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Results for “Host Microbial Interactions”

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PubMed1994

Foscarnet. A reappraisal of its antiviral activity, pharmacokinetic properties and therapeutic use in immunocompromised patients with viral infections.

The DNA polymerase of human herpes viruses, including cytomegalovirus (CMV), and the reverse transcriptase of human immunodeficiency virus (HIV) are selectively inhibited in vitro by the pyrophosphate analogue foscarnet. Inhibition is reversible on withdrawal of foscarnet and additive or synergistic effects have been demonstrated in vitro with other antiviral drugs, including ganciclovir and zidovudine. Foscarnet appears to have negligible effects on host enzymes and cells. Complete or partial clinical resolution of ocular symptoms is obtained in more than 89% of patients with acquired immunodeficiency syndrome (AIDS) and CMV retinitis during foscarnet induction therapy, but relapse occurs soon after ceasing treatment. Maintenance treatment given daily can extend the period of remission considerably. Foscarnet and ganciclovir monotherapy had similar efficacy in the treatment of CMV retinitis in patients with AIDS in several studies, and have been used concomitantly in immunocompromised patients with recalcitrant CMV infections. In 1 trial, patients receiving foscarnet survived for significantly longer than those receiving ganciclovir. Foscarnet has been used successfully in the treatment of limited numbers of immunocompromised patients with CMV-associated gastrointestinal (improvement in over 67% of patients) and other infections. Aciclovir-resistant herpes simplex infections in immunocompromised patients have also been treated successfully with foscarnet. Almost 90% of a foscarnet dose is excreted in the urine. Reversible nephrotoxicity is common during foscarnet therapy, but may be reduced by dosage adjustment and adequate hydration. Anaemia, nausea and vomiting, disturbances in electrolyte levels and genital ulceration have also been associated with administration of the drug. The different tolerability profiles of foscarnet and zidovudine facilitate the use of these agents in combination in patients with AIDS and CMV infection; whereas ganciclovir, like zidovudine, is associated with dose-limiting haematological toxicity. The apparent survival benefits seen in these patients when receiving foscarnet and zidovudine (possibly linked to synergy between zidovudine and foscarnet and/or the inherent anti-HIV activity of foscarnet), appear to offer potentially important advantages for foscarnet over ganciclovir in the treatment of selected patients with AIDS and CMV infections.

AIDS-Related Opportunistic Infections↗

PubMed1986

The human intestinal microflora.

The major host defense mechanisms against bacterial overgrowth in the small bowel are the normal propulsive activity of the bowel itself and gastric acid secretion. Microbial interactions are a major factor in regulating the indigenous bacterial flora. Studies of the bacterial enzymes of the gut suggest that changes in diet may lead to marked changes in the colonic flora. Antibiotics affect the composition of the colonic microflora. The microflora also influence the degradation of mucin, the conversion of urobilin to urobilinogen, of cholesterol to coprostanol, and the production of short chain fatty acids. Current interests are focused on the bacterial flora of tropical sprue, the role of bacteria in colorectal cancer, and the involvement of intestinal microflora in the enterohepatic circulation of sex steroid hormones.

Animals↗

PubMed2006

The pursuit of cryptococcal pathogenesis: heterologous hosts and the study of cryptococcal host-pathogen interactions.

Analysis of the molecular mechanisms by which a pathogen interacts with the human host is most commonly performed using a mammalian model of infection. However, several virulence-related genes previously shown to be involved in mammalian infection with Cryptococcus neoformans have also been shown to play a role in the interaction of these pathogens with invertebrates, such as Acanthamoeba castellanii, Caenorhabditis elegans, Dictyostelium discoideum, Drosophila melanogaster and Galleria mellonella. The study of host-pathogen interactions using these model hosts has allowed rapid screening of mutant libraries and can be used for the study of evolutionarily preserved aspects of microbial virulence and host response.

Animals↗

PubMed1984

Carbohydrates as recognition determinants in phagocytosis and in lectin-mediated killing of target cells.

