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Results for “host:pathogen interactions”

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PubMed1992

[The role of iron in immunologic processes].

Iron, apart a for long time well-known function connected with: transportation (hemoglobin), storage (myoglobin), and utilize (cytochromes, cytochrome oxidase) oxygen for respiration, has a critical role in host-pathogen interactions. Iron is essential for microbial growth, but also for immune function. The role of iron in infection, thermoregulation, acute lymphocytic leukemia, neoplasia, rheumatoid arthritis, stimulation of free radical reactions, and studies with iron chelation therapy are discussed.

Arthritis, Rheumatoid↗
PubMed2003

Bioinformatic strategies for better understanding of immune function.

Novartis Foundation sponsored a Symposium which brought together a group of experimental immunologists, theoretical immunologists, and bioinformaticians to discuss the new field of immunoinformatics. The discussion focused on immunological databases, antigen processing and presentation, immunogenomics, host-pathogen interactions, and mathematical modelling of the immune system. A main conclusion of the meeting is the critical role played by immunoinformatics in current immunology research. In particular, immunoinformatics provides a foundation for the emerging fields of systems immunology and immunogenomics.

Allergy and Immunology↗
PubMed1992

Lipoarabinomannan. Multiglycosylated form of the mycobacterial mannosylphosphatidylinositols.

The lipopolysaccharides of mycobacteria, lipoarabinomannan (LAM) and lipomannan (LM), of key importance in host-pathogen interaction, were recently shown to contain a phosphatidylinositol "anchoring domain." We now have established that LAM and LM are based on the phosphatidylinositol mannosides, the characteristic glycophospholipids of mycobacteria. Digestion of the arabinose-free LM with an endo-alpha 1----6-mannosidase yielded evidence for the presence of the 1-(sn-glycerol-3-phospho)-D-myo-inositol-2,6-bis-alpha-D-mannopyranoside unit, indistinguishable from that derived from phosphatidylinositol dimannoside. This same inositol substitution pattern was shown to be present in LAM by methylation analysis before and after dephosphorylation. Positions C-2 and C-6 of the inositol unit of LAM are occupied by mannosyl residues and C-1 by a phosphoryl group. Partial acid hydrolysis of per-O-methylated LAM and comparison by gas chromatography-mass spectrometry of the resulting derivatized oligosaccharides with like products from phosphatidylinositol hexamannoside demonstrated that the C-6 of inositol is the point of attachment of the mannan core of LAM, which consists of an alpha 1----6-linked backbone with considerable alpha-1----2 side chains. Thus, a structural and presumably biosynthetic relationship is established between some of the membranous mannosylphosphatidylinositols described some 25 years ago and the newly emerging, biologically active lipopolysaccharides of mycobacteria.

Carbohydrate Conformation↗
PubMed2004

Marker-assisted selection for leaf rust resistance genes Lr19 and Lr24 in wheat (Triticum aestivum L.).

Leaf rust caused by Puccinia recondita f.sp. tritici is a wheat disease of worldwide importance. Wheat genotypes known to carry specific rust resistance genes and segregating lines that originated from various cross combinations and derived from distinct F2 lineage, so as to represent a diverse genetic background, were included in the present study for validation of molecular markers for Lr19 and Lr24. STS markers detected the presence of the leaf rust resistance gene Lr19 in a Thatcher NIL (Tc*Lrl9) and Inia66//CMH81A575 and of the gene Lr24 in the genotypes Arkan, Blue Boy II, Agent and CI 17907. Validation of molecular markers for Lr19 and Lr24 in parental lines, followed by successful detection of these genes in F3 lines from various cross combinations, was carried out. The molecular test corresponded well with the host-pathogen interaction test response of these lines.

Crosses, Genetic↗
PubMed2004

A novel genomics approach for the identification of drug targets in pathogens, with special reference to Pseudomonas aeruginosa.

Complete genome sequences of several pathogenic bacteria have been determined, and many more such projects are currently under way. While these data potentially contain all the determinants of host-pathogen interactions and possible drug targets, computational tools for selecting suitable candidates for further experimental analyses are currently limited. Detection of bacterial genes that are non-homologous to human genes, and are essential for the survival of the pathogen represents a promising means of identifying novel drug targets. We have used three-way genome comparisons to identify essential genes from Pseudomonas aeruginosa. Our approach identified 306 essential genes that may be considered as potential drug targets. The resultant analyses are in good agreement with the results of systematic gene deletion experiments. This approach enables rapid potential drug target identification, thereby greatly facilitating the search for new antibiotics. These results underscore the utility of large genomic databases for in silico systematic drug target identification in the post-genomic era.

