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Results for “Host Microbial Interactions”

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PubMed1997

Of microbes, macrophages and nitric oxide.

One of the most prominent functions of nitric oxide (NO) is its participation in antimicrobial and antiviral defense. This paper summarizes the evidence for this function and compiles the infectious agents which are currently thought to be controlled via high out-put generation of NO as it occurs in activated macrophages and other cells expressing the inducible isoform of NO-synthase (iNOS, NOS-2). Several less appreciated forms of interaction between NO and microbes will also be reviewed, including the role of NO as an immunosuppressive or tissue-destructive molecule during the course of infections, the regulation of microbial antioxidant systems by host cell-derived NO, the contribution of NO to parasite stage conversion, the induction or suppression of macrophage iNOS by microbial products, and the existence of endogenous NO synthase pathways in certain bacteria and parasites.

Animals↗

PubMed2004

Candida albicans and Saccharomyces cerevisiae induce interleukin-8 production from intestinal epithelial-like Caco-2 cells in the presence of butyric acid.

Intestinal epithelial cells (IEC) are important in initiation and regulation of immune responses against numerous foreign substances including food, microorganisms and their metabolites in the intestine. Since the responses of IEC against yeasts have not yet been well understood, we investigated the effects of Candida albicans, Saccharomyces cerevisiae, and their cell wall components on interleukin-8 (IL-8) secretion by the IEC-like Caco-2 cells. Live cells of both yeast species stimulated Caco-2 cells to produce IL-8 only in the presence of butyric acid, which is a metabolite produced by intestinal bacteria. S. cerevisiae zymosan and glucan also enhanced IL-8 secretion. Treatment of Caco-2 cells with butyric acid increased the expression of mRNAs coding for Toll-like receptor 1 (TLR1), TLR6 and dectin-1, which recognize zymosan. C. albicans induced more IL-8 secretion and also decreased transepithelial electrical resistance more rapidly than S. cerevisiae. These results suggest that both yeasts in the intestine stimulate the host's mucosal immune systems by interacting with IEC.

Butyric Acid↗

PubMed2006

Cellular and molecular hemocyte responses of the Pacific oyster, Crassostrea gigas, following bacterial infection with Vibrio aestuarianus strain 01/32.

The strategies used by bacterial pathogens to circumvent host defense mechanisms remain largely undefined in bivalve molluscs. In this study, we investigated experimentally the interactions between the Pacific oyster (Crassostrea gigas) immune system and Vibrio aestuarianus strain 01/32, a pathogenic bacterium originally isolated from moribund oysters. First, an antibiotic-resistant V. aestuarianus strain was used to demonstrate that only a limited number of bacterial cells was detected in the host circulatory system, suggesting that the bacteria may localize in some organs. Second, we examined the host defense responses to V. aestuarianus at the cellular and molecular levels, using flow-cytometry and real-time PCR techniques. We showed that hemocyte phagocytosis and adhesive capabilities were affected during the course of infection. Our results also uncovered a previously-undescribed mechanism used by a Vibrio in the initial stages of host interaction: deregulation of the hemocyte oxidative metabolism by enhancing the production of reactive oxygen species and down-regulating superoxide dismutase (Cg-EcSOD) gene expression. This deregulation may provide an opportunity to the pathogen by impairing hemocyte functions and survival. These findings provide new insights into the cellular and molecular bases of the host-pathogen interactions in C. gigas oyster.

Animals↗

PubMed2000

Mycobacterium tuberculosis H37Rv comparative gene-expression analysis in synthetic medium and human macrophage.

