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Results for “host:pathogen interactions”

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PubMed2001

Lung surfactant and reactive oxygen-nitrogen species: antimicrobial activity and host-pathogen interactions.

Surfactant protein (SP) A and SP-D are members of the collectin superfamily. They are widely distributed within the lung, are capable of antigen recognition, and can discern self versus nonself. SPs recognize bacteria, fungi, and viruses by binding mannose and N-acetylglucosamine residues on microbial cell walls. SP-A has been shown to stimulate the respiratory burst as well as nitric oxide synthase expression by alveolar macrophages. Although nitric oxide (NO.) is a well-recognized microbicidal product of macrophages, the mechanism(s) by which NO. contributes to host defense remains undefined. The purpose of this symposium was to present current research pertaining to the specific role of SPs and reactive oxygen-nitrogen species in innate immunity. The symposium focused on the mechanisms of NO*-mediated toxicity for bacterial, human, and animal models of SP-A- and NO.-mediated pathogen killing, microbial defense mechanisms against reactive oxygen-nitrogen species, specific examples and signaling pathways involved in the SP-A-mediated killing of pulmonary pathogens, the structure and binding of SP-A and SP-D to bacterial targets, and the immunoregulatory functions of SP-A.

Animals↗

PubMed2003

The use of transepithelial models to examine host-pathogen interactions.

Many pathogens must overcome an epithelial barrier in order to establish an infection. Unsurprisingly, such pathogens have evolved different mechanisms to overcome this obstacle, targeting specific epithelial structures or functions. These include disruption of epithelial barrier function, transcytosing from the apical to the basolateral membrane domain or inducing cell movement such as neutrophil recruitment. When studying these processes in vivo, animal models often fail to mimic the disease observed in humans and present a complex system in which many variables cannot be controlled. Therefore, in vitro transepithelial models that permit the study of a relevant biological surface have been developed, to integrate not only interactions between bacteria and epithelial cells but also, under certain conditions, to integrate a third cell type, such as neutrophils or dendritic cells. Such models are particularly useful for studying the bacteria-host relationship as it would occur in the microenvironment of the human epithelium and have enhanced our understanding of the unique strategies by which pathogenic bacteria exploit host cells to overcome the initial epithelial hurdle.

Animals↗

PubMed2001

Host-pathogen interactions promoting inflammatory Lyme arthritis: use of mouse models for dissection of disease processes.

Recent studies have confirmed the infectious and inflammatory nature of arthritis induced by Borrelia burgdorferi, or Lyme arthritis. This arthritis is directed by the presence of the bacteria in joint tissue, and is mediated through activation of the Toll-like receptor 2 (TLR2) signaling pathways by borrelial lipoproteins. Several host genes regulate the severity of arthritis, possibly by regulating the balance of pro- and anti-inflammatory responses.

Animals↗

PubMed2001

Dynamic nature of host-pathogen interactions in Mycobacterium marinum granulomas.

Mycobacterium marinum causes long-term subclinical granulomatous infection in immunocompetent leopard frogs (Rana pipiens). These granulomas, organized collections of activated macrophages, share many morphological features with persistent human tuberculous infection. We examined organs of frogs with chronic M. marinum infection using transmission electron microscopy in conjunction with immunohistochemistry and acid phosphatase cytochemistry to better define the bacterium-host interplay during persistent infection. Bacteria were always found within macrophage phagosomes. These phagosomes were often fused to lysosomes, in sharp contrast to those formed during in vitro infection of J774 macrophage-like cells by M. marinum. The infected macrophages in frog granulomas showed various levels of activation, as evidenced by morphological changes, including epithelioid transformation, recent phagocytic events, phagolysosomal fusion, and disintegration of bacteria. Our results demonstrate that even long-term granulomas are dynamic environments with regard to the level of host cell activation and bacterial turnover and suggest a continuum between constantly replicating bacteria and phagocytic killing that maintains relatively constant bacterial numbers despite an established immune response. Infection with a mutant bacterial strain with a reduced capacity for intracellular replication shifted the balance, leading to a greatly reduced bacterial burden and inflammatory foci that differed from typical granulomas.

Animals↗

PubMed2000

Caenorhabditis elegans for the study of host-pathogen interactions.

