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Results for “host-pathogen interaction”

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PubMed1982

Comparative studies of gastrointestinal colonization and systemic spread by Candida albicans and nonlethal yeast in the infant mouse.

Studies of host-parasite interactions involved in gastrointestinal and systemic candidosis have been hampered by the lack of suitable animal models which mimic the disease in humans. The infant mouse has proved to be a realistic and useful model for studies of candidosis. Oral-intragastric inoculation of infants leads to systemic spread and lethality without use of compromising procedures. Not all species or strains of Candida inoculated via this route are lethal to the infant mouse nor do they demonstrate the same degree of persistence. Certain strains of C. albicans display long term colonization of the GI tract and such persistently infected mice resemble the situation in humans with C. albicans as a common, but quantitatively minor, component of the flora of the alimentary tract. The infant mouse model thereby has the potential of providing an excellent tool for experimental modification of the GI flora which reflects the situation in debilitated and compromised humans that leads to alterations of the host-pathogen balance favoring development of candidosis. This paper provides additional evidence for the validity of the infant mouse model for investigations of gastrointestinal and systemic candidosis by comparing colonization and systemic spread of two strains of C. albicans (Ca 30 and NS 33), C. guilliermondii, Saccharyomyces cerevisiae and latex beads.

Animals↗
PubMed2004

Inferring the dynamics of a spatial epidemic from time-series data.

Spatial interactions are key determinants in the dynamics of many epidemiological and ecological systems; therefore it is important to use spatio-temporal models to estimate essential parameters. However, spatially-explicit data sets are rarely available; moreover, fitting spatially-explicit models to such data can be technically demanding and computationally intensive. Thus non-spatial models are often used to estimate parameters from temporal data. We introduce a method for fitting models to temporal data in order to estimate parameters which characterise spatial epidemics. The method uses semi-spatial models and pair approximation to take explicit account of spatial clustering of disease without requiring spatial data. The approach is demonstrated for data from experiments with plant populations invaded by a common soilborne fungus, Rhizoctonia solani. Model inferences concerning the number of sources of disease and primary and secondary infections are tested against independent measures from spatio-temporal data. The applicability of the method to a wide range of host-pathogen systems is discussed.

Disease Outbreaks↗
PubMed2003

Dynamics and genealogy of strains in spatially extended host-pathogen models.

We examine the dynamics of evolution in a generic spatial model of a pathogen infecting a population of hosts, or an analogous predator-prey system. Previous studies of this model have found a range of interesting phenomena that differ from the well-mixed version. We extend these studies by examining the spatial and temporal dynamics of strains using genealogical tracing. When transmissibility can evolve by mutation, strains of intermediate transmissibility dominate even though high-transmissibility mutants have a short-term reproductive advantage. Mutant strains continually arise and grow rapidly for many generations but eventually go extinct before dominating the system. We find that, after a number of generations, the mutant pathogen characteristics strongly impact the spatial distribution of their local host environment, even when there are diverse types coexisting. Extinction is due to the depletion of susceptibles in the local environment of these mutant strains. Studies of spatial and genealogical relatedness reveal the self-organized spatial clustering of strains that enables their impact on the local environment. Thus, we find that selection acts against the high-transmissibility strains on long time-scales as a result of the feedback due to environmental change. Our study shows that averages over space or time should not be assumed to adequately describe the evolutionary dynamics of spatially distributed host-pathogen systems.

Animals↗
PubMed1996

The Dynamics of Insect-Pathogen Interactions in Seasonal Environments

Models of insect-pathogen interactions in highly seasonal environments are developed. The models apply to insects such as many temperate forest pests that have a single generation per year and which are susceptible to viral disease only during their larval period. The disease kills the hosts after a fixed time period when infectious pathogen particles are released into the environment. Depending on the time taken to kill the host, one to many cycles of pathogen replication may occur during the portion of the year when susceptible hosts are present. A baseline model with linear disease transmission is always unstable although a stable equilibrium can be achieved if there is sufficient density dependence in the transmission process. Persistent, long-period cycles are virtually never observed. The release of pathogen particles prior to host death contributes towards stability although it does not result in limit cycles. Long-period cycles were found in two other extensions of the baseline model, one in which some hosts carry a sublethal infection which is transmitted to their offspring; and a second which includes a reservoir where pathogen particles are relatively long lived although unable to cause new infections. The relationship between this work and previous host-pathogen and host-parasitoid models is discussed.

Journal Article↗
PubMed1992

Epizootics of Salmonella infection in poultry may be the result of modern selective breeding practices.