Mycobacteria are intracellular pathogens that survive and grow in host macrophages. Following phagocytosis, sustained intracellular bacterial growth depends on its ability to avoid destruction by macrophage-mediated host defences such as lysosomal enzymes, reactive oxygen and the reactive nitrogen intermediates. This suggests that the interaction between host cell and microbe is delicately balanced, and can be tipped in favour of either organism. The identification of Mycobacterium tuberculosis H37Rv (MTB) genes expressed within host cells would contribute greatly to the development of new strategies to fight tuberculosis. In the present study, we compared MTB gene expression in the course of intra- (human macrophages) and extracellular growth (Sauton's medium) to ascertain whether differences might occur between gene-expression patterns in the two habitats of replication. Using reverse-transcriptase polymerase chain reaction (RT-PCR) on a group of 14 MTB-Complex-specific genes, we found that MT10Sa (a small stable RNA), 35 kDa (unknown), ahpC (alkyl hydroperoxide reductase, AhpC), sigF (alternative RNA Polymerase sigma factor), and katG (catalase-peroxidase, HPI) genes are expressed in both the environments, while Ag85B, Ag85C (members of the Antigen 85 Complex), rpoV (RNA Polymerase sigma factor) and ESAT6 (early secretory antigen, 6 kDa) are expressed only in the in vitro culture; on the other hand, Ag85A (Antigen 85 Complex), rpoB (RNA Polymerase beta sub-unit), pab (Protein antigen b), invA and invB genes (encoding proteins that show homologies with p60 of Listeria monocytogenes) are expressed only inside the macrophage. Positive RT-PCR products on cDNAs for these genomic regions were not obtained from approximately 1000-fold more bacteria grown in Laboratory Broth. Identification of M. tuberculosis genes expressed in response to phagocytosis by human macrophages increases our basic understanding of the host-pathogen interaction, and helps to identify bacterial factors necessary for in vivo survival and growth.

Colony Count, Microbial↗

PubMed2002

The meaning of microbial exposure, infection, colonisation, and disease in clinical practice.

The basic lexicon of infectious diseases includes the terms exposure, infection, colonisation, and disease, which are used to describe the clinical states in which the presence of a microbe in a host is suspected or discovered. Therefore, the lexicon is used to articulate an implied association between a host and a microbe. However, since it is often difficult to use the available clinical and diagnostic tools to discriminate the different ways in which microbes can exist in a host, the lexicon is often used in an ambiguous and imprecise manner. Another factor contributing to imprecise use of the lexicon is that microbial factors are often held responsible for disease pathogenesis. This relegates the part that the host plays in microbial pathogenesis to an exception, which leads to the need for qualification and modification of the terminology of infectious diseases. Recently, we proposed the "damage-response framework" to incorporate the contributions of both the host and the microbe in microbial pathogenesis in a synthesis whereby host damage was used as the common denominator to describe the outcome of the host-microbe relation. In this article, we illustrate how the application of the damage-response framework to clinical infectious diseases can clarify and make more precise the terminology used to convey the outcome of microbial infection in clinical practice.

Bacteria↗

PubMed1970

Comparative studies with tox plus and tox minus corynebacteriophages.

The characteristics of nine inducible temperate corynebacteriophages designated alpha(tox+), beta(tox+), P(tox+), gamma(tox-), pi(tox+), K(tox-), rho(tox-), L(tox+), and delta(tox+) have been compared. Virion morphology and ability to recombine genetically with the well-studied phage beta(tox+) have been correlated with other properties of the phages, and the distribution of the genetic marker tox+ among related and relatively unrelated corynebacteriophages has been analyzed. The immunity specificity, host range, and plaque morphology of each phage were determined. The phages can be separated into five groups with different immunity specificities. Each type of host range previously recognized in mutants of phage beta(tox+) was present in one or more of the phages included in the present study, and the phages were found to produce plaques of several different morphological types. Representative phages with each of the five types of immunity specificity were further characterized with respect to virion morphology, ability to recombine with phage beta(tox+), latent period, average burst size, and neutralization by homologous and heterologous antiphage sera. All of these phages have polyhedral heads and long slender tails, but two distinct morphological types were distinguished by the sizes and proportions of the components of the virions. Only phages of the same morphological type as beta(tox+) were capable of genetic recombination with beta(tox+), but morphological similarity between phages was not sufficient to insure interfertility. The phages which recombined with beta(tox+) resembled one another in plaque morphology, latent period, and average burst size, whereas phages which failed to recombine with beta(tox+) differed in these characteristics. The phages capable of genetic recombination with beta(tox+) were found to differ from each other in immunity specificity, host range, neutralization by antiphage sera, and toxinogenicity. Thus, these latter characteristics are of limited value in establishing the extent of relatedness between corynebacteriophages. The genetic marker tox+ was not consistently correlated with any other property of the corynebacteriophages analyzed in this study. The most striking finding regarding the distribution of the tox+ marker is its presence both in beta(tox+) and delta(tox+), phages which fail to recombine genetically and which differ in virion morphology. The presence of the tox+ marker in genetically unrelated corynebacteriophages poses many questions concerning the origin(s) of tox+ and the evolution of the phage-host interactions which determine the ability of corynebacteria to synthesize diphtherial toxin.