The nematode worm Caenorhabditis elegans, for which the complete genome sequence is available, has several other advantages as an experimental system, and has already been widely used as a model for the study of vertebrate biology. Recent investigations have revealed that C. elegans could also be an extremely useful model system in the study of bacterial pathogenesis and have reinforced the notion that common virulence and host defence mechanisms exist.

Animals↗

PubMed1998

Animal models for host-pathogen interaction studies.

There is no model of Helicobacter pylori infection that exactly mimics the human diseases. In a particular, there are no good models of ulceration or gastric adenocarcinoma. Patterns of gastritis induced in the animals tend to be lymphocytic and lack the neutrophil infiltration typical of H. pylori infection in the adult. However, the animal models are starting to provide valuable information with respect to factors involved in the colonisation of the gastric mucosa and the importance of host factors in the development of gastric atrophy, as well as making possible the screening of potential therapeutic agents and vaccine candidates. Models include gnotobiotic piglets, primates, cats, dogs, ferrets and a range of rodents. Recent advances in the mouse models mean that they will allow us to dissect bacterial host interactions in a novel manner due to the availability of a wide range of immunological reagents and numerous mutant or transgenic strains.

Animals↗

PubMed2006

Candida albicans biofilm development, modeling a host-pathogen interaction.

Medical device-associated infections involve the attachment of cells to a surface, production of an extracellular matrix and development of a mature biofilm. Many Candida albicans disease states involve biofilm growth. These infections have great impact on public health because organisms in biofilms exhibit dramatically reduced susceptibility to antifungal therapy. Progression to a mature biofilm is dependent on cell adhesion, extracellular matrix production and the yeast-to-hyphae transition. Numerous in vitro biofilm model systems have been successfully used to examine biofilm architecture, development, cell phenotypes and drug resistance. Although these studies have included a number of experimental variables to mimic infections in patients, it is difficult to accurately account for the multitude of host and infection-site variables that are probably important in humans. Recent studies have begun to explore C. albicans biofilms using animal biofilm infection models in order to more completely reflect the complexity of this host-fungal interaction.

Animals↗

PubMed1975

An other look at iron: role in host pathogen interaction.

Iron, as participant of many biological processes is a prerequisite for life. Uptake, internal transport and storage by organisms is handled by highly specialized chemical systems endowed with strong metal binding affinities. Apart from the homeostatic function of iron-binding compounds they appear of significance for inter-species interactions. Thus, by tight binding transferrin withholds the iron from invading microorganisms required for their optimal growth. This bacteriostatic property of the iron transport protein is however partially overcome by small molecular substances synthesized by bacteria and successfully competing for the metal. The balance of such interaction is a complex one. Yet, strong evidence points to the crucial importance of the amount of iron offered by a host to infecting agents for determining the fate of bacterial disease.

Anemia, Hypochromic↗

PubMed2005

Toward a genome-wide systems biology analysis of host-pathogen interactions in group A Streptococcus.

Genome-wide analysis of microbial pathogens and molecular pathogenesis processes has become an area of considerable activity in the last 5 years. These studies have been made possible by several advances, including completion of the human genome sequence, publication of genome sequences for many human pathogens, development of microarray technology and high-throughput proteomics, and maturation of bioinformatics. Despite these advances, relatively little effort has been expended in the bacterial pathogenesis arena to develop and use integrated research platforms in a systems biology approach to enhance our understanding of disease processes. This review discusses progress made in exploiting an integrated genome-wide research platform to gain new knowledge about how the human bacterial pathogen group A Streptococcus causes disease. Results of these studies have provided many new avenues for basic pathogenesis research and translational research focused on development of an efficacious human vaccine and novel therapeutics. One goal in summarizing this line of study is to bring exciting new findings to the attention of the investigative pathology community. In addition, we hope the review will stimulate investigators to consider using analogous approaches for analysis of the molecular pathogenesis of other microbes.

Computational Biology↗

PubMed1989

Host-Pathogen Interactions : XXXII. A Fungal Glucan Preparation Protects Nicotianae against Infection by Viruses.

