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PubMed2007

Genomics of host-pathogen interactions.

The complete sequences of hundreds of microbial genomes have provided drug discovery pipelines with thousands of new potential drug targets. Their availability has also stimulated the development of a variety of innovative approaches that allow functional studies to be performed on the entire genome of an organism. This chapter describes how these approaches have been applied to the analysis of host-pathogen interactions and discusses how such studies might facilitate the development of new antibiotics.

Anti-Bacterial Agents↗
PubMed2005

The impact of saponins or saponin-containing plant materials on ruminant production--a review.

Saponins are steroid or triterpene glycoside compounds found in a variety of plants. Some saponin-containing plants, mainly legumes, have been used as animal feed, but others are toxic. Several studies on the effect of saponins on ruminant production have also been reported. Some in vitro and in vivo experiments that demonstrate the beneficial effects of saponin such as defaunation of the rumen and manipulation of the end products of fermentation are described. Defaunation is the selective removal of protozoa from the rumen microbial ecosystem by a cell membrane cholesterol-saponin interaction, which causes cell rupture. Because protozoa in the rumen cause protein turnover by predating on bacteria, defaunation increases the nitrogen utilization of the ruminant and may lead to an increase in growth, milk, or wool production. The growth-promoting effect was evident in the high roughage diet suggesting that the application of saponins or saponin-containing plant materials may be beneficial for the subsistence farmers in developing countries. Saponins are deglycosylated by rumen microbes. Some sapogenins have been detected in the digestive tract of ruminants; however, the direct action of these compounds on the host animal is still unclear. No information on the effects of saponin on ruminant reproduction is available. There is an urgent need for a systematic evaluation of the most active structural components of the saponins, and their interaction with the microbial community, the host animal, and the diet. Along with these studies, the direct effects of saponins or their microbial degradation products on the host must be examined in order to get the full understanding of the metabolism and beneficial effects of saponins on animals.

Animals↗
PubMed2003

Helicobacter pylori virulence factors--one part of a big picture.

CONTEXT: At least half the world's population is infected with Helicobacter pylori, although only 10-20% of carriers develop gastric diseases, ranging from ulcer to MALT-lymphoma and adenocarcinoma (MALT is mucosa-associated lymphoid tissue). The clinical outcome of H pylori infection is determined by a complex interaction of environmental influences and host and microbial virulence factors. H pylori genotypes carrying the babA2 gene, encoding a bacterial adhesin mediating interaction with gastric epithelial cells, have enhanced pathogenicity. Moreover, coexistence of babA2 with other bacterial virulence factors further worsens clinical outcomes. STARTING POINT: To further elucidate the clinical relevance of babA2-genopositive H pylori strains, Carlo-Frederico Zambon and colleagues analysed the association of babA2 genotypes with gastritis, gastroduodenal ulcer disease, or intestinal metaplasia in 167 infected Italian individuals. The coexistence of babA2 with other potentially disease-related H pylori genes, such as cagA, vacA, or oipA, correlated with clinical outcome. 36% of H pylori strains were babA2(-) genopositive, and abundance of babA2 was associated with the genomic presence of the other potential virulence-factor genes. H pylori strains carrying babA2, cagA, and the vacA genotype s1m1 were associated with the highest risk of developing intestinal metaplasia, whereas this condition was rarely (<10%) associated with strains with a cagA-, babA2-, vacA s2m2 genotype. Whilst the risk of developing more serious gastric lesions increased as the number of virulence factor genes accumulated in a given H pylori strain, there was no indication of any one specific bacterial gene-pattern being associated with a particular clinical disease. WHERE NEXT? Identifying the factors responsible for the enhanced pathogenicity of H pylori leading to development of life-threatening diseases in a subset of infected individuals is a mandatory task for the future. Identification of virulence-associated H pylori genes and investigation of their clinical relevance in large prospective studies will help to define such strains with increased pathogenicity. The value of H pylori genotypes as predictors of disease outcome is limited, because the pathogenic impact of bacterial virulence factors is greatly influenced by coexisting environmental and host factors.

Genotype↗
PubMed1998

Creating and maintaining the gastrointestinal ecosystem: what we know and need to know from gnotobiology.

