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Results for “Host Microbial Interactions”

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PubMed2005

The Campylobacter jejuni glycome.

Microbial cell surface glycans in the form of glycolipids and glycoproteins frequently play important roles in cell-cell interaction and host immune responses. Given the likely importance of these surface structures in the survival and pathogenesis of Campylobacter jejuni, a concerted effort has been made to characterise these determinants genetically and structurally since the genome was sequenced in 2000. We review the considerable progress made in characterising the Campylobacter glycome including the lipooligosaccharide (LOS), the capsule and O- and N-linked protein glycosylation systems, and speculate on the roles played by glycan surface structures in the life-cycle of C. jejuni.

Animals↗

PubMed1998

Active resistance of entomophagous rhabditid Heterorhabditis bacteriophora to insect immunity.

A specific extracellular proteinase, degrading selectively the cecropin-based defence system of insects, is secreted into the larval body during parasitism of the greater wax moth by the Heterorhabditis bacteriophora/Photorhabdus luminescens complex and by phase 1 of P. luminescens. The proteolytic digestion of insect inducible cecropin-like immune molecules was demonstrated by the disappearance of the Galleria mellonella cecropins and purified Hyalophora cecropin B peptide PAGE bands upon exposure to infected extracts, and a similar abrogation of antibacterial activity using an agar diffusion assay. Proteolytic activity of infected extracts produced by nematode/bacterial complex and phase 1 variant of P. luminescens was shown to be correlated with cecropin-inhibitory activity, suggesting that this anti-cecropin agent may be responsible for the ability of bacteria to establish infection and the insecticidal nature of H. bacteriophora. Antibacterial activity of Galleria lysozyme and that of chicken egg-white lysozyme to which P. luminescens is insensitive, was unaffected by H. bacteriophora proteinase.

Animals↗

PubMed1977

Activation of the alternative complement pathway due to resistance of zymosan-bound amplification convertase to endogenous regulatory mechanisms.

The surface of zymosan (Zy), by affording a protected microenvironment for C3b and the amplification convertase stabilized by properdin, P,C3b,Bb, shifts the alternative complement pathway from slow fluid phase turnover to the amplification phase of its expression. This mode of activation is in contradistinction to that of the classical pathway, which follows conversion of a proenzyme, Cl, to its active form, C1. Under conditions in which the control proteins, C3b inactivator (C3bINA) and beta1H, completely, inactivated C3b on the sheep erythrocyte intermediate, EAC4b,3b, the activity of C3b bound to Zy,ZyC3b, was diminished by only one-third. Further, when ZyC3b was converted to ZyC3b,Bb,P there was an additional point of deregulation in that the convertase was resistant to beta1H-mediated decay-dissociation while P,C3b,Bb on the sheep erythrocyte exhibited the usual susceptibility to beta1H. That Zy alone could indeed promote rapid C3 cleavage by the alternative pathway through assembly and protection of the amplification convertase on its surface was demonstrated with a mixture of alternative pathway proteins, C3,B,D,P, C3bINA, and beta1H, that had each been purified to homogeneity. Interaction of these proteins at one-tenth their relative serum concentrations with Zy permitted low-grade inactivation of C3 and B to advance to the level of amplification after a 15 min lag period. Because the reaction of the purified proteins proceeded spontaneously when either regulatory protein was deleted, the effect of Zy was attributed to deregulation rather than to conversion of one of the proteins to a specific initiating state. The alternative pathway, through the normal presence of D, interacts with a microbial surface, such as Zy, to amplify deposition of C3b by circumvention of endogenous regulatory mechanisms, thereby augmenting host defense.

Animals↗

PubMed1991

Immunosuppressive effects of Prevotella intermedia on in vitro human lymphocyte activation.