A glucan preparation obtained from the mycelial walls of the fungus Phytophthora megasperma f.sp. glycinea and known as an elicitor of phytoalexins in soybean was shown to be a very efficient inducer of resistance against viruses in tobacco. The glucan preparation protected against mechanically transmitted viral infections on the upper and lower leaf surfaces. Whether the glucan preparation was applied by injection, inoculation, or spraying, it protected the plants if applied before, at the same time as, or not later than 8 hours after virus inoculation. At concentrations ranging from 0.1 to 10 micrograms per milliliter, the glucan preparation induced protection ranging from 50 to 100% against both symptom production (necrotic local lesions, necrotic rings, or systemic mosaic) and virus accumulation in all Nicotiana-virus combinations examined. However, no significant protection against some of the same viruses was observed in bean or turnip. The host plants successfully protected included N. tabacum (9 different cultivars), N. sylvestris, N. glutinosa, and N. clevelandii. The viruses belonged to several taxonomic groups including tobacco mosaic virus, alfalfa mosaic virus, and tomato black ring virus. The glucan preparation did not act directly on the virus and did not interfere with virus disassembly; rather, it appeared to induce changes in the host plant that prevented infections from being initiated or recently established infections from enlarging. The induced resistance does not depend on induction of pathogenesis-related proteins, the phenylpropanoid pathway, lignin-like substances, or callose-like materials. We believe the induced resistance results from a mechanism that has yet to be described.

Journal Article↗

PubMed1989

Differential clearance and host-pathogen interactions of YopE- and YopK- YopL- Yersinia pestis in BALB/c mice.

This study characterized infections in BALB/c mice by the nonpigmented Yersinia pestis KIM and its derivatives lacking the low-Ca2+-response virulence plasmid pCD1 or failing to express selected yersinial outer membrane proteins (YOPs). The parent Y. pestis showed net growth in the spleen by 2 h and in the liver after 7 h; exponential growth in both the liver and spleen culminated in death of the mice starting on day 4, with total bacterial numbers of less than 10(8) in the blood, liver, and spleen together. The histopathology progressed from microabscesses to extensive coagulative necrosis unaccompanied by further immigration of inflammatory cells. This, together with the relatively low bacterial numbers, suggests a toxigenic mechanism. YopE- or YopK- YopL- yersiniae were cleared from the spleen but grew in the liver after an initial lag. Their growth was curbed after 1 to 2 days and entered a plateau that lasted 5 to 6 days; viable numbers then decline rapidly. This suggests that these Yop- mutations distinguish, at least kinetically, between host responses in liver and spleen. Both strains caused acute inflammation in liver that evolved into structured lesions surrounded by progressively mononuclear inflammation suggestive of a granulomatous response. Accordingly, YOP E and YOPs K and L are necessary in the early days of the infection for net growth in spleen and prolonged growth in the liver; their absence is reflected morphologically by the emergence of cell-mediated immunity in the liver. The YopE- and YopK- YopL- mutants bound only slightly increased amounts of C3, suggesting that YOPs E, K, and L are protective through mechanisms other than interfering with the binding of complement.

Animals↗

PubMed2003

Molecular host-pathogen interaction in brucellosis: current understanding and future approaches to vaccine development for mice and humans.

Brucellosis caused by Brucella spp. is a major zoonotic disease. Control of brucellosis in agricultural animals is a prerequisite for the prevention of this disease in human beings. Recently, Brucella melitensis was declared by the Centers for Disease Control and Prevention to be one of three major bioterrorist agents due to the expense required for the treatment of human brucellosis patients. Also, the economic agricultural loss due to bovine brucellosis emphasizes the financial impact of brucellosis in society. Thus, vaccination might efficiently solve this disease. Currently, B. abortus RB51 and B. melitensis REV.1 are used to immunize cattle and to immunize goats and sheep, respectively, in many countries. However, these genetically undefined strains still induce abortion and persistent infection, raising questions of safety and efficiency. In fact, the REV.1 vaccine is quite virulent and apparently unstable, creating the need for improved vaccines for B. melitensis. In addition, Brucella spp. may or may not provide cross-protection against infection by heterologous Brucella species, hampering the acceleration of vaccine development. This review provides our current understanding of Brucella pathogenesis and host immunity for the development of genetically defined efficient vaccine strains. Additionally, conditions required for an effective Brucella vaccine strain as well as the future research direction needed to investigate Brucella pathogenesis and host immunity are postulated.