Carbohydrate-lectin interactions serve as the basis of recognition by phagocytic cells of particles and of various target cells. Such interactions occur in the following systems: between sugars on the surface of the phagocytic cells and lectins on the surface of other cells--the best studied example is the binding of mannose-specific Escherichia coli and related organisms via their surface lectins to oligo-mannose residues on macrophages; between lectins on the surface of phagocytic cells and sugars on particles or other cells--phagocytosis of zymosan and of sialidase-treated erythrocytes, mediated respectively by mannose-specific and galactose-specific lectins on macrophages, belongs to this category; by extracellular lectins that form bridges between sugars on both types of cell--as shown by enhancement of phagocytosis of staphylococci by wheat germ agglutinin, and by lectin-dependent killing of target cells by macrophages. These interactions may play an important role in the activities of phagocytic cells in vivo. They may provide an initial host defense mechanism immediately after microbial infection, operate in tissues where phagocytic activity is poor, and participate in tumor rejection.

Animals↗

PubMed2006

Mutual enhancement of virulence by enterotoxigenic and enteropathogenic Escherichia coli.

Enterotoxigenic Escherichia coli (ETEC) and enteropathogenic E. coli (EPEC) are common causes of diarrhea in children in developing countries. Dual infections with both pathogens have been noted fairly frequently in studies of diarrhea around the world. In previous laboratory work, we noted that cholera toxin and forskolin markedly potentiated EPEC-induced ATP release from the host cell, and this potentiated release was found to be mediated by the cystic fibrosis transmembrane conductance regulator. In this study, we examined whether the ETEC heat-labile toxin (LT) or the heat-stable toxin (STa, also known as ST) potentiated EPEC-induced ATP release. We found that crude ETEC culture filtrates, as well as purified ETEC toxins, did potentiate EPEC-induced ATP release in cultured T84 cells. Coinfection of T84 cells with live ETEC plus EPEC bacteria also resulted in enhanced ATP release compared to EPEC alone. In Ussing chamber studies of chloride secretion, adenine nucleotides released from the host by EPEC also significantly enhanced the chloride secretory responses that were triggered by crude ETEC filtrates, purified STa, and the peptide hormone guanylin. In addition, adenosine and LT had additive or synergistic effects in inducing vacuole formation in T84 cells. Therefore, ETEC toxins and EPEC-induced damage to the host cell both enhance the virulence of the other type of E. coli. Our in vitro data demonstrate a molecular basis for a microbial interaction, which could result in increased severity of disease in vivo in individuals who are coinfected with ETEC and EPEC.

Adenosine Triphosphate↗

PubMed1988

Normal flora and mucosal immunity of the head and neck.

The study of the human resident flora has grown from Antony van Leeuwenhoek's simple descriptions some 300 years ago to the sophisticated investigations being done today. The acquisition of organisms and the subsequent course of either stable colonization or invasion of the host involve complex host-parasite interactions. From one perspective, clearly host factors are operative that appear to select against certain species while being permissive for others. From another perspective, microbial species that are successful at colonization must overcome certain host factors to maintain a selective advantage and flourish within a particular body habitat. It is intriguing that whereas host mucosal defenses are a significant influence contributing to selection of the resident flora, it is this established flora that provides the host with perhaps its most important local defense system. In the head and neck areas, many of these mucosal surfaces are contiguous and thus for the most part share a common resident flora. These organisms are rarely involved in infection unless some breach of the mucosal surface or some upset in the balance of the normal flora occurs. On these occasions, the host is susceptible to infection from both newly acquired organisms and those previously present, which may now become invasive. In any event, it is clear that improved knowledge of the normal flora of the head and neck is essential for understanding and for effective treatment of infectious processes in this area. It is hoped that a better appreciation of the important role of the normal flora in maintaining the host mucosal defenses will further focus our attention on its preservation.

Head↗

PubMed2026

The value of a prophage-borne defense system in phage-phage competition.