In this study, we have assessed four strains of Prevotella intermedia, isolated from periodontally involved lesions, for their ability to inhibit lymphocyte functions. All four strains were found to cause a dose-dependent inhibition of B- and T-cell proliferation in response to mitogens and antigens. This was reflected in altered DNA, RNA, and protein syntheses. Furthermore, P. intermedia appeared to affect the early stages of cell activation. This was ascertained by kinetic analysis in which it was determined that the extract had to be present during the first 24 h of incubation to cause suppression. Moreover, direct assessment of the early stages of cell activation indicated that release of cytokines and expression of the interleukin 2 receptor and CD69 on T cells were inhibited by P. intermedia sonic extracts. Finally, preliminary characterization of the immunosuppressive agent indicates that it has a molecular mass of approximately 50 kDa and is heat labile. It has been proposed that impaired host defense may play a pivotal role in the pathogenesis of many infections. The data presented in this paper suggest that microbially mediated immunosuppression may contribute to the pathogenesis of periodontal disease by altering the nature and consequences of host-parasite interactions.

Bacteroides↗

PubMed2002

Bench-to-bedside review: Toll-like receptors and their role in septic shock.

The Toll-like receptors (TLRs) are essential transmembrane signaling receptors of the innate immune system that alert the host to the presence of a microbial invader. The recent discovery of the TLRs has rapidly expanded our knowledge of molecular events that initiate host-pathogen interactions. These functional attributes of the cellular receptors provide insights into the nature of pattern recognition receptors that activate the human antimicrobial defense systems. The fundamental significance of the TLRs in the generation of systemic inflammation and the pathogenesis of septic shock is reviewed. The potential clinical implications of therapeutic modulation of these recently characterized receptors of innate immunity are also discussed.

Animals↗

PubMed2000

Anti-adhesive strategies in the prevention of infectious disease at mucosal surfaces.

Binding of microbial cell surface adhesins to host receptor molecules is a critical early step in microbial infection and pathogenesis. Anti-adhesive strategies aimed at blocking this interaction offer an attractive means of preventing infection at an early stage. The strategy should reduce the likelihood of resistant strains of microorganisms emerging, since those that do not bind will not be subjected to sustained selective pressure, as may occur with antibiotic therapy. Three classes of adhesion-blocking agent have been investigated, namely anti-adhesin antibodies, adhesin analogues and receptor analogues. The effectiveness of a number of these adhesion-blocking compounds has been demonstrated in human and animal models of infection. Direct application to the tooth surface of anti-adhesin monoclonal antibody, or a synthetic peptide adhesion epitope, prevented infection with the oral pathogen, Streptococcus mutans in humans. Intranasal administration of a soluble receptor analogue significantly reduced virus production and symptoms following experimental infection with rhinovirus. Similarly, all three types of anti-adhesion agent protected against a variety of infections at other mucosal surfaces in animal models. A common finding from these studies is the long duration of protection, which cannot be due to persistence of the anti-adhesion agent, but may be the result of competitive exclusion by members of the normal flora at specific mucosal surfaces. Development of these novel antimicrobial agents is particularly timely in view of the increasing concern over the spread of antibiotic resistance.

Adhesins, Bacterial↗

PubMed1991

Etiology of periodontal diseases.

Periodontal diseases are a series of complex, distinct, pathologic entities caused by the interaction of bacterial plaque and the host. This interaction results in destruction of the supporting alveolar bone and connective tissue. Although bacterial plaque has been implicated as the primary etiologic agent in most forms of periodontal disease, there are local and systemic factors which may modify both microbial and host components. Local factors may favor plaque accumulation and maturation, while systemic factors may modulate and decrease the host's protective response.

Dental Occlusion, Traumatic↗

PubMed1990

The neutrophil and leukotrienes--role in health and disease.