Studying the cross talk between nonpathogenic organisms and their mammalian hosts represents an experimental challenge because these interactions are typically subtle and the microbial societies that associate with mammalian hosts are very complex and dynamic. A large, functionally stable, climax community of microbes is maintained in the murine and human gastrointestinal tracts. This open ecosystem exhibits not only regional differences in the composition of its microbiota but also regional differences in the differentiation programs of its epithelial cells and in the spatial distribution of its component immune cells. A key experimental strategy for determining whether "nonpathogenic" microorganisms actively create their own regional habitats in this ecosystem is to define cellular function in germ-free animals and then evaluate the effects of adding single or several microbial species. This review focuses on how gnotobiotics-the study of germ-free animals-has been and needs to be used to examine how the gastrointestinal ecosystem is created and maintained. Areas discussed include the generation of simplified ecosystems by using genetically manipulatable microbes and hosts to determine whether components of the microbiota actively regulate epithelial differentiation to create niches for themselves and for other organisms; the ways in which gnotobiology can help reveal collaborative interactions among the microbiota, epithelium, and mucosal immune system; and the ways in which gnotobiology is and will be useful for identifying host and microbial factors that define the continuum between nonpathogenic and pathogenic. A series of tests of microbial contributions to several pathologic states, using germ-free and ex-germ-free mice, are proposed.

Animals↗
PubMed2001

Glycan mimicry as a basis for novel anti-infective drugs.

The idea of using carbohydrate-based drugs to prevent attachment of microbial pathogens to host tissues has been around for about three decades. This concept evolved from the observation that many pathogenic microbes bind to complex carbohydrate sequences on the surface of host cells. It stands to reason, therefore, that analogs of the carbohydrate sequences pathogens bind to could be used to competitively inhibit these interactions, thereby preventing microbial damage to the host. This article will summarize some of the recent advances in developing such carbohydrate-based anti-infective drugs.

Animals↗
PubMed2004

Impact of commensal microbiota on murine gastrointestinal tract gene ontologies.

The gastrointestinal tract (GIT) of eukaryotes is colonized by a vast number of bacteria, where the commensal microbiota play an important role in defining the healthy gut. To investigate the influence of commensal bacteria on multiple regions of the host GIT transcriptome, the gene expression profiles of the corpus, jejunum, descending colon, and rectum of conventional (n = 3) and germ-free mice (n = 3) were examined using the Affymetrix Mu74Av2 GeneChip. Differentially regulated genes were identified using the global error assessment model, and a novel method of Gene Ontology (GO) clustering was used to identify significantly modulated biological functions. The microbiota modify the greatest number of genes in the jejunum (267 genes with an alpha < 0.001) and the fewest in the rectum (137 genes with an alpha < 0.001). Clustering genes by GO biological process and molecular function annotations revealed that, despite the large number of differentially regulated genes, the residential microbiota most significantly modified genes involved in such biological processes as immune function and water transport all along the length of the mouse GIT. Additionally, region-specific communication between the host and microbiota were identified in the corpus and jejunum, where tissue kallikrein and apoptosis regulator activities were modulated, respectively. These findings identify important interactions between the microbiota and the mouse gut tissue transcriptome and, furthermore, suggest that interactions between the microbial population and host GIT are implicated in the coordination of region-specific functions.

Animals↗
PubMed1981

Fermentation in the rumen and human large intestine.

Fermentation of food by the microbial community of the rumen is essential for the maintenance and growth of ruminants. The microbial ecosystem and its interaction with the host are described, along with recent attempts to manipulate the composition and activity of the microbial community by adding antibiotics and other chemicals to ruminant diets. A similar microbial community and fermentation occur in the large intestine or cecum of most nonruminant animals including the large intestine of humans. The microbial ecosystems of the rumen and human large intestine are compared.

Animals↗
PubMed2001

Persistent Chlamydia trachomatis infections resist apoptotic stimuli.

Microbial modulation of apoptosis has added a new dimension of understanding to the dynamic interaction between the human host and its microbial invaders. Persistent infection can be a by-product of inhibition of apoptosis and may significantly impact the pathogenesis of diseases caused by organisms such as Chlamydia trachomatis. We compared apoptotic responses among HeLa 229 cells acutely and persistently infected and mock infected with serovar A/HAR-13. Persistence was induced by gamma interferon at 0.2 and 2.0 ng/ml. Cells were treated with etoposide or staurosporine at 24-h intervals and assayed for apoptosis by cell count, DNA ladder formation, and cytochrome c translocation. From the 24- to 120-h time points, infected cultures were 87 and 90% viable for etoposide and staurosporine treatment, respectively, and produced no DNA ladder, and cytochrome c remained in the mitochondria. In contrast, mock-infected cells were 22 and 37% viable for etoposide (P = 0.0001) and staurosporine (P = 0.01), respectively, and displayed characteristic DNA ladders, and cytochrome c was translocated. We found that resistance to apoptotic stimuli was identical in acute and persistent infections. Since cytochrome c was not translocated from the mitochondrion, caspase-9 activity was likely not involved. The expression of chlamydial hsp60, a known stimulator of inflammation in vivo, was measured in both active and persistent infections by Western blot, with increased production in the latter with or without staurosporine treatment. Chlamydial disregulation of apoptosis and the ensuing persistence of organisms offer an alternative pathogenic mechanism for chlamydial scarring observed in trachoma and infertility populations via sustained inflammation induced by immunoreactive molecules such as hsp60.

