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Results for “Host Microbial Interactions”

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At least 415 records · Page 23Linked to original sources
PubMed2003

CD8+ immunoregulatory cells in the graft-versus-host reaction: CD8 T cells activate dendritic cells to secrete interleukin-12/interleukin-18 and induce T helper 1 autoantibody.

Initiation of cell-mediated immunity or autoimmunity requires secretion of interleukin (IL)-12 from dendritic cells (DC), which drives the generation of T helper 1 (Th1) effector cells in synergy with IL-18. Induction of IL-12 can be triggered by microbial stimuli but also requires signals from activated T cells. We investigated interactions between alloreactive CD4 and CD8 T cells in mixed lymphocyte reactions (MLR) in vitro and in the graft-versus-host reaction (GVHR) in vivo. In a parent-into-F1 model of GVHR, donor CD8 cells were found to suppress the hyper-immunoglobulin E (IgE) syndrome, anti-DNA immunoglobulin G1 (IgG1) autoantibodies and donor CD4-cell expansion, but were essential for Th1-dependent immunoglobulin G2a (IgG2a) autoantibody production and release of serum IL-12 p40. In vitro, addition of alloreactive CD8 cells to CD4 cells and mature DC enhanced Th1 development. CD4 and CD8 T cells induced IL-18 from DC and primed for IL-12 p70 secretion via interferon-gamma (IFN-gamma) or tumour necrosis factor-alpha (TNF-alpha). However CD8 T cells, but not CD4 cells, released IFN-gamma/TNF-alpha after primary stimulation. The data suggest that rapid release of inflammatory cytokines from central memory-type CD8 cells early in immunity is critical for induction of Th1 cells via DC activation and IL-12 production. This pathway could provide a means for amplification of cell-mediated autoimmunity in the absence of microbial stimuli.

Animals↗
PubMed2002

Interactions between the microbiota and the intestinal mucosa.

The intestinal microflora can be considered as a postnatally aquired organ composed of a large diversity of bacterial cells that can perform different functions for the host. This organ is highly exposed to environmental influences and thus modulated in its composition and functions by external factors, such as nutrition. Specific components of the intestinal microflora, including lactobacilli and bifidobacteria, have been associated with beneficial effects on the host, such as promotion of gut maturation and integrity, antagonisms against pathogens and immune modulation. In addition, the microflora seem to play a significant role in the maintenance of intestinal immune homeostasis and prevention of inflammation. At the present time, the contribution of intestinal epithlial cell in the first line of defence against pathogenic bacteria and microbial antigens has been recognized, in contrast, the interactions of intestinal epithelial cells with commensal bacteria are less understood. The present work summarizes the increasing scientific attention for mechanisms of the innate immune response of the host to different components of the autochthonous microflora and suggests a potential role for selected probiotic bacteria in the regulation of intestinal inflammation.

Bifidobacterium↗
PubMedDate not supplied

Iron status, immune response and susceptibility to infection.

Nutritional factors can modulate immune responses. The concentration of iron, amongst other nutrients, influences host defence mechanisms. In experimentally induced iron deficiency in animals, morbidity and mortality on bacterial challenge are increased several-fold. Cell-mediated immunity and intra-cellular bacterial killing by polymorphonuclear leucocytes are impaired in iron-deficient individuals. This impairment is likely to be mediated by the effect of iron lack on cell proliferation, DNA synthesis and activity of iron-containing and iron-dependent enzymes involved in killing and elimination of microbes. Conversely, the availability of the free iron is a critical determinant for bacterial multiplication. It is not surprising then that epidemiological and clinical data on the frequency of infections--bacterial, fungal and others--in iron-deficient, iron-overloaded and healthy groups differ so widely. Vulnerability to infection based on the individual's iron status must be the net result of the effect of iron, or the lack of it, on microbial growth on the one hand and on immunocompetence of the host on the other. The key to keeping these interactions within physiological bounds is 'optimal iron nutrition'.

Anemia, Hypochromic↗
PubMed2006

HC-toxin.

HC-toxin is a cyclic tetrapeptide of structure cyclo(D-Pro-L-Ala-D-Ala-L-Aeo), where Aeo stands for 2-amino-9,10-epoxi-8-oxodecanoic acid. It is a determinant of specificity and virulence in the interaction between the producing fungus, Cochliobolus carbonum, and its host, maize. HC-toxin qualifies as one of the few microbial secondary metabolites whose ecological function in nature is understood. Reaction to C. carbonum and to HC-toxin is controlled in maize by the Hm1 and Hm2 loci. These loci encode HC-toxin reductase, which detoxifies HC-toxin by reducing the 8-carbonyl group of Aeo. HC-toxin is an inhibitor of histone deacetylases (HDACs) in many organisms, including plants, insects, and mammals, but why inhibition of HDACs during infection by C. carbonum leads to disease is not understood. The genes for HC-toxin biosynthesis (collectively known as the TOX2 locus) are loosely clustered over >500 kb in C. carbonum. All of the known TOX2 genes are present in multiple, functional copies and are absent from natural toxin non-producing isolates. The central enzyme in HC-toxin biosynthesis is a 570-kDa non-ribosomal synthetase encoded by a 15.7-kb open reading frame. Other genes known to be required for HC-toxin encode alpha and beta subunits of fatty acid synthase, which are presumed to contribute to the synthesis of Aeo; a pathway-specific transcription factor; an efflux carrier; a predicted branched-chain amino acid aminotransferase; and an alanine racemase.