Temperate phages that incorporate into their bacterial hosts' genomes often encode defense systems that protect their hosts from superinfection by unrelated phages. Yet the evolutionary value of such defenses to the phage remains unclear. We present a minimal theoretical framework to quantify the selective advantage of a prophage-borne defense system in competition between temperate phages infecting the same bacterial host. The model reveals regimes in which a "defensive phage" can invade and persist despite growth costs, regimes of bistability, and others in which all phage types coexist due to a rock-paper-scissors-like dynamic between defensive, non-defensive, and defense-loss variants. Because defense systems can be non-transitive, true rock-paper-scissors relations can lead to persistent oscillations. These results identify simple conditions under which phage-encoded defense systems are evolutionarily stable, providing testable predictions for the prevalence and maintenance of these systems in natural microbial communities.

Prophages↗

PubMed1994

Diversity within diversity: molecular approaches to studying microbial interactions with insects.

DNA sequence information has greatly augmented the number of characters available for analysis in phylogenetic research. Nowhere is this more evident than in studies of microbial evolution. Ribosomal DNA sequence data has simultaneously permitted the distinction between individual species and the inference of their phylogenetic relationships in many cases where both were formerly impossible. These have contributed to our understanding of the ecology of particular microbe-host interactions and the history of these relationships over evolutionary time. We describe examples from two ends of the ecological spectrum in insect/bacterial associations: one in which bacteria mediate host cytoplasmic incompatibility and parthenogenesis, and the other in which mycetocyte bacteria augment host nutrition. In the former, the pattern of bacterial interaction is general, with the same or closely related strains of the genus Wolbachia associating with a wide range of insect taxa. In the latter, concordance between host and microbe phylogenies suggests cospeciation between bacteria and host, although it is as yet unclear whether this process has involved step-wise, reciprocal coevolution. We conclude with a discussion of how developments in molecular techniques may aid in analyzing more complex interactions between insects and microbes.

Animals↗

PubMed2006

Innate defences against methicillin-resistant Staphylococcus aureus (MRSA) infection.

The innate immune system is the primary defence against bacterial infection. Among the factors involved in innate defence, anti-microbial peptides produced by humans have recently attracted attention due to their relevance to some diseases and also to the development of new chemotherapeutic agents. Staphylococcus aureus is one of the major human pathogens, causing a variety of infections from suppurative disease to food poisoning. Methicillin-resistant S. aureus (MRSA) is a clinical problem and with the recent emergence of a vancomycin-resistant strain, this will pose serious problems in the near future. In investigating the molecular biology of S. aureus infections to develop new chemotherapeutic agents against MRSA infections, knowledge of the interaction of innate anti-microbial peptides with S. aureus is important. In vitro and in vivo experiments demonstrate that exposure of S. aureus to host cells can induce the anti-microbial peptides beta-defensin-2 (hBD2), hBD3, and LL37/CAP18. The induction level of these peptides differs among strains, as does the susceptibility of the strains, with MRSA strains exhibiting lower susceptibility. In summary, the susceptibility of S. aureus strains, including MRSA strains, to components of the innate immune system varies, with the MRSA strains showing more resistance to both innate immune factors and chemotherapeutic agents.

Anti-Bacterial Agents↗

PubMed1993

In vitro susceptibility of Pityrosporum ovale (Malassezia furfur) to human androgenic steroids.

Cells of Pityrosporum ovale that colonize human pilosebaceous units are constantly exposed to cutaneous androgenic steroids. The aim of our study was to find out whether P. ovale is susceptible to these hormones. Three strains of P. ovale were grown in vitro in the presence of various concentrations of testosterone, dehydroepiandrosterone, androstenedione, androstanedione, 5-alpha-dihydrotestosterone and progesterone (10, 100, and 1000 micrograms/ml; agar dilution assays). In addition, three strains of Candida albicans were also exposed to equal concentrations of the same androgens. As a result, all P. ovale strains were suppressed by 1000 micrograms/ml androstenedione, which was the strongest inhibitor. The other androgenic steroids also significantly reduced P. ovale growth at different concentrations, depending on the hormone used and the strain tested. Progesterone was inhibitory at the highest concentration for one P. ovale strain only. Candida albicans was not affected by any of the androgens. These findings demonstrate an in vitro susceptibility of P. ovale to high concentrations of human androgenic steroids. A relevance of this interaction for the in vivo fungus-host relation is not apparent.