This paper discusses the hypothesis that a major factor in the epizootics of Salmonella infection in poultry is a declining host genetic diversity. A computer model is described which is based on models that have been previously used to investigate host-pathogen coevolution in cereal crops. It is shown that, as host genetic diversity declines, parasite diversity also declines to a lower equilibrium level. With a highly diverse host, parasite numbers decline to zero. With a homogeneous host population, after an initial decline, there is a rapid increase in parasite numbers, due to the selection of a particularly well adapted parasite strain. This simple computer simulation is used as the basis for a discussion of the literature supporting the suggestion that a major factor in the epizootic of Salmonella in poultry is related to the low genetic diversity of commercial poultry flocks.

Animals↗
PubMed2004

MHC polymorphism under host-pathogen coevolution.

The genes encoding major histocompatibility (MHC) molecules are among the most polymorphic genes known for vertebrates. Since MHC molecules play an important role in the induction of immune responses, the evolution of MHC polymorphism is often explained in terms of increased protection of hosts against pathogens. Two selective pressures that are thought to be involved are (1) selection favoring MHC heterozygous hosts, and (2) selection for rare MHC alleles by host-pathogen coevolution. We have developed a computer simulation of coevolving hosts and pathogens to study the relative impact of these two mechanisms on the evolution of MHC polymorphism. We found that heterozygote advantage per se is insufficient to explain the high degree of polymorphism at the MHC, even in very large host populations. Host-pathogen coevolution, on the other hand, can easily account for realistic polymorphisms of more than 50 alleles per MHC locus. Since evolving pathogens mainly evade presentation by the most common MHC alleles in the host population, they provide a selective pressure for a large variety of rare MHC alleles. Provided that the host population is sufficiently large, a large set of MHC alleles can persist over many host generations under host-pathogen coevolution, despite the fact that allele frequencies continuously change.

Computer Simulation↗
PubMed2003

Three types of defense-responsive genes are involved in resistance to bacterial blight and fungal blast diseases in rice.

Bacterial blight and fungal blast diseases of rice, caused by Xanthomonas oryzae pv. oryzae and Pyricularia grisea Sacc., respectively, are two of the most devastating diseases in rice worldwide. To study the defense responses to infection with each of these pathogens, expression profiling of 12 defense-responsive genes was performed using near-isogenic rice lines that are resistant or susceptible to bacterial blight and fungal blast, respectively, and rice cultivars that are resistant or susceptible to both pathogens. All 12 genes showed constitutive expression, but expression levels increased in response to infection. Based on their expression patterns in 12 host-pathogen combinations, these genes could be classified into three types, pathogen non-specific (6), pathogen specific but race non-specific (4) and race specific (2). Most of the 12 genes were only responsive during incompatible interactions. These results suggest that bacterial blight and fungal blast resistances share common pathway(s), but are also regulated by different defense pathways in rice. Activation of the corresponding R gene is the key step that initiates the action of these genes in defense responses. The chromosomal locations and pathogen specificities of seven of the 12 genes were consistent with those of previously identified quantitative trait loci for rice disease resistance, which indicates that some of the 12 genes studied may have a phenotypic impact on disease resistance in rice.

Bacteria↗
PubMed2002

Ultrastructure of the host-pathogen interface in daylily leaves infected by the rust fungus Puccinia hemerocallidis.

Transmission electron microscopy was used to examine details of the host-pathogen interface in daylily leaf cells infected by the rust fungus Puccinia hemerocallidis. Samples were prepared for study by high-pressure freezing followed by freeze substitution. The outstanding preservation of ultrastructural details afforded by this fixation protocol greatly facilitated the study of this host-pathogen interface. The extrahaustorial membrane that separated each dikaryotic haustorium from the cytoplasm of its host cell was especially well preserved and appeared almost completely smooth in profile. Large aggregations of tubular cytoplasmic elements were present near haustoria in infected host cells. Many of these tubular elements were found to be continuous with the extrahaustorial membrane and conspicuous electron-dense deposits present in the extrahaustorial matrix extended into these elements. The use of gold-conjugated wheat germ agglutinin for labeling of chitin revealed that these deposits were not part of the haustorial wall. Portions of many of the tubular elements associated with haustoria were conspicuously beaded in appearance. Some tubular elements were found to be continuous with flattened cisternae that in turn bore short beaded chains. Distinctive tubular-vesicular complexes previously reported only in cryofixed rust haustoria also were found in the haustoria of P. hemerocallidis.

Basidiomycota↗
PubMed2004

Mycobacterial granulomas: keys to a long-lasting host-pathogen relationship.

