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Results for “Host Microbial Interactions”

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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↗

PubMed2026

KG-Microbe: Building modular and scalable knowledge graphs for microbiome and microbial sciences.

BACKGROUND: The integration of many disparate forms of data is essential for understanding the microbial world and its interaction with the environment and human health. Doing so is particularly challenging in the context of microbe-host and microbe-microbe interactions that contribute to health or environmental outcomes. There are thousands of relevant microbial species, and millions of interactions among those microbes and with their environment or host. Integrated information (e.g., about host and microbial physiology, genetics, and metabolism) facilitates deeper understanding of complex mechanisms and helps interpret correlative results. RESULTS: The KG-Microbe construction framework is a novel approach to harmonizing bacterial and archaeal data in the form of a findable, accessible, interoperable, reusable and AI-ready knowledge graph (KG). Starting from a core KG with organismal traits, environments, and growth preferences and the integration of established ontologies, the framework generates a hierarchy of related KGs targeting specific use cases, including the human microbiome in the context of disease, or environmental microbiomes. The framework supports customizable taxa subsets representing communities or clades of interest. Evaluations of the KG-Microbe KGs through a series of competency questions demonstrate the accuracy and effectiveness of the data harmonization, and the utility of the resulting KGs in studies of inflammatory bowel disease and Parkinson's disease. Finally, the predictive and environmental capabilities of the KGs are demonstrated by predicting growth preferences using graph features. CONCLUSIONS: The KG-Microbe framework unifies microbial contexts in a single resource to support integrative analyses across biomedical, host, and environmental domains. KG-Microbe is a flexible, modular enabling technology for humans and machine learning methods to uncover candidate mechanistic explanations of microbial associations.

Microbiota↗

PubMed2002

Bacteriophage-host interaction in the enhanced biological phosphate removing activated sludge system.

Bacteriophages were isolated from a laboratory scale enhanced biological phosphate removing (EBPR) activated sludge process, and their host range was examined. Bacterial isolates to host the bacteriophages were isolated from the EBPR activated sludge process. Bacteriophages were eluted from the EBPR activated sludge, enriched by incubation with the bacterial isolates, and then tested for plaque formation on each of the bacterial isolates. Out of 12 bacterial isolates isolated, 4 supported plaque formation. Four bacteriophages were obtained from the plaques. The host range test was conducted with the combination of the bacteriophage isolates and the bacterial isolates. Three of the bacteriophages were found to form plaques on more than one host, and one of them formed plaques on both gram +ve and gram -ve bacterial isolates. Two of the four bacteriophages failed to form plaques on their original bacterial host, indicating the existence of mutation on either both or one of the host and the bacteriophage. This study strongly suggests that bacteriophages are an active part of the activated sludge microbial ecosystem, having very complex interaction with their host bacteria.

Bacteriophages↗

PubMedDate not supplied

Leucine-rich repeats in host-pathogen interactions.

Leucine-rich repeats (LRRs) are versatile binding motifs found in a variety of proteins and are involved in protein-protein interactions. The LRR domain is composed of repeats forming a characteristic solenoid horse-shoe structure, which provides a scaffold for numerous insertions involved in binding to pathogen-associated molecular patterns and surface receptors. LRRs have been shown to be involved in the host defense systems of both plants (resistance genes) and mammals (Toll-like receptors and nucleotide-binding oligomerisation domain proteins), where they sense specific pathogen-associated molecules and activate the innate immune system. Paradoxically, LRRs have also been shown to be part of microbial virulence factors involved in the interaction with host cells and establishment of infection. The potential of LRRs to bind a vast array of structurally unrelated ligands and their well-documented involvement in microbial pathogenesis make them a potential target for vaccines and new drugs. The recent identification of LRRs in the obligate intracellular protozoan parasite Leishmania and their participation in the macrophage-parasite interaction have added new insight into the role of LRRs in the host cell invasion.

Amino Acid Sequence↗

PubMed2004

Cell-to-cell signalling in Escherichia coli and Salmonella enterica.