Androgens↗

PubMed2002

Cellular hijacking: a common strategy for microbial infection.

Eukaryotic cells are under constant attack from microbial intruders seeking a selective advantage for survival, propagation and dissemination. Microbial infections can often result in disease and might even be lethal to the host if they are not combatted effectively. Studies of host-pathogen interactions have revealed that virulence often requires the usurpation of existing cell signaling pathways or membrane traffic machinery of the host. Such studies provide a rich source of cell biological data that will probably prove essential for future efforts designed to either thwart these attacks or learn from them.

ADP Ribose Transferases↗

PubMed1989

Correlation between electrophoretic types B1 and B2 of carboxylesterase B and sex of patients in Escherichia coli urinary tract infections.

One hundred and sixty-eight strains of Escherichia coli isolated from 84 men and 84 women who had urinary tract infections (134 cases) or bacteremia of urinary tract origin (34 cases) were assessed for their carboxylesterase B electrophoretic types B1 and B2, alpha-haemolysin production, the presence of mannose resistant haemagglutinin (MRHA) and antibiotic susceptibility. Electrophoretic type B2 was phenotypically linked with alpha-haemolysin and MRHA productions. The strains isolated from males were more frequently of type B2, haemolytic and both haemolytic and haemagglutinating than those isolated from females. The strains isolated during bacteremia were more frequently haemolytic and haemagglutinating than those obtained from urinary tract infections. Type B1 strains were more frequently resistant to antimicrobial agents than type B2 strains. The results reinforced the distinction, in terms of virulence and antibiotic sensitivity, between B1 and B2 strains and demonstrated the influence of the sex of patients on the host-parasite interaction during urinary tract infections.

Bacterial Proteins↗

PubMed1997

Structural and antigenic types of cell wall polysaccharides from viridans group streptococci with receptors for oral actinomyces and streptococcal lectins.

Lectin-mediated interactions between oral viridans group streptococci and actinomyces may play an important role in microbial colonization of the tooth surface. The presence of two host-like motifs, either GalNAc beta1-->3Gal (Gn) or Gal beta1-->3GalNAc (G), in the cell wall polysaccharides of five streptococcal strains accounts for the lactose-sensitive coaggregations of these bacteria with Actinomyces naeslundii. Three streptococcal strains which have Gn-containing polysaccharides also participate in GalNAc-sensitive coaggregations with strains of Streptococcus gordonii and S. sanguis. Each Gn- or G-containing polysaccharide is composed of a distinct phosphodiester-linked hexa- or heptasaccharide repeating unit. The occurrence of these polysaccharides on 19 additional viridans group streptococcal strains that participate in lactose-sensitive coaggregations with actinomyces was examined. Negatively charged polysaccharides that reacted with Bauhinia purpurea agglutinin, a Gal and GalNAc binding plant lectin, were isolated from 17 strains by anion exchange column chromatography of mutanolysin-cell wall digests. Results from nuclear magnetic resonance and immunodiffusion identified each of 16 polysaccharides as a known Gn- or G-containing structural type and one polysaccharide as a new but closely related Gn-containing type. Unlike the reactions of lectins, the cross-reactions of most rabbit antisera with these polysaccharides were correlated with structural features other than the host-like motifs. Gn-containing polysaccharides occurred primarily on the strains of S. sanguis and S. oralis while G-containing polysaccharides were more common among the strains of S. gordonii and S. mitis examined. The findings strongly support the hypothesis that lectin-mediated recognition of these streptococci by other oral bacteria depends on a family of antigenically diverse Gn- and G-containing cell wall polysaccharides, the occurrence of which may differ between streptococcal species.

