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Results for “host-pathogen interaction”

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At least 505 records · Page 28Linked to original sources
PubMed1998

Effect of bacterial invasion of macrophages on the outcome of assays to assess bacterium-macrophage interactions.

In vitro assays to quantify killing of bacteria by macrophages provide useful insights into host-pathogen relations. In the present study, we used strains of Yersinia enterocolitica and Escherichia coli which varied in their ability to invade mammalian cells to evaluate these assays. The results showed that 30 min and 24 h after incubation with murine bone marrow-derived macrophages, strains of Y. enterocolitica and E. coli which expressed invasin (an outer membrane protein which allows bacteria to penetrate mammalian cells) achieved significantly greater numbers in macrophages than otherwise isogenic bacteria which lacked this protein (P < 0.01). When the 24-h data were corrected for the number of bacteria ingested by macrophages initially, the differences between invasin-positive and -negative bacteria were no longer evident (P> 0.2). This study has shown (1) that invasin-mediated penetration of macrophages by bacteria is not associated with enhanced intracellular survival, and (2) that invasion of macrophages by bacteria may influence the interpretation of assays for bactericidal capacity unless allowance is made for the number of bacteria ingested during the early phase of the assay.

Animals↗
PubMed2001

Interactions between sources of mortality and the evolution of parasite virulence.

A well-known result from the theory of the evolution of virulence is the prediction that the virulence of a pathogen (i.e. the rate of parasite-induced host mortality) always evolves to higher levels when host background mortality rates increase. This prediction, however, is derived from models that assume that host mortality sources combine additively to determine the overall host mortality rate. In this paper, we suggest that such additivity is probably rare for many host-pathogen systems, and explore how the predictions for the evolution of virulence are altered when interactions between host mortality sources are incorporated into the theory. Our results indicate that if mortality-source interactions are sufficiently strong then the evolutionarily stable level of virulence can actually decrease as the background mortality rate increases. Consequently, a detailed mechanistic description of how parasites and other mortality sources combine to cause host mortality is required before reliable predictions about virulence evolution can be made. Moreover, mortality-source interactions make empirical comparisons of the virulence of different parasites a much more subtle issue.

Animals↗
PubMed2000

Interaction of Shigella flexneri IpaC with model membranes correlates with effects on cultured cells.

Invasion of enterocytes by Shigella flexneri requires the properly timed release of IpaB and IpaC at the host-pathogen interface; however, only IpaC has been found to possess quantifiable activities in vitro. We demonstrate here that when added to cultured cells, purified IpaC elicits cytoskeletal changes similar to those that occur during Shigella invasion. This IpaC effect may correlate with its ability to interact with model membranes at physiological pH and to promote entry by an ipaC mutant of S. flexneri.

Antigens, Bacterial↗
PubMed2003

Modelling pathogen transmission: the interrelationship between local and global approaches.

We describe two spatial (cellular automaton) host-pathogen models with contrasting types of transmission, where the biologically realistic transmission mechanisms are based entirely on 'local' interactions. The two models, fixed contact area (FCA) and fixed contact number (FCN), may be viewed as local 'equivalents' of commonly used global density- (and frequency-) dependent models. Their outputs are compared with each other and with the patterns generated by these global terms. In the FCN model, unoccupied cells are bypassed, but in the FCA model these impede pathogen spread, extending the period of the epidemic and reducing the prevalence of infection when the pathogen persists. Crucially, generalized linear modelling reveals that the global transmission terms betaSI and beta'SI/N are equally good at describing transmission in both the FCA and FCN models when infected individuals are homogeneously distributed and N is approximately constant, as at the quasi-equilibrium. However, when N varies, the global frequency-dependent term beta'SI/N is better than the density-dependent one, betaSI, at describing transmission in both the FCA and FCN models. Our approach may be used more generally to compare different local contact structures and select the most appropriate global transmission term.

Animals↗
PubMedDate not supplied

Giardiasis: host-pathogen biology.

Giardiasis is the most common waterborne diarrheal disease in the United States and is highly prevalent throughout the world. The clinical spectrum of disease ranges from asymptomatic infection to persistent severe malabsorption. The precise interaction between Giardia and its human host remains conjectural because of the paucity of published studies that address the details of its pathogenesis. The immune system of the host responds to this protozoan parasite, and the intestinal epithelium is a site of interaction between parasite and host. Possible mechanisms whereby Giardia may alter the host's absorption of nutrients at the epithelial level include direct physical interference, toxin secretion, direct physical alteration of the epithelium, competition for nutrients, induction of an inflammatory response, and coincidental infection of the host with a second organism. The host's immune system may play both a protective and a pathogenic role.

Adult↗
PubMed2002

Evolutionary ecology of plant diseases in natural ecosystems.

Plant pathogens cause mortality and reduce fecundity of individual plants, drive host population dynamics, and affect the structure and composition of natural plant communities. Pathogens are responsible for both numerical changes in host populations and evolutionary changes through selection for resistant genotypes. Linking such ecological and evolutionary dynamics has been the focus of a growing body of literature on the effects of plant diseases in natural ecosystems. A guiding principle is the importance of understanding the spatial and temporal scales at which plants and pathogens interact. This review summarizes the effects of diseases on populations of wild plants, focusing in particular on the mediation of plant competition and succession, the maintenance of plant species diversity, as well as the process of rapid evolutionary changes in host-pathogen symbioses.

Adaptation, Physiological↗
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↗
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↗
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↗
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↗
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↗