The granulocyte plays a major role in inflammatory processes by its capability to produce and release proinflammatory mediators such as the leukotrienes. This class of mediators exerts multiple functions in various physiological and pathophysiological processes. The interdependent interaction among the various mediator cascades, the inflammatory cells as well as the neuroendocrine system are areas of current interest. Appropriate stimuli (immunological, non immunological) by their defined pattern of signal transduction are responsible for priming, cellular activation and deactivation of granulocytes as it is shown for microbial infection. Thus the mediators may provide the prerequisites for a balanced homeostasis during host defense. It is clear that among the complexity of mediators not a single factor but the interaction of multiple mediator cascades reflect the final outcome of the disease process. In this regard the actual concentrations at local sites are obviously more relevant as those in whole body fluids.

Humans↗

PubMed2004

Enteropathogenic Escherichia coli infection leads to appearance of aberrant tight junctions strands in the lateral membrane of intestinal epithelial cells.

Infection of intestinal epithelial cells with enteropathogenic Escherichia coli (EPEC) disrupts tight junction (TJ) architecture and barrier function. The aim of this study was to determine the impact of EPEC on TJ protein interactions and localization. Human intestinal epithelial cells (T84) were infected for 1, 3 or 6 h with EPEC. To probe the TJ protein-protein interactions, co-immunoprecipitations were performed. The associations between ZO-1, occludin and claudin-1 progressively decreased after infection. Corresponding morphological changes were analysed by immunofluorescence confocal microscopy. Tight junction proteins progressively lost their apically restricted localization. Freeze-fracture electron microscopy revealed the appearance of aberrant strands throughout the lateral membrane that contained claudin-1 and occludin as determined by immunogold labelling. These structural alterations were accompanied by a loss of barrier function. Mutation of the gene encoding EspF, important in the disruption of TJs by EPEC, prevented the disruption of TJs. Tight junction structure normalized following eradication of EPEC with gentamicin and overnight recovery. This is the first demonstration that a microbial pathogen can cause aberrant TJ strands in the lateral membrane of host cells. We speculate that the disruption of integral and cytoplasmic TJ protein interactions following EPEC infection allows TJ strands to form or diffuse into the lateral plasma membrane.

Cell Line↗

PubMed1995

Nonopsonic phagocytosis of microorganisms.

Nonopsonic phagocytosis mediated by phagocyte receptors that recognize corresponding adhesins on microbial surfaces has attracted increasing interest as a potential host defense mechanism against extracellular pathogens and as a means of survival in the host for intracellular pathogens. Three types of nonopsonic phagocytosis involving carbohydrate-protein interactions (also termed lectinophagocytosis), protein-protein interactions, and hydrophobic interactions are discussed. A prominent receptor on phagocytic cells involved in recognizing pathogens belongs to the CD11/CD18 integrins. It mediates both opsonophagocytosis and nonopsonic phagocytosis and exhibits multiple specificity for different microbial adhesins. In other cases, similar specificity toward a microbial ligand (e.g. the Klebsiella pneumoniae capsule) is shared by dual molecules, one of which (e.g. the mannose-binding protein in serum) mediates opsonophagocytosis and the other (e.g. the macrophage mannose receptor) mediates nonopsonic phagocytosis of the microorganisms. In addition, we discuss how nonopsonic phagocytosis can trigger the phagocytes to release inflammatory agents and cause tissue injury. Further studies of the molecular mechanisms of nonopsonic phagocytosis, in particular those underlying the up-regulation of the phagocytic receptors by various agents, should lead to the development of new approaches for the prevention of infectious diseases.

Amino Acid Sequence↗

PubMed2001

Microbes and microbial toxins: paradigms for microbial-mucosal interactions. VII. Enteropathogenic Escherichia coli: physiological alterations from an extracellular position.

Enteropathogenic Escherichia coli (EPEC) is primarily associated with infantile diarrhea in developing countries. This intriguing pathogen exerts numerous physiological effects on its host target tissue, the intestinal epithelium, all from an extracellular location. Expression of a type III secretory apparatus allows this organism to transfer bacterial effector molecules directly into host cells. As a result of EPEC attachment to and/or translocation of proteins into intestinal epithelial cells, many signaling cascades are activated. Ultimately, host functions are perturbed, including alteration of ion transport, disruption of the tight junction barrier, and activation of the inflammatory response.