Anti-Bacterial Agents↗
PubMedDate not supplied

[Latency of baculoviruses].

Due to their widespread natural occurrence, baculoviruses and their insect hosts are a convenient model to study the pathogen-host interactions. However, the absence of reliable techniques for the detection of latent viral infection, which is common in insect populations, is among the constraints of such studies. The recent progress in molecular biology techniques made it possible to obtain the fundamental data on the detection of latent viruses in different insect species as well as on the mechanism of latent infection induction, which are reviewed below. The obtained data in many respects expand our knowledge about the role of latency in the system of interactions between baculoviruses and their insect hosts at different ecological levels.

Animals↗
PubMed2005

[Apoptosis of immune system cells in tuberculosis infection].

The review summarizes information on the role of apoptosis in distinct cell subsets in tuberculosis infection. It is emphasizes that the apoptotic death of Mycobacterium-infected macrophages and immune T cells may have differences for the protection of the host. Macrophageal apoptosis may be considered as an important mechanism involved in defense against Mycobacterium tuberculosis, by reducing the viability of mycobacteria and inhibiting their spread in the organs. In contrast, elimination of mycobacteria-specific T cells through the apoptotic mechanism of activation-induced cell death rather prevents the long-term responsiveness to mycobacterial antigens, leading to the persistence of infection and unfavorable tuberculosis progression. The findings suggest the complexity of host-pathogen interactions and emphasize the importance of studies of the molecular mechanisms involved in protection and pathology.

Animals↗
PubMed1990

Antigenic protein from Mycobacterium leprae released in macrophages in vitro as indicator of viability of bacteria.

Peritoneal macrophages from randombred, Swiss white mice, when cultured and infected with Mycobacterium leprae for 24 hours, are able to show the presence of antigen(s) with binding affinity to antibodies present in the sera of bacteriologically positive, lepromatous leprosy patients. Such antibodies are not seen in sera from normal and healthy persons, tuberculoid leprosy patients, or long-term-treated, bacteriologically negative, lepromatous leprosy patients. The production of the antigen(s) is blocked by the anti-M leprae drug rifampin. Other mycobacteria when incubated with macrophages from mice show very little antigens in the lysate but the antigens have an equal affinity for antibodies in sera from both normal individuals and lepromatous patients. Only the lysates from macrophages exposed to live M. leprae could discriminate and could exhibit differential binding to sera from leprosy patients compared to sera from normal individuals. This antigen(s) does not have any binding ability to the monoclonal antibodies available to the antigens of M. leprae identified at present and shown to be specific to M. leprae. This indicates a separate identity of this product which has potential for further exploitation in exploring host-pathogen interactions related specifically to the leprosy infection and the tolerance of M. leprae inside cells.

Animals↗
PubMed1990

Epidemiology in bone and joint infection.

The studies of community-acquired infection indicate the importance of the environment in which the host-pathogen interaction takes place. Whereas the high incidence rates at the extremes of life are compatible with a hypothesis of diminished immune competence, the varying rates of acute osteomyelitis during growth, and its predominantly metaphyseal site, suggest that further studies of the molecular biology of this rather specific infection would be revealing. Molecular biology has a role, too, in improving understanding of the epidemiology of resistance and pathogenicity in hospital-acquired infections. Although antibiotic prescription and other medical practices influence the environment profoundly, we should remember that we may be experiencing long-term trends beyond our present understanding. As more and more reconstructive bone and joint surgery is carried out, careful observational epidemiology remains a vital tool.

Arthritis, Infectious↗
PubMed1982

Pathogen-host jujitsu: phagocyte impotence caused by internalized bacterial adenylate cyclase.

Humans and animals infected with Bordetella species show evidence of impaired host defenses. These pathogenic bacteria produce a unique adenylate cyclase which enters human phagocytes and catalyzes the unregulated formation of cAMP, a known cellular inhibitor. This unique pathogen-host interaction may explain the unusual features of human B. pertussis infection and represents a powerful new probe for the investigation of cAMP-governed processes.