Apoptosis↗
PubMed2006

Role of the innate immune system and host-commensal mutualism.

Host organisms live in intimate contact with indigenous microflora. The interactions between the host and commensal microbiota are highly complex and heterogeneous. A growing body of evidence indicates that commensal symbionts provide many benefits to the host physiology, particularly in the gastrointestinal system. The molecular mechanisms of the mutualistic interactions between the host and commensals are largely unknown but can be due either to bioactivity of the commensals or to the reaction of the host immune system to the commensal-derived products. Recent advances in our understanding of the innate immune system allow re-evaluation of some of the older findings regarding the mechanisms of benefits conferred by microflora. Here we review the examples of the benefits of host-commensal interactions that are due to recognition of commensal microbial products by the host innate immune system.

Animals↗
PubMed2006

[Recurrent urinary tract infections in women. Virulence of pathogens and host reaction].

The interactions of host-specific and microbial factors are responsible for recurrent urinary tract infections (rUTI). The anatomical properties of the female urogenital tract favor colonization by uropathogens. Local factors such as glucose concentration of the urine, stability of the lactobacilli population, the influence of estrogens, the activity of Tamm-Horsfall protein or of defensins, and disturbance of the systemic defense mechanisms dictate the course of an infection. The most prominent uropathogen is E. coli. It expresses various virulence factors including adhesions, toxins, iron uptake systems, and a capsule. It is still unclear if there are virulence factors characteristic for E. coli strains causing rUTI. The formation of intracellular reservoirs by invasion of uroepithelial cells by E. coli could be another, as yet little noticed cause for rUTI. Therefore, in cases of rUTI the application of intracellularly active antibiotics should be considered.

Animals↗
PubMed2006

MNN5 encodes an iron-regulated alpha-1,2-mannosyltransferase important for protein glycosylation, cell wall integrity, morphogenesis, and virulence in Candida albicans.

The cell walls of microbial pathogens mediate physical interactions with host cells and hence play a key role in infection. Mannosyltransferases have been shown to determine the cell wall properties and virulence of the pathogenic fungus Candida albicans. We previously identified a C. albicans alpha-1,2-mannosyltransferase, Mnn5, for its novel ability to enhance iron usage in Saccharomyces cerevisiae. Here we have studied the enzymatic properties of purified Mnn5 and characterized its function in its natural host. Mnn5 catalyzes the transfer of mannose to both alpha-1,2- and alpha-1,6-mannobiose, and this activity requires Mn2+ as a cofactor and is regulated by the Fe2+ concentration. An mnn5Delta mutant showed a lowered ability to extend O-linked, and possibly also N-linked, mannans, hypersensitivity to cell wall-damaging agents, and a reduction of cell wall mannosylphosphate content, phenotypes typical of many fungal mannosyltransferase mutants. The mnn5Delta mutant also exhibited some unique defects, such as impaired hyphal growth on solid media and attenuated virulence in mice. An unanticipated phenotype was the mnn5Delta mutant's resistance to killing by the iron-chelating protein lactoferrin, rendering it the first protein found that mediates lactoferrin killing of C. albicans. In summary, MNN5 deletion impairs a wide range of cellular events, most likely due to its broad substrate specificity. Of particular interest was the observed role of iron in regulating the enzymatic activity, suggesting an underlying relationship between Mnn5 activity and cellular iron homeostasis.

Alcian Blue↗
PubMed1997

Targeted delivery of antigen to hamster nasal lymphoid tissue with M-cell-directed lectins.

The nasal cavity of a rodent is lined by an epithelium organized into distinct regional domains responsible for specific physiological functions. Aggregates of nasal lymphoid tissue (NALT) located at the base of the nasal cavity are believed to be sites of induction of mucosal immune responses to airborne antigens. The epithelium overlying NALT contains M cells which are specialized for the transcytosis of immunogens, as demonstrated in other mucosal tissues. We hypothesized that NALT M cells are characterized by distinct glycoconjugate receptors which influence antigen uptake and immune responses to transcytosed antigens. To identify glycoconjugates that may distinguish NALT M cells from other cells of the respiratory epithelium (RE), we performed lectin histochemistry on sections of the hamster nasal cavity with a panel of lectins. Many classes of glycoconjugates were found on epithelial cells in this region. While most lectins bound to sites on both the RE and M cells, probes capable of recognizing alpha-linked galactose were found to label the follicle-associated epithelium (FAE) almost exclusively. By morphological criteria, the FAE contains >90% M cells. To determine if apical glycoconjugates on M cells were accessible from the nasal cavity, an M-cell-selective lectin and a control lectin in parallel were administered intranasally to hamsters. The M-cell-selective lectin was found to specifically target the FAE, while the control lectin did not. Lectin bound to M cells in vivo was efficiently endocytosed, consistent with the role of M cells in antigen transport. Intranasal immunization with lectin-test antigen conjugates without adjuvant stimulated induction of specific serum immunoglobulin G, whereas antigen alone or admixed with lectin did not. The selective recognition of NALT M cells by a lectin in vivo provides a model for microbial adhesin-host cell receptor interactions on M cells and the targeted delivery of immunogens to NALT following intranasal administration.