Cell-to-cell signalling in prokaryotes that leads to co-ordinated behaviour has been termed quorum sensing. This type of signalling can have profound impacts on microbial community structure and host-microbe interactions. The Gram-negative quorum-sensing systems were first discovered and extensively characterized in the marine Vibrios. Some components of the Vibrio systems are present in the classical genetic model organisms Escherichia coli and Salmonella enterica. Both organisms encode a signal receptor of the LuxR family, SdiA, but not a corresponding signal-generating enzyme. Instead, SdiA of Salmonella detects and responds to signals generated only by other microbial species. Conversely, E. coli and Salmonella encode the signal-generating component of a second system (a LuxS homologue that generates AI-2), but the sensory apparatus for AI-2 differs substantially from the Vibrio system. The only genes currently known to be regulated by AI-2 in Salmonella encode an active uptake and modification system for AI-2. Therefore, it is not yet clear whether Salmonella uses AI-2 as a signal molecule or whether AI-2 has some other function. In E. coli, the functions of both SdiA and AI-2 are unclear due to pleiotropy. Genetic strategies to identify novel signalling systems have been performed with E. coli and Providencia stuartii. Several putative signalling systems have been identified, one that uses indole as a signal and another that releases what appears to be a peptide. The latter system has homologues in E. coli and Salmonella, as well as other bacteria, plants and animals. In fact, the protease components from Providencia and Drosophila are functionally interchangeable.

Bacterial Proteins↗

PubMed1991

A host-host-pathogen model with free-living infective stages, applicable to microbial pest control.

A model has been investigated of the dynamics of the interaction between two hosts which are both attacked by a common pathogen, where the pathogen has free-living infective stages the population size of which must itself be modelled explicitly, and where the host species do not interact with one another except through their shared pathogen. If either host interacted with the pathogen alone, three broad classes of dynamics would be possible: host regulation, pathogen persistence and pathogen extinction. Here, all possible types of combinations of hosts are examined: regulation-regulation (both hosts would be regulated if they interacted with the pathogen alone), regulation-persistence, regulation-extinction, persistence-persistence persistence-extinction and extinction-extinction. A wide range of dynamics is generated, including a number of patterns quite unlike those found in the one-host pathogen case (e.g. persistence in one host, elimination of the other host) and behaviour contingent on initial densities in the system. For clarity and pertinence, attention is focused on the case where one host is a pest, the pathogen is a potential microbial control agent, and the other host is a non-target species which it is undesirable to harm. The model suggests, broadly, that non-targets are unlikely to be seriously threatened in such cases, and also that non-targets, far from undermining pest control, are quite likely to contribute to its efficacy.

Animals↗

PubMed1995

The diversity and origins of toxins in ciguatera fish poisoning.

The source of the diversity of phytotoxins found in the marine food web is not well understood. It is not clear what roles these secondary metabolites might have in the phytoplankton that produce them. The phytotoxins do not appear to be deterrents of predation, although the production of antibiotics by marine macroalgae might be considered in this light (86). It is equally doubtful that the production and/or presence of these toxins confers a selective advantage on the phytoplankton producers, when in fact the diversity of naturally occurring phytoplankton species may well be maintained by lytic viral infections (22,64). On the other hand, these multiple, diverse toxins may be the products of the different adaptations and interactions that take place between microalgal vectors and the highly variable spectrum of their microbial symbionts. We do not know what selective signals these toxic products may be providing in the maintenance of the symbiont-host consortia in which they are produced, however, their diversity most likely reflects the diversity of symbiotic interactions that exist in these consortia. Woven into the very fabric of the traditional marine food web is an invisible empire of marine micro-organisms, that by its very existence may determine the intense diversity of toxins found in marine biota. Marine bacteria are very likely the most abundant organisms in the sea and to a large degree maintain a food web of their own, often referred to as the microbial loop (64). This microbial web sustains the biogeochemical cycles in the sea. Much of the food produced by phytoplankton and cyanobacteria is consumed by bacteria in the microbial loop and may never enter the food web of larger invertebrates and fishes. Traditionally, the marine food web has been viewed, so to speak, from the top, however, it is now clear that there is an enormous marine microbial food web from which the food web of larger invertebrates and fishes emanates (Figure 13). In many respects the phytotoxins are biomarkers of the interactions between these two food webs. In their very diversity these toxins reflect an amalgam of interacting collaborating forms of life, a complex of phytoplankton hosts and their microbial symbionts producing multiple toxins and their derivatives that ultimately result in the complex medical symptoms they produce in human consumers of poisoned seafood. The term ciguatera has been employed to describe the syndrome of the illness contracted by persons who have eaten tropical and semitropical finfish poisoned by ciguatoxin.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗

PubMed2001

Adaptation of bacteria to the intestinal niche: probiotics and gut disorder.