Animals↗

PubMed2003

Quantification of disease progression of several microbial pathogens on Arabidopsis thaliana using real-time fluorescence PCR.

An accurate monitoring of disease progression is important to evaluate disease susceptibility phenotypes. Over the years, Arabidopsis thaliana has become the model species to serve as a host in plant-pathogen interactions. Despite the efforts to study genetic mechanisms of host defense, little efforts are made for a thorough pathogen assessment, often still depending on symptomology. This manuscript describes the use of real-time polymerase chain reaction (PCR) to assess pathogen growth in the host Arabidopsis for a number of frequently studied pathogens. A wide range of correlations between pathogen biomass and fluorescence is demonstrated, demonstrating the theoretical sensitivity of the technique. It is also demonstrated that host DNA does not interfere with the quantification of pathogen DNA over a wide range. Finally, quantification of pathogen biomass in different plant genotypes with a varying degree of resistance shows the capability of this technique to be used for assessment of pathogen development in disease progression.

Alternaria↗

PubMed2002

Porphyromonas gingivalis lipopolysaccharide displays functionally diverse interactions with the innate host defense system.

Periodontitis is a bacterially induced chronic inflammatory disease and a major cause of tooth loss in the world. The tissue damage and alveolar bone resorption characteristic of the disease are believed to be due to a destructive innate host response to a pathogenic subgingival biofilm. Porphyromonas gingivalis, a Gram-negative bacterium, is a member of this mixed microbial community that has been designated an etiologic agent of periodontitis. The innate host response to lipopolysaccharide (LPS) obtained from P. gingivalis is unusual in that different studies have reported that it can be an agonist for Toll-like receptor (TLR) 2 as well as an antagonist or agonist for TLR4. In addition, human monocytes respond to this LPS by secreting a variety of different inflammatory mediators, while endothelial cells do not. We have examined highly purified preparations of P. gingivalis LPS and found that they activate both TLR2 combined with TLR1 and TLR4 in transiently transfected human embryonic kidney (HEK) 293 cells. We have further demonstrated that highly purified P. gingivalis LPS preparations contain at least 3 major different lipid A species. We speculate that P. gingivalis lipid A structural heterogeneity contributes to the unusual innate host response to this LPS and its ability to interact with different TLR molecules.

Cell Line↗

PubMed1987

Bacterial adherence to respiratory tract mucosa--a dynamic interaction leading to colonization.

Normally, the mucosa of the nasooropharynx, trachea, and, perhaps, the major bronchi is colonized with aerobic and anaerobic microbes. This epithelial surface coexists with the microbial flora and is not overgrown with it. Moreover, the physiologic functions of the mucosa--including a protective barrier, mucociliary clearance and humidification, and warming of respired air--are not impeded. How this flora is controlled and what is amiss when virulent or pathogenic bacteria can cause infection are fascinating questions. A balance is maintained during health in which epithelial cell integrity--a function of proper nutrition, available secretory immunoglobulins and glycoproteins, and ciliary motion--resists the microbe's attempt to attach via specialized receptors (pili) or by proteolytic destruction of local proteins. These interactions are reviewed in detail. When colonization is excessive and aspiration of more microbes into the lower airway occurs, infection is more probable. Certain bacteria such as Streptococcus pneumoniae and Hemophilus influenzae, which are associated with chronic bronchitis, illustrate a mechanism in which the host-microbial balance may be upset by selective impairment of a host protein, secretory IgA1. Alternatively, viral infection or cilotoxic microbes (mycoplasma) can favor colonization of bacteria when mucosal clearance mechanisms are impaired. Last, mucosal integrity can be breached by noxious gases or inflammation that may allow bacteria entry into the submucosal that provides a nidus for infection.