Chronic infection with mycobacteria is controlled by the formation of granulomas. The failure of granuloma maintenance results in reactivation of disease. Macrophages are the dominant cell type in granulomas, but CD4+ T cells are the master organizers of granuloma structure and function. Recent work points to an unrecognized role for nonspecific T cells in maintaining granuloma function in the chronic phase of infection. In addition, it has become clear that mycobacteria and host T cells collaborate in formation of granulomas. Further understanding of how nonspecific T cells contribute to granuloma formation, as well as how bacteria and T cells maintain a harmonious relationship over the life of the host, will facilitate the development of new strategies to treat mycobacterial disease.

Animals↗
PubMed2002

The pathology of brucellosis reflects the outcome of the battle between the host genome and the Brucella genome.

The successful co-existence of each Brucella spp. with its preferred host is the outcome of ancient co-evolutionary relationships and selection pressures that often result in a stalemate where the pathogen has evolved to survive within the biological systems of the host, and the host has evolved innate and acquired immune systems which allow controlled survival of infection by the pathogen, ultimately supporting the survival of the host-pathogen system. In general, Brucella spp. have evolved a similar fundamental pathogenesis of facultative intracellular parasitism though the predominant route of natural exposure varies from oropharynx to genital tract, as does the preferred tissue and cellular tropism, e.g. non-professional placental trophoblasts, fetal lung, professional macrophages of reticulendothelial system, and the male and female reproductive tracts. The morphogenesis of the pyogranulomatous lesions stimulated by Brucella reflects the nature of the persistent parasitism, i.e. genome versus genome. The question is, how can this perplexing array of survival mechanisms be unraveled? Fortunately, the integration of real-time image analysis, cell biology, genome-wide analysis, proteomics and bioinformatics holds the most promise ever for the global analysis of the Brucella infectious process and the host:pathogen interface leading to a clearer understanding of the interactions of these biological systems. These discoveries will be expected to provide a frameshift in rationales for interrupting and/or controlling brucellosis at host and/or pathogen levels.

Animals↗
PubMed2002

Functional and comparative genomics of pathogenic bacteria.

Microarray expression profiling and the development of data-mining tools and new statistical instruments affords an unprecedented opportunity for the genome-scale study of bacterial pathogenicity. Expression profiles obtained from bacteria grown in media simulating host microenvironments yield a portrait of interacting metabolic pathways and multistage developmental programs and disclose regulatory networks. The analysis of closely related strains and species by microarray-based comparative genomics provides a measure of genetic variability within natural populations and identifies crucial differences between pathogen and commensal. In the near future, the combined use of bacterial and host microarrays to study the same infected tissue will reveal the host-pathogen dialogue in a gene-by-gene and site- and time-specific manner. This review discusses the use of microarray-based expression profiling to identify genes of pathogenic bacteria that are differentially regulated in response to host-specific signals. Additionally, the review describes the application of microarray methods to disclose differences in gene content between taxonomically related strains that vary with respect to pathogenic phenotype.

Animals↗
PubMed1998

Signaling and host cell invasion by Trypanosoma cruzi.

Signal transduction events triggered in mammalian host cells by the obligate intracellular parasite Trypanosoma cruzi are required for invasion. Infective T. cruzi trypomastigotes elicit Ca2+ signaling in mammalian host cells and activate transforming growth factor-beta receptor signaling pathways. The elevation of Ca2+ in T. cruzi, induced by host-cell contact, is also required for invasion, extending the concept of host-pathogen 'cross-talk' to invasive protozoan pathogens.

Animals↗
PubMed1997

Macrophage apoptosis in microbial infections.

Upon infection with a pathogen, eukaryotic cells can undergo programmed cell death as an ultimate response. Therefore, modulation of apoptosis is often a prerequisite to establish a host-pathogen relationship. Some pathogens kill macrophages by inducing apoptosis and thus overcome the microbicidal arsenal of the phagocyte. Apoptotic macrophages, on the other hand, can elicit an inflammation by secretion of proinflammatory cytokines. Shigella flexneri, the aetiological agent of bacillary dysentery, induces apoptosis in macrophages which, in agony, specifically release mature interleukin-1 beta (IL-1 beta). This cytokine attracts neutrophils (PMN) to the site of infection resulting in the massive colonic inflammation characteristic of bacillary dysentery. Shigellosis represents a paradigm of a proinflammatory apoptosis in a bacterial infection. The molecular link between apoptosis and inflammation is interleukin-1 beta converting enzyme (ICE) which is activated during macrophage apoptosis and binds to IpaB, a secreted Shigella protein.

Animals↗
PubMed2001

Human cytomegalovirus and natural killer-mediated surveillance of HLA class I expression: a paradigm of host-pathogen adaptation.

