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Results for “host-pathogen interaction”

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PubMed1991

Ecological and genetic models of host-pathogen coevolution.

A model is presented to analyse the forces that maintain genetic polymorphism in interactions between host plants and their pathogens. Genetic variability in hosts occurs for specific resistance to different pathogen races and variability in pathogens occurs for specific virulence to different host races. The model tracks both fluctuating population sizes and changing gene frequencies. Analyses over a range of parameters show that ecological and demographic factors, such as birth and death rates, often have a more profound effect on the amount of polymorphism than genetic parameters, such as the pleiotropic costs of resistance and virulence associated with different alleles. A series of simple measures are proposed to predict the amount of genetic polymorphism expected in particular host-pathogen interactions. These measures can be used to develop and test a comparative theory of genetic polymorphism in host-pathogen coevolution.

Biological Evolution↗
PubMed1990

Virulence plasmids of Salmonella typhimurium and other salmonellae.

Related high molecular weight plasmids of several serotypes and species of Salmonella have been associated with virulence in a variety of animal models of infection. The primary virulence plasmid phenotype is in the ability of salmonellae to spread beyond the initial site of infection, the intestines. The mechanism of this plasmid-mediated invasive infection has not been identified, but may be a complex interaction in the host-pathogen relationship. A common region of the salmonella plasmids has been associated with virulence, and specific virulence genes and their products are now being identified; however, much is yet to be accomplished in this field. The combined analysis of pathogenesis and genetics associated with the salmonella virulence plasmids may identify new systems of bacterial virulence and the genetic basis for this virulence.

Animals↗
PubMed2025

Stepping out of the dark: how metabolomics shed light on fungal biology.

Metabolomics, a critical tool for analyzing small-molecule metabolites, integrates with genomics, transcriptomics, and proteomics to provide a systems-level understanding of fungal biology. By mapping metabolic networks, it elucidates regulatory mechanisms driving physiological and ecological adaptations. In fungal pathogenesis, metabolomics reveals host-pathogen dynamics, identifying virulence factors like gliotoxin in Aspergillus fumigatus and metabolic shifts, such as glyoxylate cycle upregulation in Candida albicans. Ecologically, it highlights fungal responses to abiotic stressors, including osmolyte production like trehalose, enhancing survival in extreme environments. These insights highlight metabolomics' role in decoding fungal persistence and niche colonization. In drug discovery, it aids target identification by profiling biosynthetic pathways, supporting novel antifungal and nanostructured therapy development. Combined with multi-omics, metabolomics advances insights into fungal pathogenesis, ecological interactions, and therapeutic innovation, offering translational potential for addressing antifungal resistance and improving treatment outcomes for fungal infections. Its progress shed light on complex fungal molecular profiles, advancing discovery and innovation in fungal biology.

Metabolomics↗
PubMed2000

The phytopathogenic bacteria Erwinia carotovora infects Drosophila and activates an immune response.

Although Drosophila possesses potent immune responses, little is known about the microbial pathogens that infect Drosophila. We have identified members of the bacterial genus Erwinia that induce the systemic expression of genes encoding antimicrobial peptides in Drosophila larvae after ingestion. These Erwinia strains are phytopathogens and use flies as vectors; our data suggest that these strains have also evolved mechanisms for exploiting their insect vectors as hosts. Erwinia infections induce an antimicrobial response in Drosophila larvae with a preferential expression of antibacterial versus antifungal peptide-encoding genes. Antibacterial peptide gene expression after Erwinia infection is reduced in two Drosophila mutants that have reduced numbers of hemocytes, suggesting that blood cells play a role in regulating Drosophila antimicrobial responses and also illustrating that this Drosophila-Erwinia interaction provides a powerful model for dissecting host-pathogen relationships.

Animals↗
PubMedDate not supplied

Epidemiology of Clostridium difficile-induced intestinal disease.

The epidemiology of Clostridium difficile-induced intestinal disease is an intriguing subject about which there are few answers but many remaining questions. Although it is accepted that altered intestinal microecology (usually the result of antimicrobial therapy) is a major predisposition to disease, the details of microbial interactions are not yet known and clearly involve more than simple overgrowth of a resistant member of the resident flora. A variety of reservoirs of C. difficile are recognized. These include endogenous carriage, environmental contamination, and zoonoses, but the relative epidemiologic importance of these varied sources is yet to be determined. Because minor variations in methods for cultivation of C. difficile can markedly affect the ability to detect the organism, even the prevalence of endogenous carriage by various populations is not fully defined. There is good evidence for nosocomial acquisition of disease, but the frequency of this event and the usefulness of preventive measures need to be determined. The development of a typing system would provide a valuable tool for investigating many of the remaining questions. Finally, in addition to the recognized risk factors, which include the apparently predisposing alteration in intestinal microecology and exposure to C. difficile, there appear to be other, as yet undefined, variables that help to determine whether disease will occur. Perhaps the elucidation of the details of the pertinent microbial interactions as well as an understanding of the relevant host-pathogen relationships will provide important insights into the epidemiology of C. difficile-induced disease.

Anti-Bacterial Agents↗
PubMed2000

Host-pathogen studies in the post-genomic era.

Several studies are starting to show the power of DNA microarrays to identify interactions between animal hosts and their pathogens, and have revealed interesting correlations between host responses to different infectious agents.

Animals↗
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↗
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↗
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↗
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↗
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↗
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

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↗
PubMedDate not supplied

The genetics of host-pathogen coevolution: implications for genetic resource conservation.

The results of long-term studies of coevolution in the Hordeum vulgare-Rhynchosporium secalis pathosystem are summarized. The genetic systems of barley (host) and R. secalis (pathogen) are complementary: Gene-for-gene interactions among loci affect many traits, leading to self-regulating adjustments over generations between host and pathogen populations. Different pathotypes differ widely in their ability to damage the host, and different host-resistance alleles differ widely in their ability to protect the host from the pathogen. Among 29 resistance loci in the specific host population studied, several played major roles in providing stable resistance, but many had net detrimental effects on the yield and reproductive ability of the host. Resistance alleles that protected against the most damaging pathotypes increased sharply in frequency in the host populations. It is concluded that the evolutionary processes that take place in genetically variable populations propagated under conditions of cultivation can be highly effective in increasing the frequency of desirable alleles and useful multilocus genotypes. This enhances the value of the evolving populations as sources of genetic variability in breeding for disease resistance and other characters that affect adaptedness.

Biological Evolution↗