Animals↗

PubMed2005

Single gene effects in mouse models of host: pathogen interactions.

Inbred mouse strains have been known for many years to vary in their degree of susceptibility to different types of infectious diseases. The genetic basis of these interstrain differences is sometimes simple but often complex. In a few cases, positional cloning has been used successfully to identify single gene effects. The natural resistance-associated macrophage protein 1 (Nramp1) gene (Slc11a1) codes for a metal transporter active at the phagosomal membrane of macrophages, and Nramp1 mutations cause susceptibility to Mycobacterium, Salmonella, and Leishmania. Furthermore, recent advances in gene transfer technologies in transgenic mice have enabled the functional dissection of gene effects mapping to complex, repeated parts of the genome, such as the Lgn1 locus, causing susceptibility to Legionella pneumophila in macrophages. Finally, complex traits such as the genetically determined susceptibility to malaria can sometimes be broken down into multiple single gene effects. One such example is the case of pyruvate kinase, where a loss-of-function mutation was recently shown by our group to be protective against blood-stage infection with Plasmodium chabaudi. In all three cases reviewed, the characterization of the noted gene effect(s) has shed considerable light on the pathophysiology of the infection, including host response mechanisms.

Animals↗

PubMed2001

Fish monocytes as a model for mycobacterial host-pathogen interactions.

Mycobacterium marinum, a relatively rapid-growing fish and human pathogen, has become an important model for the investigation of mycobacterial pathogenesis. M. marinum is closely related to the Mycobacterium tuberculosis complex and causes a disease in fish and amphibians with pathology similar to tuberculosis. We have developed an in vitro model for the study of M. marinum virulence mechanisms using the carp monocytic cell line CLC (carp leukocyte culture). We found that fish monocytes can differentiate between pathogenic and nonpathogenic mycobacterial species. Interestingly, M. marinum enters fish monocytes at a 40- to 60-fold-higher rate than Mycobacterium smegmatis. In addition, M. marinum survives and replicates in fish monocytes while M. smegmatis is killed. We also found that M. marinum inhibits lysosomal fusion in fish monocytes, indicating that these cells may be used to dissect the mechanisms of intracellular trafficking in mycobacteria. We conclude from these observations that monocytic cells from fish, a natural host for M. marinum, provide an extremely valuable model for the identification and characterization of mycobacterial virulence determinants in the laboratory.

Animals↗

PubMedDate not supplied

Immune regulation during pregnancy and host-pathogen interactions in infectious abortion.

The immunological mechanisms that govern the success of pregnancy in outbred mammals are complex. During placental formation the invasion of fetal cells into maternal tissue must be controlled to prevent damage to the mother. Equally, maternal recognition of pregnancy must be such that allorejection of the fetus does not occur. Despite the complexity of this phenomenon, it is clear that cytokines play a crucial role at the maternofetal interface and in the periphery to ensure that pregnancy proceeds successfully. Inflammatory cytokines such as tumour necrosis factor-alpha (TNF-alpha) and interferon-gamma (IFN-gamma) can exert detrimental effects in the placenta and tend to be present at low concentrations, whereas the regulatory cytokines interleukin (IL)-10 and tranforming growth factor-beta (TGF-beta) are beneficial and tend to predominate. This means that infection with pathogens that target the placenta and that elicit inflammatory responses may cause abortion by giving rise to a detrimental combination of cytokines that causes damage but does not control the disease. Infectious abortion is discussed in the context of the modulation of host immune responses during pregnancy, taking into account the different placental structures present in human beings, rodents and ruminants.

Abortion, Septic↗

PubMed1990

Outer membrane proteins of E. coli in the host-pathogen interaction in urinary tract infection.