Diarrhea↗

PubMed2000

Micronutrients and infection: interactions and implications with enteric and other infections and future priorities.

Symposium presentations have focused on the elegant molecular science and the biologic mechanisms by which micronutrients play critical roles in cellular and humoral immune responses, cellular signaling and function, and even in the evolution of microbial virulence. The concluding session examined the practical issues of how best to evaluate the nutritionally at-risk host, especially in the areas of greatest need-an analytical model of nutrient-immune interactions, implications of nutritional modulation of the immune response for disease, and the implications for international research and child health. This overview illustrated how malnutrition may be a major consequence of early childhood diarrhea and enteric infections, as enteric infections may critically impair intestinal absorptive function with potential long-term consequences for growth and development. The potentially huge, largely undefined DALY (disability-adjusted life years) impact of early childhood diarrheal illnesses demonstrates the importance of quantifying the long-term functional impact of largely preventable nutritional and infectious diseases, especially in children in developing areas.

Child↗

PubMed2006

Symbiosis insights through metagenomic analysis of a microbial consortium.

Symbioses between bacteria and eukaryotes are ubiquitous, yet our understanding of the interactions driving these associations is hampered by our inability to cultivate most host-associated microbes. Here we use a metagenomic approach to describe four co-occurring symbionts from the marine oligochaete Olavius algarvensis, a worm lacking a mouth, gut and nephridia. Shotgun sequencing and metabolic pathway reconstruction revealed that the symbionts are sulphur-oxidizing and sulphate-reducing bacteria, all of which are capable of carbon fixation, thus providing the host with multiple sources of nutrition. Molecular evidence for the uptake and recycling of worm waste products by the symbionts suggests how the worm could eliminate its excretory system, an adaptation unique among annelid worms. We propose a model that describes how the versatile metabolism within this symbiotic consortium provides the host with an optimal energy supply as it shuttles between the upper oxic and lower anoxic coastal sediments that it inhabits.

Animals↗

PubMed1999

The interaction of intestinal epithelial cells and intraepithelial lymphocytes in host defense.

Intestinal intraepithelial lymphocytes (i-IEL) are located at the basolateral surfaces of intestinal epithelial cells (i-EC) and play important roles in the homeostasis of intestinal microenvironment. i-IEL comprise unique T cell populations including CD4-CD8alphaalpha+ T cells expressing T cell receptor (TCR)alphabeta or TCRgammadelta and CD4+ CD8alphaalpha+ T cells expressing TCR alphabeta. We show here that CD4+ CD8alphaalpha+ i-IEL belongs to Th1 type T cells capable of responding to self-MHC class I on i-EC and that a significant fraction of i-IEL expressed Fas ligand (Fas-L) and induced apoptosis in the i-EC via Fas-dependent pathway. i-IEL may recognize and eliminate the effete i-EC for homeostatic regulation of intestinal epithelia. The interaction of i-EC and i-IEL through E-cadherin/alphaEbeta7 integrin is important for homing and maintenance of i-IEL in intestine. Listeria monocytogenes are also known to interact with E-cadherin on i-EC and invade into the epithelial cells. Invasion of L. monocytogenes into i-EC activated NFkappa-B and subsequently up-regulated the expression of IL-15 gene, which has a NFkappa-B binding site at the promoter region. i-IEL, especially gammadelta T cells, were significantly activated to produce Th1 type cytokines at the early stage after oral infection with L. monocytogenes in mice and rats. The activation of i-IEL coincided with a peak response of IL-15 production by i-EC after infection. Taken together, mutual interaction of i-IEL and i-EC may be important not only for homeostatic regulation but also host defense against microbial infection in intestine.

