells within 48-72 h after initial exposure in media above 700 mOsm kg(-1). Disruption of the integrity of the gill cell monolayers could be noted within 30 min of exposure to the amoeba suspensions by changes in transepithelial resistance (TER) compared with control cell monolayers maintained in the exposure media. This was significantly different by 2 h (P < 0.05) compared with control cells and remained significantly different (P < 0.01) for the remaining 72 h that the TER was monitored. The RTgill-W1 cell line is thus a convenient model for growing N. pemaquidensis and for studying host-pathogen interactions in AGD.

Analysis of Variance↗

PubMed1996

Surface antigen cross-linking triggers forced exit of a protozoan parasite from its host.

We used the common fish pathogen Ichthyophthirius multifiliis as a model for studying interactions between parasitic ciliates and their vertebrate hosts. Although highly pathogenic, Ichthyophthirius can elicit a strong protective immune response in fish after exposure to controlled infections. To investigate the mechanisms underlying host resistance, a series of passive immunization experiments were carried out using mouse monoclonal antibodies against a class of surface membrane proteins, known as immobilization antigens (or i-antigens), thought to play a role in the protective response. Such antibodies bind to cilia and immobilize I. multifiliis in vitro. Surprisingly, we found that passive antibody transfer in vivo caused rapid exit of parasites from the host. The effect was highly specific for a given I. multifiliis serotype. F(ab)2 subfragments had the same effect as intact antibody, whereas monovalent Fab fragments failed to protect. The activity of Fab could, nevertheless, be restored after subsequent i.p. injection of bivalent goat anti-mouse IgG. Parasites that exit the host had detectable antibody on their surface and appeared viable in all respects. These findings represent a novel instance among protists in which protective immunity (and evasion of the host response) result from an effect of antibody on parasite behavior.

Animals↗

PubMed1995

Interaction of avian sarcoma/leukemia viruses with heterologous hosts: inference for host-range and some pathogenic properties of human immunodeficiency viruses.

Although there are substantial differences between retroviruses originating from avian and primate species, a comparison of these two different biological systems reveals that interaction of these retroviruses with heterologous hosts involves similar biological principles. Retroviral isolates with high replicative capacity in natural targets (e.g. CD4+ lymphocytes and macrophages for human immunodeficiency viruses (HIVs) can infect other cell types [e.g. CD- astrocytes, follicular dendritic cells (FDC) in vivo and/or CD4+ neoplastic T cells in vitro] as well. These viral isolates may have a potential of infecting heterologous cells in vitro and can enlarge their host-range by establishing infection in other species, distantly related. Strains of avian sarcoma/leukemia viruses (ASLV) originating from their natural hosts, chickens, and infectious for other avian species, ducks, can frequently infect mammals (rodents). Similarly, HIV-1 strains infectious for chimpanzees possess capacity of establishing chronic infection in pig-tailed macaques. The broad host-range of retroviral isolates in both viral systems is accompanied by presence of additional structures in viral envelope. These novel or additional envelope structures may recognize alternate viral receptor(s). Moreover, the enlarged host range of primary HIV-1 isolates is evaluated by infection of neoplastic CD4+ permanent cell line, MT2, and serves as a predictive marker of progression of the viral infection toward AIDS.

Alpharetrovirus↗

PubMed1996

Host immunity to ticks.

The tick-host-pathogen interface is characterized by complex immunological interactions. Tick feeding induces host immune regulatory and effector pathways involving antibodies, complement, antigen-presenting cells, T lymphocytes, and other bioactive molecules. Acquired resistance impairs tick engorgement, ova production, and viability. Tick countermeasures to host defenses reduce T-lymphocyte proliferation, elaboration of the TH1 cytokines interleukin-2 and interferon-gamma, production of macrophage cytokines interleukin-1 and tumor necrosis factor, and antibody responses. The dynamic balance between acquired resistance and tick modulation of host immunity affects engorgement and pathogen transmission. A thorough understanding of acquired immunity to ticks is essential for rational development of antitick vaccines.

Animals↗

PubMed2004

Diversity and specificity in the interaction between Caenorhabditis elegans and the pathogen Serratia marcescens.

BACKGROUND: Co-evolutionary arms races between parasites and hosts are considered to be of immense importance in the evolution of living organisms, potentially leading to highly dynamic life-history changes. The outcome of such arms races is in many cases thought to be determined by frequency dependent selection, which relies on genetic variation in host susceptibility and parasite virulence, and also genotype-specific interactions between host and parasite. Empirical evidence for these two prerequisites is scarce, however, especially for invertebrate hosts. We addressed this topic by analysing the interaction between natural isolates of the soil nematode Caenorhabditis elegans and the pathogenic soil bacterium Serratia marcescens. RESULTS: Our analysis reveals the presence of i) significant variation in host susceptibility, ii) significant variation in pathogen virulence, and iii) significant strain- and genotype-specific interactions between the two species. CONCLUSIONS: The results obtained support the previous notion that highly specific interactions between parasites and animal hosts are generally widespread. At least for C. elegans, the high specificity is observed among isolates from the same population, such that it may provide a basis for and/or represent the outcome of co-evolutionary adaptations under natural conditions. Since both C. elegans and S. marcescens permit comprehensive molecular analyses, these two species provide a promising model system for inference of the molecular basis of such highly specific interactions, which are as yet unexplored in invertebrate hosts.

Animals↗

PubMed2006

55 kDa outer-membrane protein from short-chain fatty acids exposed Salmonella enterica serovar Typhi induces apoptosis in macrophages.