Adenylyl Cyclases↗
PubMed1994

[Infections of cutaneous wounds].

Infection of cutaneous wounds can be defined as proliferation of microorganisms at an interruption in the mucocutaneous covering. The phenomenon depends on an association of local and general factors which disturb the balance in host-pathogen interactions, in favor of the latter. In addition to infections by nonspecific pyogenic germs, whether posttraumatic or postsurgical, there are specific infections where the wound is the departure point for a systemic infection. Even today, tetanus and gaseous gangrene should be apprehended and systematically prevented. Similarly, the high incidence of infection of bite or scratch wounds (animal or human) should suggest prophylactic antibiotic treatment as well as evaluation of the risk of rabies in the case of animal bites or scratches. In any case, even if antibiotic treatment must be undertaken as an emergency measure, previous bacteriological investigation should be carried out if possible since it permits subsequent adaptation in case of failure of the initial antibiotic treatment.

Animals↗
PubMed1996

Antibiotics, cytokines, and endotoxin: a complex and evolving relationship in gram-negative sepsis.

Compelling experimental evidence now exists that antimicrobial agents induce the release of endotoxin from Gram-negative bacteria during the process of bacteriolysis. Different antimicrobial classes, particularly those which act upon the outer membrane of bacteria, vary in the amount of free endotoxin released from Gram-negative organisms. Despite this in vitro evidence, clinically important consequences of antibiotic-induced endotoxin release have yet to be consistently documented. Complexities in the host-pathogen interactions during actual infection with Gram-negative bacteria may account for the difficulties in demonstrating this phenomena in vivo. This brief review analyses these interactions and defines clinical settings where antibiotic-induced endotoxin release may prove to be clinically relevant.

Anti-Bacterial Agents↗
PubMed1999

Identification of quantitative trait loci governing arthritis severity and humoral responses in the murine model of Lyme disease.

A spectrum of disease severity has been observed in patients with Lyme disease, with approximately 60% of untreated individuals developing arthritis. The murine model of Lyme disease has provided strong evidence that the genetic composition of the host influences the severity of arthritis following infection with Borrelia burgdorferi: infected C3H mice develop severe arthritis while infected C57BL/6N mice develop mild arthritis. Regions of the mouse genome controlling arthritis severity and humoral responses during B. burgdorferi infection were identified in the F2 intercross generation of C3H/HeNCr and C57BL/6NCr mice. Rear ankle swelling measurements identified quantitative trait loci (QTL) on chromosomes 4 and 5, while histopathological scoring identified QTL on a unique region of chromosome 5 and on chromosome 11. The identification of QTL unique for ankle swelling or histopathological severity suggests that processes under distinct genetic control are responsible for these two manifestations of Lyme arthritis. Additional QTL that control the levels of circulating Igs induced by B. burgdorferi infection were identified on chromosomes 6, 9, 11, 12, and 17. Interestingly, the magnitude of the humoral response was not correlated with the severity of arthritis in infected F2 mice. This work defines several genetic loci that regulate either the severity of arthritis or the magnitude of humoral responses to B. burgdorferi infection in mice, with implications toward understanding the host-pathogen interactions involved in disease development.

Animals↗
PubMed2026

Tree Killer, Qu'est-ce Que C'est? Insights From Forest Pathogen Genomes.

Forests are central to planetary health but are increasingly challenged by emerging diseases driven by climate change, global trade, and anthropogenic disturbance. Despite the apparent resilience of long-lived, genetically diverse tree hosts, forest ecosystems have repeatedly experienced landscape-level pathogen-driven transformations. Advances in genomics, transcriptomics, and functional biology have transformed our understanding of how fungal and oomycete pathogens interact with their hosts across a continuum of lifestyles, from saprotrophy and necrotrophy to biotrophy. Here, we synthesize insights from comparative and population genomics and functional studies across diverse forest pathosystems to examine the traits that characterize successful tree pathogens. We highlight how lifestyle plasticity, adaptations to woody tissues, vector-mediated transmission, and biotrophic stealth enable pathogens to colonize perennial hosts and persist over long temporal scales. We further examine how genome plasticity, hybridization, and horizontal gene transfer generate adaptive potential that often outpaces host evolutionary responses under current environmental change. Finally, we discuss emerging genomic tools, including biosurveillance, machine learning-based classification, and genome editing, that are beginning to link genotype to phenotype and inform assessments of disease risk. By integrating genomic, ecological, and evolutionary perspectives, this review outlines general principles governing forest pathogen success and identifies priorities for future research aimed at improving understanding, early detection, and management of forest diseases in a changing world.