Among various strategies to evade the host immune response, some viruses like human cytomegalovirus (HCMV) interfere with surface MHC class I expression and antigen presentation to T lymphocytes. The ability of natural killer (NK) cells to detect MHC class I molecules through inhibitory receptors can be envisaged as an adaptation of the immune system for responding to such pathological alterations. To fulfil that role, rodents use members of the Ly49 C-type lectin superfamily, whereas primates employ killer immunoglobulin-like receptors and the immunoglobulin-like transcript 2/leucocyte immunoglobulin-like receptor-1 receptor. CD94/NKG2 lectin-like heterodimers represent the most conserved receptor system for MHC class I molecules; by interacting with human HLA-E or murine Qa-1b, CD94/NKG2A inhibitory receptors broadly probe the biosynthesis pathway of other class I molecules. Reciprocally, HCMV has developed mechanisms to evade the NK response while modulating HLA class Ia expression. The ability of HCMV to maintain surface levels of HLA-E and to express an HLA class I surrogate (UL18) are herein discussed in the context of the interplay with human NKR systems.

Adaptation, Physiological↗
PubMed2004

The combined effects of pathogens and predators on insect outbreaks.

The economic damage caused by episodic outbreaks of forest-defoliating insects has spurred much research, yet why such outbreaks occur remains unclear. Theoretical biologists argue that outbreaks are driven by specialist pathogens or parasitoids, because host-pathogen and host-parasitoid models show large-amplitude, long-period cycles resembling time series of outbreaks. Field biologists counter that outbreaks occur when generalist predators fail, because predation in low-density defoliator populations is usually high enough to prevent outbreaks. Neither explanation is sufficient, however, because the time between outbreaks in the data is far more variable than in host-pathogen and host-parasitoid models, and far shorter than in generalist-predator models. Here we show that insect outbreaks can be explained by a model that includes both a generalist predator and a specialist pathogen. In this host-pathogen-predator model, stochasticity causes defoliator densities to fluctuate erratically between an equilibrium maintained by the predator, and cycles driven by the pathogen. Outbreaks in this model occur at long but irregular intervals, matching the data. Our results suggest that explanations of insect outbreaks must go beyond classical models to consider interactions among multiple species.

Animals↗
PubMed2001

Identification of functional regions within invasion plasmid antigen C (IpaC) of Shigella flexneri.

Shigella flexneri causes bacillary dysentery with symptoms resulting from the inflammation that accompanies bacterial entry into the cells of the colonic epithelium. The effectors of S. flexneri invasion are the Ipa proteins, particularly IpaB and IpaC, which are secreted at the host-pathogen interface following bacterial contact with a host cell. Of the purified Ipa proteins, only IpaC has been shown to possess quantifiable in vitro activities that are related to cellular invasion. In this study, ipaC deletion mutants were generated to identify functional regions within the IpaC protein. From these data, we now know that the N-terminus and an immunogenic central region are not required for IpaC-dependent enhancement of cellular invasion by S. flexneri. However, to restore invasiveness to an ipaC null mutant of S. flexneri, the N-terminus is essential, because IpaC mutants lacking the N-terminus are not secreted by the bacterium. Deletion of the central hydrophobic region eliminates IpaC's ability to interact with phospholipid membranes, and fusion of this region to a modified form of green fluorescent protein converts it into an efficient membrane-associating protein. Meanwhile, deletion of the C-terminus eliminates the mutant protein's ability to establish protein-protein contacts with full-length IpaC. Interestingly, the mutant form of ipaC that restores partial invasiveness to the S. flexneri ipaC null mutant also restores full contact-mediated haemolysis activity to this bacterium. These data support a model in which IpaC possesses a distinct functional organization that is important for bacterial invasion. This information will be important in defining the precise role of IpaC in S. flexneri pathogenesis and in exploring the potential effects of purified IpaC at mucosal surfaces.

Antigens, Bacterial↗
PubMed1987

Resilience and variability in pathogens and hosts.

Adaptability by means of phenotype variability in host-pathogen systems is studied using a model that resembles a class of array systems known as cellular automata. Each automaton in this model is characterized by a network of n x m processors that process the information contained in levels 0 to m. The effect of the automaton's architecture on its ability to satisfy variations in constraints is analysed, and automata-evolution experiments are described. Increasing the number of organization levels in the automaton is shown to increase its efficiency in buffering external changes, and the mechanism of modulating the processing rules appears more efficient than the mechanism of controlling the mutation rate. Analogy with biological systems suggests that hosts and pathogens evolve towards increasing modulation of their genomic information processing and that single mature lymphocytes should be able to generate more than one antigen receptor. These hypotheses can provide an explanation for the sequential ordered expression of different antigen genes in trypanosomes, as well as for immunosuppression and autoimmune phenomena.

Animals↗