The gastrointestinal tract is a complex ecosystem host to a diverse and highly evolved microbial community composed of hundreds of different microbial species. The interactions that occur between this complex microbial community and the human host have become the focus of scientific research due to increases in the incidence of illnesses associated with deficient or compromised microflora (e.g., gastrointestinal tract infections, inflammatory bowel disease (Crohn's disease and ulcerative colitis), irritable bowel syndrome, antibiotic-induced diarrhea, constipation, food allergies, cardiovascular disease, and certain cancers). Effective multidisciplinary research programs now complement conventional microbiology with molecular ecology techniques to provide culture-independent analysis of the gastrointestinal ecosystem. Furthermore, as we acquire an understanding of gut microflora composition and processes such as intestinal adherence, colonization, translocation, and immunomodulation, we are also elucidating mechanisms by which these can be influenced. This knowledge not only allows scientists to define the activities and interactions of "functional food"-borne beneficial bacteria in the gut, but will also provide the scientific basis for the development of innovative biotechnology-based products tailored to prevent specific diseases and promote overall human gastrointestinal health.

Bacterial Physiological Phenomena↗

PubMedDate not supplied

Receptins: a novel term for an expanding spectrum of natural and engineered microbial proteins with binding properties for mammalian proteins.

A new term 'receptin', derived from recipere (lat.), is proposed to denote microbial binding proteins that interact with mammalian target proteins. An example of such a 'receptin' is staphyloccocal protein A which binds to the Fc part of many mammalian immunoglobulins. Several other types of 'receptins' are listed. This term may easily be distinguished from the similar term 'receptor', describing a binding site on a cell surface, mostly eukaryotic, where a secondary effect is induced inside the cell upon binding to a ligand. A receptin, however, does not necessarily have to induce a secondary event. Receptins include so called MSCRAMMs, adhesins, and also engineered receptins, affibodies, and engineered ligands. It denotes any protein of microbial origin, cell-bound or soluble, which can bind to a mammalian protein. It fulfills the need for an umbrella terminology for a large group of binding structures. In contrast, the term 'lectin' represents a group of proteins with affinity for carbohydrate structures. The new term 'receptin' includes a number of key microbial proteins involved in host-parasite interactions and in virulence. Some receptins are promising vaccine candidates.

Animals↗

PubMed1999

A natural variant of the cysteine protease virulence factor of group A Streptococcus with an arginine-glycine-aspartic acid (RGD) motif preferentially binds human integrins alphavbeta3 and alphaIIbbeta3.

The human pathogenic bacterium group A Streptococcus produces an extracellular cysteine protease [streptococcal pyrogenic exotoxin B (SpeB)] that is a critical virulence factor for invasive disease episodes. Sequence analysis of the speB gene from 200 group A Streptococcus isolates collected worldwide identified three main mature SpeB (mSpeB) variants. One of these variants (mSpeB2) contains an Arg-Gly-Asp (RGD) sequence, a tripeptide motif that is commonly recognized by integrin receptors. mSpeB2 is made by all isolates of the unusually virulent serotype M1 and several other geographically widespread clones that frequently cause invasive infections. Only the mSpeB2 variant bound to transfected cells expressing integrin alphavbeta3 (also known as the vitronectin receptor) or alphaIIbbeta3 (platelet glycoprotein IIb-IIIa), and binding was blocked by a mAb that recognizes the streptococcal protease RGD motif region. In addition, mSpeB2 bound purified platelet integrin alphaIIbbeta3. Defined beta3 mutants that are altered for fibrinogen binding were defective for SpeB binding. Synthetic peptides with the mSpeB2 RGD motif, but not the RSD sequence present in other mSpeB variants, blocked binding of mSpeB2 to transfected cells expressing alphavbeta3 and caused detachment of cultured human umbilical vein endothelial cells. The results (i) identify a Gram-positive virulence factor that directly binds integrins, (ii) identify naturally occurring variants of a documented Gram-positive virulence factor with biomedically relevant differences in their interactions with host cells, and (iii) add to the theme that subtle natural variation in microbial virulence factor structure alters the character of host-pathogen interactions.