Animals↗

PubMed2006

Early days: genomics and human responses to infection.

DNA microarray-based gene transcript-profiling of the responses of primates to infection has begun to yield new insights into host-pathogen interactions; this approach, however, remains plagued by challenges and complexities that have yet to be adequately addressed. The rapidly changing nature over time of acute infectious diseases in a host, and the genetic diversity of microbial pathogens present unique problems for the design and interpretation of functional-genomic studies in this field. In addition, there are the more common problems related to heterogeneity within clinical samples, the complex, non-standardized confounding variables associated with human subjects and the complexities posed by the analysis and validation of highly parallel data. Whereas various approaches have been developed to address each of these issues, there are significant limitations that remain to be overcome. The resolution of these problems should lead to a better understanding of the dialogue between the host and pathogen.

Animals↗

PubMed2006

Selection for Staphylococcus aureus small-colony variants due to growth in the presence of Pseudomonas aeruginosa.

Opportunistic infections are often polymicrobial. Two of the most important bacterial opportunistic pathogens of humans, Pseudomonas aeruginosa and Staphylococcus aureus, frequently are coisolated from infections of catheters, endotracheal tubes, skin, eyes, and the respiratory tract, including the airways of people with cystic fibrosis (CF). Here, we show that suppression of S. aureus respiration by a P. aeruginosa exoproduct, 4-hydroxy-2-heptylquinoline-N-oxide (HQNO), protects S. aureus during coculture from killing by commonly used aminoglycoside antibiotics such as tobramycin. Furthermore, prolonged growth of S. aureus with either P. aeruginosa or with physiological concentrations of pure HQNO selects for typical S. aureus small-colony variants (SCVs), well known for stable aminoglycoside resistance and persistence in chronic infections, including those found in CF. We detected HQNO in the sputum of CF patients infected with P. aeruginosa, but not in uninfected patients, suggesting that this HQNO-mediated interspecies interaction occurs in CF airways. Thus, in all coinfections with P. aeruginosa, S. aureus may be underappreciated as a pathogen because of the formation of antibiotic-resistant and difficult to detect small-colony variants. Interspecies microbial interactions, analogous to those mediated by HQNO, commonly may alter not only the course of disease and the response to therapy, but also the population structure of bacterial communities that promote the health of host animals, plants, and ecosystems.

Cell Proliferation↗

PubMed1979

Augmentation of macrophage complement receptor function in vitro. I. Characterization of the cellular interactions required for the generation of a T-lymphocyte product that enhances macrophage complement receptor function.

The function of complement receptors of mouse peritoneal macrophages was converted in vitro from mediating only attachment of macrophage complement receptor function was achieved by treating freshly explanted macrophages with supernates from cultures containing T lymphocytes and appropriately triggered macrophages. Fc receptor-mediated phagocyctosis by macrophages was required for the production of active supernates, for neither ingestion via the cells' complement receptors nor ingestion via nonimmunologic means was a sufficient stimulus for the macrophages' participation in the generation of supernatant activity. Fc receptor-triggered macrophages interacted by a contact dependent, but histocompatibility independent, mechanism with T lymphocytes, thereby signalling the lymphocytes to elaborate the active product. The possible significance of enhanced macrophage complement receptor function in inflammation, host defense against microbial pathogens, immune complex disease, and neoplasia is discussed.

Animals↗

PubMed2003

Oral microbial biofilms and plaque-related diseases: microbial communities and their role in the shift from oral health to disease.