Administration, Intranasal↗
PubMed1979

A rat model of chronic respiratory infection with Pseudomonas aeruginosa.

Chronic, nonlethal, pulmonary infection of rats by Pseudomonas aeruginosa can be initiated by intratracheal inoculation of 10(4) bacteria enmeshed in agar beads. The number of bacteria recoverable from the lung increased to approximately 10(6) within 3 days and remained at that number during 35 days of observation. Histologic examination of the infected lungs revealed lesions resembling those seen in lung tissue of humans with acute or chronic nonbacteremic, Pseudomonas aeruginosa pneumonia, including the presence of goblet-cell hyperplasia, focal areas of necrosis, and acute and chronic inflammatory infiltrate. This model should be useful for investigating the interactions between microbial virulence factors and host defense mechanisms.

Animals↗
PubMed1997

Bacterial attachment to uro-epithelial cells: mechanisms and consequences.

Microbial attachment to mucosal surfaces is a first step in mucosal infection. Specific interactions between microbial surface ligands and host receptors influence the distribution of microbes in their sites of infection. Adhesion has often been regarded as a sufficient end point, explaining tissue tropism and bacterial persistence at mucosal sites. Adherence, however, is also a virulence factor through which microbes gain access to host tissues, upset the integrity of the mucosal barrier, and cause disease. The induction of mucosal inflammation is one aspect of this process. Bacterial attachment to mucosal surfaces activates the production of pro-inflammatory cytokines that cause both local and systemic inflammation. Epithelial cells are one source of these cytokines. The binding of fimbrial lectins to epithelial cell receptors triggers transmembrane signaling events that upregulate cytokine-specific mRNA and increase cytokine secretion. P fimbriae that bind the globoseries of glycolipids cause the release of ceramides and activation of the ceramide signaling pathway which contributes to the IL-6 response. Spread of cytokines and other pro-inflammatory mediators from the local site contributes to the symptoms and signs of infection.

Adhesins, Bacterial↗
PubMed2006

Regenerative dental medicine: stem cells and tissue engineering in dentistry.

The dawn of this century is brightened by the growing understanding and experimentation with stem cells as primary tools in the expanding regenerative medicine and tissue engineering revolution. The tradition of using prosthetic artificial implants to restore lost or damaged dental tissue will gradually be supplanted by more natural alternatives, including biological tooth replacement or induction. The practice of dentistry is likely to be revolutionized by biological therapies based on growth and differentiation factors that accelerate and/or induce a natural biological regeneration. This prospect has flourished from the gained knowledge provided by the molecular biological characterization of the genetic makeup of human cells and from a growing understanding of the effect of environmental factors. Prevention of dental diseases will also gain new ground as more insight is gained into the genetic makeup of microbial pathogens, their interactions with the host, and the host repair mechanisms. This review summarizes current knowledge, barriers, and challenges in the clinical use of stem cells with an emphasis on applications in dentistry.

Animals↗
PubMed2006

[Three cases of tuberculosis children who demonstrated paradoxical worsening during different stage of treatment].

We report three tuberculosis children aged seven-month-old to 11-year-old who had paradoxical worsening of tuberculosis of lung and lymph nodes, lymph nodes, and intracranial tuberculoma at different treatment stages. In these children, paradoxical worsening occurred at about 14 days after start of anti-tuberculosis treatment, about six months after the start, and about three months after the completion of treatment. No alteration was done in the method of anti-tuberculosis treatment against expanding lesions, and predonisolone was prescribed in two subjects. Expanded lesions then improved one- to five-months later. The mechanisms of paradoxical worsening is unclear. However, these cases suggest that paradoxical worsening may occur at any time after starting anti-tuberculosis treatment based on interaction between the microbial factors and host immunological factors in lung, lymph nodes, intracranial tuberculosis lesions.

Child↗
PubMed1986

Pseudomonas aeruginosa and cystic fibrosis: unusual bacterial adaptation and pathogenesis.

Pseudomonas aeruginosa is an adaptable, saprophytic bacterium with the potential to cause a variety of opportunistic infections in compromised hosts. In patients with cystic fibrosis, chronic pulmonary colonization with mucoid alginate-producing mutants of P. aeruginosa is a major cause of morbidity and mortality and is an interesting example of microbial adaptation and host-bacterium interaction.

Adaptation, Physiological↗