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Results for “host‐pathogen interactions”

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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↗

PubMed1994

Tick-induced modulation of the host immune response.

The tick-host-pathogen interface is characterised by complex immunological interactions. Host immune responses to tick infestation and infection with tick-borne pathogens involve cytokines, antibodies, complement and T lymphocyte regulatory and effector pathways. A successful host-parasite relationship is a balance between limiting the parasite by host defenses and the ability of the parasite to modulate, evade or restrict the host response. Hosts acquire immunological based resistance to tick infestation, which reduces engorgement, production of ova and viability. Salivary glands of ixodid ticks produce a complex array of immunogens and pharmacologically active molecules. Tick salivary gland derived material can modulate host cytokine, antibody and cell mediated immune responses. Both immunoregulatory and immune effector pathways of the host are suppressed. Tick feeding impairs the ability to develop a primary immune response to a thymic dependent immunogen. Lymphocytes obtained from tick infested hosts are reduced in their ability to proliferate in vitro to T lymphocyte mitogens, while responses to B lymphocyte polyclonal activators are unaltered. Normal macrophages and lymphocytes were exposed to female tick salivary gland extracts prepared daily during the course of engorgement. All extracts reduced lymphocyte responses to T cell mitogens and enhanced in vitro proliferation in the presence of a B lymphocyte mitogen. Macrophage elaboration of tumour necrosis factor alpha and interleukin-1 are significantly reduced in a differential manner. Production of interleukin-2 and interferon-gamma by T lymphocytes is reduced. Tick modulation of the host immune response could enhance the ability of the arthropod to obtain a blood meal and facilitate pathogen transmission to an immunocompetent host.

Animals↗

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↗

PubMed1989

The predicted protein product of a pathogenicity locus from Pseudomonas syringae pv. phaseolicola is homologous to a highly conserved domain of several procaryotic regulatory proteins.

A ca. 20-kilobase (kb) region (hrp) that controls the interaction of Pseudomonas syringae pv. phaseolicola with its host (pathogenicity) and nonhost plants (hypersensitive reaction) was previously cloned and partially characterized. In this study we defined the limits and determined the nucleotide sequence of a hrp locus (hrpS), located near the right end of the hrp cluster. The largest open reading frame (ORF302) in hrpS has a coding capacity for a 302-amino-acid polypeptide. The predicted amino acid sequence of the translation product of ORF302 (HrpS) shows significant similarity to several procaryotic regulatory proteins, including the NtrC, NifA, and DctD proteins of Rhizobium spp., the NtrC and NifA proteins of Klebsiella pneumoniae, and the TyrR protein of Escherichia coli. These proteins regulate diverse operons involved in nitrogen fixation, transport and metabolism of amino acids, and transport of C-4 dicarboxylic acids. The HrpS protein appears to be the shortest naturally occurring member of this family of proteins, corresponding for the most part to the highly conserved central domain of these proteins, which contains a putative ATP-binding site. A C-terminal segment analogous to the less-well-conserved domain, involved in DNA binding of NtrC and NifA, is also present in HrpS. These similarities suggest that HrpS is a regulatory protein. In line with this prediction is the finding that a functional hrpS gene is necessary for the activation of another hrp locus during the plant-bacterium interaction.

Amino Acid Sequence↗

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↗

PubMed1991

A host-host-pathogen model with free-living infective stages, applicable to microbial pest control.

A model has been investigated of the dynamics of the interaction between two hosts which are both attacked by a common pathogen, where the pathogen has free-living infective stages the population size of which must itself be modelled explicitly, and where the host species do not interact with one another except through their shared pathogen. If either host interacted with the pathogen alone, three broad classes of dynamics would be possible: host regulation, pathogen persistence and pathogen extinction. Here, all possible types of combinations of hosts are examined: regulation-regulation (both hosts would be regulated if they interacted with the pathogen alone), regulation-persistence, regulation-extinction, persistence-persistence persistence-extinction and extinction-extinction. A wide range of dynamics is generated, including a number of patterns quite unlike those found in the one-host pathogen case (e.g. persistence in one host, elimination of the other host) and behaviour contingent on initial densities in the system. For clarity and pertinence, attention is focused on the case where one host is a pest, the pathogen is a potential microbial control agent, and the other host is a non-target species which it is undesirable to harm. The model suggests, broadly, that non-targets are unlikely to be seriously threatened in such cases, and also that non-targets, far from undermining pest control, are quite likely to contribute to its efficacy.

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↗

PubMed2025

Multi-scale phylodynamic modelling of rapid punctuated pathogen evolution.

Computational multi-scale pandemic modelling remains a major and timely challenge. Here we identify specific requirements for a new class of models simulating pandemics across three scales: (1) pathogen evolution, often punctuated by the rapid emergence of new variants, (2) human interactions within a heterogeneous population, and (3) public health responses which constrain individual actions to control the disease transmission. We then present a pandemic modelling framework satisfying these requirements and capable of simulating feedback loops between dynamics unfolding at these different scales. The developed framework comprises a stochastic agent-based model of pandemic spread, coupled with a phylodynamic model that incorporates within-host pathogen evolution. It is validated with a case study, modelling the punctuated evolution of SARS-CoV-2, based on global and contemporary genomic surveillance data, which captures a large heterogeneous population. We demonstrate that the model replicates the essential features of the COVID-19 pandemic and virus evolution, while retaining computational tractability and scalability.