Actinomyces↗

PubMed2006

Protective and destructive immunity in the periodontium: Part 1--innate and humoral immunity and the periodontium.

Based on the results of recent research in the field, the present paper will discuss the protective and destructive aspects of the innate vs. adaptive (humoral and cell-mediated) immunity associated with the bacterial virulent factors or antigenic determinants during periodontal pathogenesis. Attention will be focused on: (i) the Toll-like receptors (TLR), the innate immune repertoire for recognizing the unique molecular patterns of microbial components that trigger innate and adaptive immunity for effective host defenses, in some general non-oral vs. periodontal microbial infections; (ii) T-cell-mediated immunity, Th-cytokines, and osteoclastogenesis in periodontal disease progression; and (iii) some molecular techniques developed and used to identify critical microbial virulence factors or antigens associated with host immunity (using Actinobacillus actinomycetemcomitans and Porphyromonas gingivalis as the model species). Therefore, further understanding of the molecular interactions and mechanisms associated with the host's innate and adaptive immune responses will facilitate the development of new and innovative therapeutics for future periodontal treatments.

Adaptor Proteins, Signal Transducing↗

PubMed2006

Cytokine responses of bovine macrophages to diverse clinical Mycobacterium avium subspecies paratuberculosis strains.

BACKGROUND: Mycobacterium avium subsp. paratuberculosis (MAP), the causative agent of Johne's disease (JD) persistently infects and survives within the host macrophages. While it is established that substantial genotypic variation exists among MAP, evidence for the correlates that associate specific MAP genotypes with clinical or sub-clinical disease phenotypes is presently unknown. Thus we studied strain differences in intracellular MAP survival and host responses in a bovine monocyte derived macrophage (MDM) system. RESULTS: Intracellular survival studies showed that a bovine MAP isolate (B1018) and a human MAP isolate (Hu6) persisted in relatively higher numbers when compared with a sheep MAP isolate (S7565) at 24-hr, 48-hr and 96-hr post infection (PI). MDMs stimulated with B1018 up-regulated IL-10 at the transcript level and down-regulated TNFalpha at the protein and transcript levels compared with stimulations by the S7565 and Hu6. MDMs infected with Hu6 showed a down regulatory pattern of IL-10 and TNFalpha compared to stimulations by S7565. Cells stimulated with B1018 and Hu6 had low levels of matrix metalloprotease-3 (MMP3) and high levels of tissue inhibitor of metalloprotease-1 (TIMP1) at 96-hr PI relative to MDMs stimulated by S7565. CONCLUSION: Taken together, results suggest that the bovine (B1018) and the human (Hu6) MAP isolates lead to anti-inflammatory and anti-invasive pathways in the macrophage environment whereas the sheep (S7565) MAP isolate induces a pro-inflammatory pathway. Thus the infecting strain genotype may play a role in polarizing the host immune responses and dictate the clinicopathological outcomes in this economically important disease.

Animals↗

PubMed2000

Rhizosphere Interactions and the Exploitation of Microbial Agents for the Biological Control of Plant-Parasitic Nematodes.

A range of specialist and generalist microorganisms in the rhizosphere attacks plant-parasitic nematodes. Plants have a profound effect on the impact of this microflora on the regulation of nematode populations by influencing both the dynamics of the nematode host and the structure and dynamics of the community of antagonists and parasites in the rhizosphere. In general, those organisms that have a saprophytic phase in their life cycle are most affected by environmental conditions in the rhizosphere, but effects on obligate parasites have also been recorded. Although nematodes influence the colonization of roots by pathogenic and beneficial microorganisms, little is known of such interactions with the natural enemies of nematodes in the rhizosphere. As nematodes influence the quantity and quality of root exudates, they are likely to affect the physiology of those microorganisms in the rhizosphere; such changes may be used as signals for nematode antagonists and parasites. Successful biological control strategies will depend on a thorough understanding of these interactions at the population, organismal, and molecular scale.

cyst nematodes↗

PubMed1999

Can we learn from the pathogenetic strategies of group A hemolytic streptococci how tissues are injured and organs fail in post-infectious and inflammatory sequelae?