Alleles↗

PubMed1983

Plasmodium berghei: diet and drug dosage regimens influencing selection of drug-resistant parasites in mice.

Two different diets for the host and three drug dosage regimens were used to select lines resistant to sulfadoxine and pyrimethamine from the parent strain of the rodent malaria parasite Plasmodium berghei [the N (K173) strain]. A higher yield of resistance was obtained when a high parasitemia was present at the beginning of the drug pressure schedule. The development of resistance to the association of sulfadoxine plus pyrimethamine was accelerated by a relatively high para-aminobenzoic acid (PABA) content diet. Reproducibility was satisfactory when one of the dosage regimens was applied independently by two different technicians at different times.

4-Aminobenzoic Acid↗

PubMed2006

Commensals upon us.

A battle to control and curtail bacterial infectious diseases is being waged in our hospitals and communities through antibiotic therapies and vaccines targeting specific species. But what effects do these interventions have on the epidemiology of infections caused by the organisms that are part of our natural microbial flora? Gram-positive and gram-negative bacteria appear as new disease agents from among commensal flora. These include vancomycin resistant enterococci (VRE), community-associated methicillin resistant Staphylococcus aureus (CA-MRSA), non-vaccine invasive serotypes of Streptococcus pneumoniae, new strains of non-type b Haemophilus influenzae and multi-drug resistant Escherichia coli. These examples illustrate how clinical improvements and widespread use and misuse of antibiotics have pushed evolution, allowing normally non-pathogenic strains to become infectious disease threats to human health.

Anti-Bacterial Agents↗

PubMed2003

Collagenous transmembrane proteins: collagen XVII as a prototype.

Collagenous transmembrane proteins are an emerging group of biologically versatile molecules which function as both cell surface receptors and matrix molecules. The seven group members have interesting structural similarities: they are integral membrane proteins in type II orientation and have one or more collagenous domains in the extracellular C-terminus; interspersed by non-collagenous stretches which confer structural flexibility to the ectodomain. A conserved coiled-coil sequence (linker domain) immediately adjacent to the extracellular face of the cell membrane presumably serves as a nucleus for trimerization and triple-helix folding of each collagen. Intriguingly, the ectodomains of at least some of these molecules are proteolytically shed from the cell surface, releasing a shorter form of the collagen into the extracellular matrix. Collagenous transmembrane proteins are expressed in many different tissues and cells, and are involved in a broad spectrum of biological functions, reaching from epithelial and neural cell adhesion, and epithelial-mesenchymal interactions during morphogenesis to host defense against microbial agents. Several group members are involved in the molecular pathology of genetic and acquired human diseases including epidermolysis bullosa, ectodermal dysplasia, bullous pemphigoid or Alzheimer disease. An extensively investigated member is collagen XVII, a keratinocyte surface protein, which attaches the epidermis to the basement membrane in the skin. In this review, the structure and functions of the currently known collagenous transmembrane proteins are summarized and, as a 'prototype' of the group, collagen XVII and its biology and pathophysiology are delineated.

Amino Acid Sequence↗

PubMed2025

16S rRNA and Metagenomic Datasets of Gastrointestinal Microbiota in Fetal and 7-Day-Old Goat Kids.

The perinatal period (from late gestation to the neonatal stage) in ruminants is a critical phase for fetal organ maturation, where ecological succession of gastrointestinal microbial communities significantly impacts livestock production efficiency. However, research remains insufficient regarding the distribution patterns and functional annotation of microbial communities across different gastrointestinal compartments during this period. This study characterized early microbiota dynamics in Hutianshi Goats using 16S rRNA sequencing (4 fetal goats at 90 ± 10 gestational days) and metagenomics (3 7-day-old goat kids). The fetal goat group generated 852,694 valid reads, yielding 688,277 high-quality reads after chimera removal for downstream analysis. The 7-day-old goat kids group produced 1,081,588,182 final valid reads, after data processing and assembly, 8,561,345 contigs were generated. Gene prediction identified 6,095,352 genes. Multi-database annotations (NR, KEGG, CAZy, etc.) revealed functional potential and antimicrobial resistance traits. The public release of this dataset facilitates academic understanding of microbial community dynamics and host-microbe interactions during this developmental stage, providing both theoretical foundations and data resources for ruminant developmental biology and precision breeding regulation.