SARS-CoV-2↗

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↗

PubMed1994

Host-host-pathogen models and microbial pest control: the effect of host self regulation.

A model has been investigated of the dynamics of the interaction between two hosts that are both attacked by a common pathogen with free-living infective stages, where the hosts are also subject to self-regulation. If either host interacted with the pathogen alone, two types of dynamics would be possible: an uninfected state where the host settles at its carrying capacity, and an infected state where the host settles at, or cycles around, a density lower than the carrying capacity. The three possible combination of two hosts have been investigated: uninfected-uninfected (both hosts uninfected if alone with the pathogen), infected-uninfected and infected-infected. A range of dynamics is generated, depending on parameter values, including infected co-existence of the two hosts (arrived at by a variety of routes), uninfected co-existence of the two hosts, exclusion of one host by the other which remains in an infected state, and a number of outcomes contingent on the initial densities in the system. Free-living infective stages make uninfected co-existence more likely and introduce additional contingency into the dynamics. The implications for microbial pest control are into the dynamics. The implications for microbial pest control are markedly different from those derived from related models without host self-regulation. There appears to be little chance of a non-target host undermining pest control, relatively little chance of the non-target enhancing pest control and a small but non-negligible threat to non-targets when parameter values are appropriate. The application of the results is commended but great caution is urged.

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↗

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↗

PubMed1996

Host-pathogen systems in a spatially patchy environment.

A discrete model for a host-pathogen system is developed and is used to represent the dynamics in each patch within a landscape of n x n patches. These patches are linked by between-generation dispersal to neighbouring patches. Important results (compared to similar 'coupled map lattice' studies) include an increase in the likelihood of metapopulation extinction if the natural loss of pathogen particles is low, and the observation of a radial wave pattern (not previously reported) where the wavefront propagates uniformly from a central focus. This result has additional significance in that it permits the system to exhibit 'intermittency' between two quasi-stable spatial patterns: spirals and radial waves. With intermittent behaviour, the dynamics may look consistent when viewed at one time scale, but over a longer time scale they can alter dramatically and repeatedly between the two patterns. There is also evidence of clear links between spatial structure and temporal metapopulation behaviour in both the intermittent and 'pure' regions, verified by results from an algorithmic complexity measure and a spectral analysis of the temporal dynamics.

Animals↗

PubMed1997

Interactions between frequency-dependent and vertical transmission in host-parasite systems.

We investigate host-pathogen dynamics and conditions for coexistence in two models incorporating frequency-dependent horizontal transmission in conjunction with vertical transmission. The first model combines frequency-dependent and uniparental vertical transmission, while the second addresses parasites transmitted vertically via both parents. For the first model, we ask how the addition of vertical transmission changes the coexistence criteria for parasites transmitted by a frequency-dependent horizontal route, and show that vertical transmission significantly broadens the conditions for parasite invasion. Host-parasite coexistence is further affected by the form of density-dependent host regulation. Numerical analyses demonstrate that within a host population, a parasite strain with horizontal frequency-dependent transmission can be driven to extinction by a parasite strain that is additionally transmitted vertically for a wide range of parameters. Although models of asexual host populations predict that vertical transmission alone cannot maintain a parasite over time, analysis of our second model shows that vertical transmission via both male and female parents can maintain a parasite at a stable equilibrium. These results correspond with the frequent co-occurrence of vertical with sexual transmission in nature and suggest that these transmission modes can lead to host-pathogen coexistence for a wide range of systems involving hosts with high reproductive rates.

Animals↗

PubMed1996

Salmonellosis: host immune responses and bacterial virulence determinants.

The lifestyle of bacterial pathogens requires them to establish infection in the face of host immunity. Upon entering a potential host, a variety of interactions are initiated, the outcome of which depends upon a myriad of attributes of each of the participants. In this review we discuss the interactions that occur between pathogenic Salmonella species and the host immune systems, but when appropriate to broaden perspective, we have provided a general overview of the interactions between bacterial pathogens and animal hosts. Pathogenic Salmonella species possess an array of invasion genes that produce proteins secreted by a specialized type III secretion apparatus. These proteins are used by the bacteria to penetrate the intestinal mucosa by invading and destroying specialized epithelial M cells of the Peyer's patches. This maneuver deposits the bacteria directly within the confines of the reticuloendothelial system. The host responds to these actions with nonspecific phagocytic cells and an inflammatory response as well as by activating specific cellular and humoral immune responses. Salmonella responds to this show of force directly. It appears that the bacteria invade and establish a niche within the very cells that have been sent to destroy them. Efforts are underway to characterize the factors that allow these intracellular bacteria to customize intracellular vacuoles for their own purposes. It is the constant play between these interactions that determines the outcome of the host infection, and clearly they will also shape the evolution of new survival strategies for both the bacterium and the host.

Animals↗