Trees↗
PubMed2025

Immune-mediated indirect interaction between gut microbiota and bacterial pathogens.

BACKGROUND: In many animals, survival during infection depends on the ability to coordinate interactions between the host immune system and gut microbiota. These tripartite interactions, in turn, potentially shape pathogen virulence evolution. A key regulator of the immune system and, hence, bipartite interactions in insects is the immune deficiency (Imd) pathway, which modulates gut microbiota and pathogens by synthesizing antimicrobial peptides (AMPs) through the NF-κB transcription factor Relish. However, whether Imd-dependent AMPs mediate indirect interactions between gut microbiota and pathogens in a tripartite context remains unclear. Using RNAi-mediated knockdown of Tenebrio molitor Relish (TmRelish), we hypothesized that Imd-dependent AMPs influence indirect interaction between Providencia burhodogranariea_B (P. b_B) infection and the gut microbiota. RESULTS: TmRelish knockdown altered bipartite interactions by disrupting gut microbiota load and composition, increasing pathogen load, and ultimately leading to higher host mortality during infection. However, we did not find support for our tripartite hypothesis that Imd-dependent AMPs mediate indirect interactions between the gut microbiota and P. b_B infection, suggesting the involvement of alternative regulatory pathways or Imd-independent mechanisms. Nevertheless, our investigations of tripartite interactions showed a positive effect of P. b_B infection on gut microbiota load, which in turn stimulated the expression of a subset of AMPs. However, this upregulation of AMPs did not result in reduced P. b_B load. Notably, the gut microbiota did not affect pathogen load but promoted host survival during P. b_B infection, indicating a role in increasing host tolerance rather than resistance. CONCLUSIONS: These findings suggest that while Imd-dependent AMPs may not mediate tripartite interactions in our system, microbiota-host interactions, such as microbiota-mediated immune priming and changes in microbiota load, can shape infection outcomes. These effects on infection outcomes almost certainly exert important selective pressures on the evolution of bacterial virulence.

Animals↗
PubMed1999

Climate change and plant disease management.

▪ Abstract Research on impacts of climate change on plant diseases has been limited, with most work concentrating on the effects of a single atmospheric constituent or meteorological variable on the host, pathogen, or the interaction of the two under controlled conditions. Results indicate that climate change could alter stages and rates of development of the pathogen, modify host resistance, and result in changes in the physiology of host-pathogen interactions. The most likely consequences are shifts in the geographical distribution of host and pathogen and altered crop losses, caused in part by changes in the efficacy of control strategies. Recent developments in experimental and modeling techniques offer considerable promise for developing an improved capability for climate change impact assessment and mitigation. Compared with major technological, environmental, and socioeconomic changes affecting agricultural production during the next century, climate change may be less important; it will, however, add another layer of complexity and uncertainty onto a system that is already exceedingly difficult to manage on a sustainable basis. Intensified research on climate change-related issues could result in improved understanding and management of plant diseases in the face of current and future climate extremes.

climate variability↗
PubMed1992

Heat shock proteins and infection: interactions of pathogen and host.

Invasive microorganisms encounter defensive attempts of the host to starve, destroy and eliminate the infection. In experimental model systems aiming to imitate defensive actions of the host, microorganisms respond by the rapid acceleration in the rate of expression of heat shock and other stress proteins. Heat shock proteins (hsp) of most if not all pathogens are major immune targets for both B- and T-cells. Host cells involved in the defensive action cannot avoid exposure to their own reactive compounds, such as oxygen radicals, resulting in premature cell death and tissue damage. Long-term consequences to the host may include cancer. In cells in tissue culture, induction of host-specific hsps occurs upon exposure to oxidants and in viral infections. Drugs that bind to members of the hsp70 family induce peroxisome proliferation and hepatocarcinoma, but may open the way for the development of novel drugs in support of antimetabolite treatment of infections and cancer.

Animals↗