Animals↗

PubMed2001

Prediction of shock in febrile medical patients with a clinical infection.

OBJECTIVE: Shock in the course of fever is likely caused by septic shock. Because septic shock carries a high mortality rate, early recognition could benefit the patient. We tried to predict the development of shock in medical patients with fever and a clinical infection, on the basis of clinical and microbiological information, and to evaluate the role therein of systemic inflammatory response syndrome (SIRS) criteria: abnormal body temperature, tachycardia, tachypnea, and abnormal white blood cell counts. DESIGN: Prospective observational study. SETTING: Department of Internal Medicine at a university hospital. PATIENTS: Patients were 212 consecutive medical patients with newly onset fever (temperature, >38.0 degrees C axillary or >38.3 degrees C rectally) and a clinical source of infection. MEASUREMENTS AND MAIN RESULTS: Of the 212 patients enrolled, 14 developed shock (i.e., a decrease in systolic arterial blood pressure of >40 mm Hg) during a maximum follow-up period of 7 days after inclusion. In univariate analyses, advanced age, prior urogenital disease, an abdominal source, nosocomial infections, and bacteremia predisposed patients to shock (p < .05). For clinical variables, obtained daily for 2 days after inclusion, a low performance (p < .001), the peak respiratory rate (p < .05), the peak heart rate (p < .05), the nadir score on the Glasgow Coma Scale (p < .005), the peak and nadir white blood cell counts (p < .005), and the nadir albumin (p < .01) and peak creatinine concentrations in blood (p < .001) predicted shock development. In multivariate analysis, the presence of bacteremia, the peak respiratory rate, the nadir Glasgow Coma Scale score, and the peak white blood cell count positively and the peak erythrocyte sedimentation rate negatively contributed to prediction of shock development. In contrast, SIRS had less predictive value, mainly because of lack of predictive value of peak heart rate and temperature in multivariate models. CONCLUSION: In febrile medical patients with a clinical infection, the development of shock involves an interaction between circulating microbial products and the host response, which can be recognized clinically by variables easily obtained at the bedside and partly different from the set used to define SIRS.

Adolescent↗

PubMed2004

Quorum sensing and signal interference: diverse implications.

Quorum sensing (QS) is a community genetic regulation mechanism that controls microbiological functions of medical, agricultural and industrial importance. Discovery of microbial QS signals and the signalling mechanisms led to identification of numerous enzymatic and non-enzymatic signal interference mechanisms that quench microbial QS signalling. Evidence is accumulating that such signal interference mechanisms can be developed as promising approaches to control microbial infection and biofilm formation. In addition, these mechanisms exist not only in microorganisms but also in the host organisms of bacterial pathogens, highlighting their potential implications in microbial ecology and in host-pathogen interactions. Investigation of QS and signal interference mechanisms might significantly broaden the scope of research in microbiology.

Animals↗

PubMed2003

The role of acquired immunity and periodontal disease progression.

Our understanding of the pathogenesis in human periodontal diseases is limited by the lack of specific and sensitive tools or models to study the complex microbial challenges and their interactions with the host's immune system. Recent advances in cellular and molecular biology research have demonstrated the importance of the acquired immune system not only in fighting the virulent periodontal pathogens but also in protecting the host from developing further devastating conditions in periodontal infections. The use of genetic knockout and immunodeficient mouse strains has shown that the acquired immune response-in particular, CD4+ T-cells-plays a pivotal role in controlling the ongoing infection, the immune/inflammatory responses, and the subsequent host's tissue destruction. In particular, studies of the pathogen-specific CD4+ T-cell-mediated immunity have clarified the roles of: (i) the relative diverse immune repertoire involved in periodontal pathogenesis, (ii) the contribution of pathogen-associated Th1-Th2 cytokine expressions in periodontal disease progression, and (iii) micro-organism-triggered periodontal CD4+ T-cell-mediated osteoclastogenic factor, 'RANK-L', which is linked to the induction of alveolar bone destruction in situ. The present review will focus on some recent advances in the acquired immune responses involving B-cells, CD8+ T-cells, and CD4+ T-cells in the context of periodontal disease progression. New approaches will further facilitate our understanding of their underlying molecular mechanisms that may lead to the development of new treatment modalities for periodontal diseases and their associated complications.

Aggregatibacter actinomycetemcomitans↗