Various pathogens including Salmonella species are known to induce apoptosis in host cell types during their infection processes. However, the bacterial components capable of inducing apoptosis have not been fully understood. It is now known that in vivo expression of virulence determinants differ from the expression under in vitro conditions. Therefore, in the present study, attempts were made to evaluate the apoptotic potential of outer-membrane protein (OMP) from short-chain fatty acids (SCFA) exposed Salmonella enterica serovar Typhi. Short-chain fatty acids exposure is one of the in vivo stresses encountered by the pathogen in the intestine. Therefore, to simulate the in vivo condition, S. enterica serovar Typhi was grown in the presence of SCFA and its OMP profile was analyzed. The apoptotic potential of 55 kDa protein expressed with enhanced intensity under the SCFA stress was evaluated. Murine peritoneal macrophages interacted with 55 kDa protein showed DNA fragmentation, changes in fluorescence and exposure of phosphatidylserine on their outer leaflets. Levels of nitrite and citrulline were found to be increased in the supernatant of macrophages after interacting them with 55 kDa protein. However, the enzymatic activity of superoxide dismutase was found to be decreased as compared to that of the control (uninteracted) macrophages. These observations indicate that increased levels of nitrite and decreased levels of superoxide dismutase may be one of the mechanisms to induce apoptosis in macrophages by SCFA induced 55 kDa OMP. These findings may help us better understand the pathophysiology of the disease during the host pathogen interactions.

Animals↗

PubMed1989

[Etiopathogenesis of HIV infection].

The knowledge of life's cycle of the acquired immune deficiency syndrome's virus (HIV) its complex genetic structure involving the interaction of positive and negative regulatory gene controlling the growth of the virus, its great genetic variability, the different pathogenic mechanisms, the cell-virus interaction, the different host-cells and the interaction of other pathogens, are all fundamentals facts for a better understanding of the various stages of infection by HIV until ultimate establishment of the Acquired Immune Deficiency Syndrome and also to explain the therapeutic difficulties until now.

Acquired Immunodeficiency Syndrome↗

PubMed1993

Helicobacter pylori: microbiology of a 'slow' bacterial infection.

The bacterium Helicobacter pylori lives in the gastric mucus layer of humans and induces a chronic inflammatory response that can result in both peptic ulceration and gastric neoplasms. Helicobacter pylori infection can be considered as a 'slow', adaptive and autoregulating process. The mechanisms by which this slow bacterial pathogen survives and interacts with the host immune system may provide a model for other persistent mucosal pathogens.

Gastritis↗

PubMed1995

Present state of research on ticks (Ixodoidea) in the Czech Republic.

Tick research in the Czech Republic started developing rapidly after World War II and was directed to the faunistics and taxonomy, biology, ecology and behaviour, physiology and genetics, disease transmission, host-parasite relationships and control. Altogether 15 tick species were reported from the territory of the Czech Republic. Most studies in biology, ecology and virus transmission were dedicated to Ixodes ricinus, but biology and ecology of Dermacentor reticulatus, I. laguri and I. hexagonus were also studied. Many studies were done on argasid ticks, mostly on pheromonal communication of Argas persicus and immunology of feeding of A. polonicus. Population variability of both these species was also studied. The present research on ticks is mostly directed to study of interaction among hosts, ticks and pathogens on the humoral, cellular and molecular level.

Adaptation, Physiological↗

PubMed2002

Listeria monocytogenes virulence and pathogenicity, a food safety perspective.

Several virulence factors of Listeria monocytogenes have been identified and extensively characterized at the molecular and cell biologic levels, including the hemolysin (listeriolysin O), two distinct phospholipases, a protein (ActA), several internalins, and others. Their study has yielded an impressive amount of information on the mechanisms employed by this facultative intracellular pathogen to interact with mammalian host cells, escape the host cell's killing mechanisms, and spread from one infected cell to others. In addition, several molecular subtyping tools have been developed to facilitate the detection of different strain types and lineages of the pathogen, including those implicated in common-source outbreaks of the disease. Despite these spectacular gains in knowledge, the virulence of L. monocytogenes as a foodborne pathogen remains poorly understood. The available pathogenesis and subtyping data generally fail to provide adequate insight about the virulence of field isolates and the likelihood that a given strain will cause illness. Possible mechanisms for the apparent prevalence of three serotypes (1/2a, 1/2b, and 4b) in human foodborne illness remain unidentified. The propensity of certain strain lineages (epidemic clones) to be implicated in common-source outbreaks and the prevalence of serotype 4b among epidemic-associated stains also remain poorly understood. This review first discusses current progress in understanding the general features of virulence and pathogenesis of L. monocytogenes. Emphasis is then placed on areas of special relevance to the organism's involvement in human foodborne illness, including (i) the relative prevalence of different serotypes and serotype-specific features and genetic markers; (ii) the ability of the organism to respond to environmental stresses of relevance to the food industry (cold, salt, iron depletion, and acid); (iii) the specific features of the major known epidemic-associated lineages; and (iv) the possible reservoirs of the organism in animals and the environment and the pronounced impact of environmental contamination in the food processing facilities. Finally, a discussion is provided on the perceived areas of special need for future research of relevance to food safety, including (i) theoretical modeling studies of niche complexity and contamination in the food processing facilities; (ii) strain databases for comprehensive molecular typing; and (iii) contributions from genomic and proteomic tools, including DNA microarrays for genotyping and expression signatures. Virulence-related genomic and proteomic signatures are expected to emerge from analysis of the genomes at the global level, with the support of adequate epidemiologic data and access to relevant strains.

Consumer Product Safety↗