Many oral pathologies, such as dental caries, periodontal disease and peri-implantitis are plaque-related. Dental plaque is a microbial biofilm formed by organisms tightly bound to a solid substrate and each other by means of an exopolymer matrix. Bacteria exhibit different properties when contained within a biofilm. Knowing the mechanisms controlling the formation and development of biofilms can help to understand the emergence and progression of such pathologies and to plan effective treatment. Most periodontal pathogens are common saprophytes of the oral cavity, expressing their virulence only in a susceptible host or when some changes come about in the oral environment. Physical, metabolic and physiological interactions may cause positive or negative effects among the various microbiota present. Such mechanisms of antagonism/synergy select the bacterial population and alterations of its composition affect the balance with the host and may lead to pathology. The effectiveness of antimicrobial agents, as measured through in vitro tests, is dramatically reduced in vivo due to the properties of the microbial community: mature, intact biofilms are less sensitive to such agents, as the exopolymer matrix, bacterial enzymes and slow growth rate hinder the action of chemotherapeutic agents. The present literature review aims to examine the most representative studies, focusing on the characteristics of bacterial communities and the crucial shift from oral health to plaque-related diseases.

Anti-Infective Agents, Local↗

PubMed2006

Microarray analysis of human epithelial cell responses to bacterial interaction.

Host-pathogen interactions are inherently complex and dynamic. The recent use of human microarrays has been invaluable to monitor the effects of various bacterial and viral pathogens upon host cell gene expression programs. This methodology has allowed the host response transcriptome of several cell lines to be studied on a global scale. To this point, the great majority of reports have focused on the response of immune cells, including macrophages and dendritic cells. These studies revealed that the immune response to microbial pathogens is tailored to different microbial challenges. Conversely, the paradigm for epithelial cells has--until recently--held that the epithelium mostly served as a relatively passive physical barrier to infection. It is now generally accepted that the epithelial barrier contributes more actively to signaling events in the immune response. In light of this shift, this review will compare transcriptional profiling data from studies that involved host-pathogen interactions occurring with epithelial cells. Experiments that defined both a common core response, as well as pathogen-specific host responses will be discussed. This review will also summarize the contributions that transcriptional profiling analysis has made to our understanding of bacterial physio-pathogensis of infection. This will include a discussion of how host transcriptional responses can be used to infer the function of virulence determinants from bacterial pathogens interacting with epithelial mucosa. In particular, we will expand upon the lessons that have been learned from gastro-intestinal and oral pathogens, as well as from members of the commensal flora.

Animals↗

PubMed2026

De Novo Genome Sequence Assembly of the Algal Endosymbiont Micractinium conductrix Derived From Its Host Paramecium bursaria 186b.

Endosymbiosis is a major driver of evolutionary innovation and underpins the function of diverse ecosystems. The origins and evolution of endosymbiosis are challenging to study experimentally due to the short-lived culturability of many microbial strains derived from endosymbiotic interactions. The facultative endosymbiosis between the ciliate, Paramecium bursaria, and the green alga, Micractinium conductrix (Chlorellaceae, Trebouxiophyceae), is ecologically widespread and has emerged as a powerful lab-tractable model system. This endosymbiosis is founded upon a reciprocal nutrient exchange, but each of the species can be cultured independently enabling quantification of symbiotic fitness effects, new partnerships to be generated in the lab, and co-associations to be subject to experimental evolution. To date, evolve-and-resequence approaches have been limited due to a lack of high-quality genome assemblies enabling gene variants to be identified. Here, we report a near telomere-to-telomere genome assembly for M. conductrix 186b, using a range of sequencing technologies. Comparative analysis shows that this is one of the most complete Chlorellaceae algal genome assemblies available to date. To aid accurate gene calling and annotation, we conducted both RNAseq and Iso-Seq transcriptome sequencing experiments. Collectively, these 'omics datasets will facilitate: (i) comparative genomics studies of endosymbiont evolution, (ii) evolve-and-resequence experiments, (iii) genome-scale metabolic modeling studies, and (iv) identification of targets for genetic modification experiments and biotechnological applications.