The purpose of this review-hypothesis is to discuss the literature which had proposed the concept that the mechanisms by which infectious and inflammatory processes induce cell and tissue injury, in vivo, might paradoxically involve a deleterious synergistic 'cross-talk', among microbial- and host-derived pro-inflammatory agonists. This argument is based on studies of the mechanisms of tissue damage caused by catalase-negative group A hemolytic streptococci and also on a large body of evidence describing synergistic interactions among a multiplicity of agonists leading to cell and tissue damage in inflammatory and infectious processes. A very rapid cell damage (necrosis), accompanied by the release of large amounts of arachidonic acid and metabolites, could be induced when subtoxic amounts of oxidants (superoxide, oxidants generated by xanthine-xanthine oxidase, HOCl, NO), synergized with subtoxic amounts of a large series of membrane-perforating agents (streptococcal and other bacterial-derived hemolysins, phospholipases A2 and C, lysophosphatides, cationic proteins, fatty acids, xenobiotics, the attack complex of complement and certain cytokines). Subtoxic amounts of proteinases (elastase, cathepsin G, plasmin, trypsin) very dramatically further enhanced cell damage induced by combinations between oxidants and the membrane perforators. Thus, irrespective of the source of agonists, whether derived from microorganisms or from the hosts, a triad comprised of an oxidant, a membrane perforator, and a proteinase constitutes a potent cytolytic cocktail the activity of which may be further enhanced by certain cytokines. The role played by non-biodegradable microbial cell wall components (lipopolysaccharide, lipoteichoic acid, peptidoglycan) released following polycation- and antibiotic-induced bacteriolysis in the activation of macrophages to release oxidants, cytolytic cytokines and NO is also discussed in relation to the pathophysiology of granulomatous inflammation and sepsis. The recent failures to prevent septic shock by the administration of only single antagonists is disconcerting. It suggests, however, that since tissue damage in post-infectious syndromes is caused by synergistic interactions among a multiplicity of agents, only cocktails of appropriate antagonists, if administered at the early phase of infection and to patients at high risk, might prevent the development of post-infectious syndromes.

Animals↗

PubMed1994

Microbial ecology of dental plaque and its significance in health and disease.

Dental plaque forms naturally on teeth and is of benefit to the host by helping to prevent colonization by exogenous species. The bacterial composition of plaque remains relatively stable despite regular exposure to minor environmental perturbations. This stability (microbial homeostasis) is due in part to a dynamic balance of both synergistic and antagonistic microbial interactions. However, homeostasis can break down, leading to shifts in the balance of the microflora, thereby predisposing sites to disease. For example, the frequent exposure of plaque to low pH leads to inhibition of acid-sensitive species and the selection of organisms with an aciduric physiology, such as mutans streptococci and lactobacilli. Similarly, plaque accumulation around the gingival margin leads to an inflammatory host response and an increased flow of gingival crevicular fluid. The subgingival microflora shifts from being mainly Gram-positive to being comprised of increased levels of obligately anaerobic, asaccharolytic Gram-negative organisms. It is proposed that disease can be prevented or treated not only by targeting the putative pathogens but also by interfering with the processes that drive the breakdown in homeostasis. Thus, the rate of acid production following sugar intake could be reduced by fluoride, alternative sweeteners, and low concentrations of antimicrobial agents, while oxygenating or redox agents could raise the Eh of periodontal pockets and prevent the growth and metabolism of obligately anaerobic species. These views have been incorporated into a modified hypothesis (the "ecological plaque hypothesis") to explain the relationship between the plaque microflora and the host in health and disease, and to identify new strategies for disease prevention.

Bacteria, Anaerobic↗