Outer membrane protein patterns (Omp) of Escherichia coli obtained directly from the urine of bacteriuric patients without passage on artificial culture media (ACM) were studied by polyacrylamide gel electrophoresis (SDS-PAGE) in an effort to determine whether in vivo conditions of growth affected the expression of these bacterial surface structures. Seventeen strains studied showed two distinct Omp patterns: one protein band appeared at the level of porin proteins (40 kDa) in both patterns, but Omp A protein was at the level of 36 kDa in the first pattern and a new protein was observed at 21.5 kDa in the second pattern suggesting that it is a fragment of Omp A. High molecular weight proteins were also observed in most of the strains and this finding was related to lack of free iron when the same strains were grown under iron restricted conditions in vitro. The same strains grown in pooled urine from normal females showed the first pattern mentioned above. Comparative growth on ACM of urinary strains and E. coli strains isolated from blood, feces and wounds showed an increase in the number of porins expressed (from 1 to 2 or 3, with some variability observed between strains). Differences in osmolality between pooled urine and ACM used, plus in vitro studies varying the osmolality of culture media, showed that osmolality accounted for differences in the number of porins expressed: porin expression decreased in urine the ACM of high osmolality, suggesting that the same phenomena occurred in vivo. It is concluded that host factors including low availability of iron and high osmolality present in the urinary tract influence the expression of several E. coli surface proteins. These proteins may relate to the ability of E. coli to colonize and invade the urinary tract by regulating the physiologic and/or metabolic state of the bacterial cell favoring survival of the organism in a hostile environment. Specific immune responses directed against porins could influence the outcome of this host-parasite interaction.

Bacterial Outer Membrane Proteins↗

PubMed1998

Host-pathogen interaction in amebiasis and progress in vaccine development.

Entamoeba histolytica, the causative organism of invasive intestinal and extraintestinal amebiasis, infects approximately 50 million people each year, causing an estimated 40 to 100 thousand deaths annually. Because amebae only infect humans and some higher non-human primates, an anti-amebic vaccine could theoretically eradicate the organism. Uncontrolled epidemiologic studies indicate that acquired immunity to amebic infection probably occurs and that such a vaccine might be feasible. Application of molecular biologic techniques has led to rapid progress towards understanding how Entamoeba histolytica causes disease, and to the identification of several amebic proteins associated with virulence. These proteins are now being evaluated as potential vaccine components. Parenteral and oral vaccine preparations containing recombinant amebic proteins have been effective in preventing disease in a gerbil model of amebic liver abscess. Although systemic and mucosal cellular and humoral immunity both appear to play a role in protection against Entamoeba histolytica, the relative importance of each in the human immune response remains unknown. No animal model of intestinal amebiasis currently exists, moreover, so it has been impossible to evaluate protection against colonization and colitis. Further investigation of the fundamental mechanisms by which Entamoeba histolytica causes disease and of the human immune response to amebic infection is necessary to assess the true feasibility of an anti-amebic vaccine.

Animals↗

PubMed2004

Advances in the biology, diagnosis and host-pathogen interactions of parvovirus B19.

Increased recognition of parvovirus B19 (B19), an erythrovirus, as a significant human pathogen that causes fetal loss and severe disease in immunocompromised patients has resulted in intensive efforts to understand the pathogenesis of B19-related disease, to improve diagnostic strategy that is deployed to detect B19 infection and blood-product contamination and, finally, to elucidate the nature of the cellular immune response that is elicited by the virus in diverse patient cohorts. It is becoming clear that at least three related erythrovirus strains (B19, A6/K71 and V9) are circulating in the general population and that viral entry into target cells is mediated by an expanding range of cellular receptors, including P antigen and beta-integrins. Persistent infection by B19 is emerging as a contributory factor in autoimmune disease, a hypothesis that is constrained by the detection of B19 in the skin of apparently healthy individuals. B19 infection during pregnancy may account for thousands of incidences of fetal loss per annum in Europe, North America and beyond, yet there is currently only minimal screening of pregnant women to assess serological status, and thereby risk of infection, upon becoming pregnant. Whilst major advances in diagnosis of B19 infection have taken place, including standardization of serological and DNA-based detection methodologies, blood donations that are targeted at high-risk groups are only beginning to be screened for B19 IgG and DNA as a means of minimizing exposure of at-risk patients to the virus. It is now firmly established that a Th1-mediated cellular immune response is mounted in immunocompetent individuals, a finding that should contribute to the development of an effective vaccine to prevent B19 infection in selected high-risk groups, including sickle-cell anaemics.

Anemia, Aplastic↗