Symbiosis↗

PubMed2004

The interaction of Pseudomonas aeruginosa PAK with human and animal respiratory tract cell lines.

A major virulence factor of a common human pathogen Pseudomonas aeruginosa, was investigated to determine if it dominated attachment interactions in a variety of in vitro cell culture systems. It was found that Type-IV pilus-type mechanisms, which mediated the attachment of P. aeruginosa to three human respiratory tract cell lines (A549, BEAS-2B and RPMI 2650) also mediated attachment to two respiratory tract cell lines from mouse (C57) and rat (L-2) to a similar degree. Significant differences were found in the number of P. aeruginosa associated with the human, rat and mouse cell lines. Additionally, differences were also found between A547, C57 and L-2 cells with respect to the moieties that P. aeruginosa interacted with at the level of the cell surface, suggesting that asialo-GM1 ligands were not the only structure that this bacterium could interact with in order to associate with host cells.

Animals↗

PubMed2004

Use of cDNA microarrays to analyze responses to pneumococcal virulence factors.

BACKGROUND & OBJECTIVES: The complex interactions that occur between host and pathogen during bacteraemia caused by Streptococcus pneumoniae are not well understood. Upon entering the blood stream the pneumococcus intiates responses through contact with naïve monocytes and macrophages resulting in an inflammatory response. To elucidate the role of microbial virulence factors in the host response to the pneumococcus, cDNA microarray analysis was used to identify genes in THP-1 cells, a human monocytic cell line, that are responsive to pneumococcal virulence factors. METHODS: S. pneumoniae D39, a serotype 2 pneumococcus, and PLN an isogenic mutant of D39 that does not express pneumolysin were used. Gene expression profiles elicited by both wild-type and mutant were compared with that of THP-1 cells not exposed to pneumococci. Results obtained from microarray analysis were confirmed and further characterized using reverse transcriptase (RT)-PCR, real-time RT-PCR, and ELISA. RESULTS: Genes in THP-1 cells that were responsive to the pneumococcus independent of the presence of the specific virulence factor, pneumolysin, were identified. THP-1 cell genes that were differentially expressed independent of pneumolysin included the ones involved in cell-to-cell signaling and antipathogen responses. Those that were responsive to pneumolysin included genes encoding adhesion molecules, chemokines, cytokine receptors, and cell cycle and apoptosis proteins. INTERPRETATION & CONCLUSION: The global transcriptional response of naïve monocytes to contact with the pneumococcus was characterized and the utility of cDNA microarray analysis in elucidating the role of specific factors in host-pathogen interactions were demonstrated.

Cell Line↗

PubMed2005

Comparative genetics and innate immune functions of collagenous lectins in animals.

Collagenous lectins such as mannan-binding lectins (MBLs), ficolins (FCNs), surfactant proteins A and D (SP-A, SP-D), conglutinin (CG), and related ruminant lectins are multimeric proteins with carbohydrate-binding domains aligned in a manner that facilitates binding to microbial surface polysaccharides. MBLs and FCNs are structurally related to C1q, but activate the lectin complement pathway via interaction with MBL-associated serine proteases (MASPs). MBLs, FCNs, and other collagenous lectins also bind to some host macromolecules and contribute to their removal. While there is evidence that some lectins and the lectin complement pathway are conserved in vertebrates, many differences in collagenous lectins have been observed among humans, rodents, and other vertebrates. For example, humans have only one MBL but three FCNs, whereas most other species express two FCNs and two MBLs. Bovidae express CG and other SP-D-related collectins that are not found in monogastric species. Some dysfunctions of human MBL are due to single nucleotide polymorphisms (SNPs) that affect its expression or structure and thereby increase susceptibility to some infections. Collagenous lectins have well-established roles in innate immunity to various microorganisms, so it is possible that some lectin genotypes or induced phenotypes influence resistance to some infectious or inflammatory diseases in animals.

Animals↗