Animals↗

PubMed1996

Metabolic constraints on voluntary intake in ruminants.

The weak point in all current methods or models of diet formulation is the prediction of intake. The major uncertainty is not in the cases in which physical constraints apply, but in those in which voluntary intake is limited by feedback from metabolic factors. Voluntary intake is, ultimately, a psychological phenomenon, involving the integration of many signals, and reflects the flexibility of biological systems evolved to cope with variability in food supply, composition and animal state. Conditions giving rise to regulatory signals may provide a framework for modeling metabolic constraints on intake. The empirical evidence for metabolic feedback shows that the animal's productive potential, which affects its ability to utilize nutrients, interacts with the balance of absorbed nutrients to regulate intake. The relative importance of the sites where nutrient imbalance occurs (microbial or host animal metabolism) is unclear, as is the relevant time scale (minutes or days) of response. A model of the effects of asynchrony of nutrient supply to ruminal microbes suggests that ammonia and microbial recycling and the contribution of hind-gut fermentation reduce the asynchrony in the balance of nutrients absorbed into the bloodstream. Hitherto, rather little progress has been made in mathematical modeling of the metabolic processes controlling intake. Models that describe the phenomenon in terms of global variables, such as total energy intake, protein supply, and protein synthetic capacity, can simulate the way constraints may operate without requiring or providing a deeper understanding of the metabolic processes involved. Models describing the flux of energy and materials down established metabolic pathways have the potential to explore constraints on intake, but until the problem of parameterizing such models can be overcome, that potential will remain untapped.

Animals↗

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↗

PubMed1991

Rumen digestive physiology and microbial ecology.

The rumen is a dynamic, continuous fermentation compartment that provides a suitable environment for a variety of species of anaerobic bacteria, protozoa, and fungi. These microorganisms have a complex series of interactions with the feeds supplied to the host, with some using particulate matter as both sources of nutrients and sites of sequestration to avoid being washed from the rumen by the rapid flow of fluids. Because of the ability to use soluble nutrients and to reproduce rapidly, other microbes associate primarily with the liquid phase of the rumen contents. Due to the metabolic activity of all microbial populations, feeds are converted to microbial matter and fermentation end products, which serve as nutrients for the ruminant. Optimum feed utilization by ruminants is dependent on achieving maximum rumen fermentation and flow of microbial protein to the duodenum. At this time, it is clear that the major nutrients required by the microbial populations include both fibrous and nonfibrous sources of carbohydrates and nitrogen in the form of ammonia, amino acids, and peptides. In spite of five decades of research, the exact quantities and sources of these nutrients that will result in optimum rumen fermentation rates and microbial yields are only partially known.

Animals↗

PubMed2003

The 10(5) bacterial growth guideline: reassessing its clinical relevance in wound healing.

The microbiology of wounds is a key determinant in healing and clinicians generally accept that a level of microbial (ie, bacterial) growth greater than 100,000 viable organisms per gram of tissue can be used to diagnose infection. Although other factors that predispose a wound to infection are widely recognized, today's wound care practitioners are influenced primarily by the 10 5 guideline, with treatment being based on the microbial count in deep or superficial tissue. However, to appropriately manage microbially challenged wounds (eg, heavily colonized and clinically infected), a more balanced awareness of the broader issues relating to micro-organisms and wounds is needed. The types of micro-organisms, their interactions with each other and with the wound environment, the local conditions, and host resistance are all key factors that collectively influence healing. From a microbiological perspective, successful wound healing is dependent on maintaining a host-manageable bioburden. If local conditions favor microbial growth, a wound may fail to heal and become infected, requiring topical antiseptics or antibiotics to supplement the host inflammatory response and restore balance in favor of the host. This paper provides a critical examination of the 10 5 guideline to enhance clinician understanding and utilization of a commonly applied diagnostic consideration.

Colony Count, Microbial↗