Animals↗
PubMed2004

Reactivity of typhoid patients sera with stress induced 55 kDa phenotype in Salmonella enterica serovar Typhi.

Salmonella faces a variety of stresses including acid and heat, in the natural environment whether in the gastrointestinal tract of mammalian host or in the external environment during transmission where survival and multiplication is a priority for the pathogen. In the present study, Salmonella enterica serovar Typhi was grown under acid (inorganic and organic) as well as heat stress and the outermembrane protein (OMP) profiles were compared. A 55 kDa OMP was found to be expressed with high intensity under the selected stress conditions in comparison to normal conditions. The protein expressed under acidic stress reacted with antibodies raised against heat shock protein indicating the similarity of atleast some of the epitopes. In vivo immunogenicity (reactivity with typhoid patient sera) revealed that the 55kDa protein under each stress condition was reactive with 83% of the typhoid sera. In the light of role of the stress induced proteins in pathogenesis of microbial infections and their immunogenic potential, these findings may be relevant for a better understanding of the host-microbe interactions and for future development of diagnostic and preventive strategies.

Acids↗
PubMed1983

Macrophage 'receptors' for bacterial cell-wall sugars and immune response genes: possible determinants of susceptibility to infection.

Recognition of bacteria, antigen presentation and regulation of the immune response by the class II antigens of the major histocompatibility complex (MHC) are among the many factors that influence a host's response to microbial infection. 'Lectin-like' receptors on the macrophage membrane recognize a variety of bacteria by interaction with their cell-wall sugars. These receptors are susceptible to environmental factors and appear to be associated with the I-A subregion of the mouse MHC. Possible effects of this recognition system on the pathogenesis of microbial infection and reactive arthritides are considered.

Animals↗
PubMed2004

A Pseudomonas aeruginosa quorum-sensing molecule influences Candida albicans morphology.

Candida albicans is an opportunistic pathogen that is commonly found as a member of the human microflora. The ability of C. albicans to alter its cellular morphology has been associated with its virulence; yeast cells are more prevalent in commensal interactions whereas filamentous cells appear important in opportunistic infections. C. albicans encounters a multitude of other microbial species in the host environment and it is likely that they impact the C. albicans transition between virulent and non-virulent states. Here, we report that C. albicans morphology is significantly affected by the presence of Pseudomonas aeruginosa, another opportunistic pathogen. In a screen using a C. albicans HWP1-lacZ strain to indicate regions of filamentous growth, we identified P. aeruginosa mutants incapable of inhibiting C. albicans filamentation. Through these studies, we found that 3-oxo-C12 homoserine lactone, a cell-cell signalling molecule produced by P. aeruginosa, was sufficient to inhibit C. albicans filamentation without affecting fungal growth rates. Both microscopic analysis and real-time reverse transcription polymerase chain reaction analysis of morphology-specific markers confirmed that filamentation was suppressed by 200 microM 3-oxo-C12 homoserine lactone. Structurally related compounds with a 12-carbon chain length, e.g. C12-acyl homoserine lactone and dodecanol also affected C. albicans filamentation at similar concentrations. In contrast, other acylated homoserine lactones of different chain lengths did not affect fungal morphology. The activity of 3OC12HSL is compared with that of farnesol, a C. albicans-produced molecule also with a C12-backbone. The effects that bacteria have on the morphology of C. albicans represents one of the ways by which bacteria can influence the behaviour of fungal cells.

4-Butyrolactone↗
PubMed2005

Differential expression of inflammatory chemokines by Th1- and Th2-cell promoting dendritic cells: a role for different mature dendritic cell populations in attracting appropriate effector cells to peripheral sites of inflammation.

Protective immunity to pathogens depends on efficient immune responses adapted to the type of pathogen and the infected tissue. Dendritic cells (DC) play a pivotal role in directing the effector T cell response to either a protective T helper type 1 (Th1) or type 2 (Th2) phenotype. Human monocyte-derived DC can be differentiated into Th1-, Th2- or Th1/Th2-promoting DC in vitro upon activation with microbial compounds or cytokines. Host defence is highly dependent on mobile leucocytes and cell trafficking is largely mediated by the interactions of chemokines with their specific receptors expressed on the surface of leucocytes. The production of chemokines by mature effector DC remains elusive. Here we assess the differential production of both inflammatory and homeostatic chemokines by monocyte-derived mature Th1/Th2-, Th1- or Th2-promoting DC and its regulation in response to CD40 ligation, thereby mimicking local engagement with activated T cells. We show that mature Th1- and Th1/Th2-, but not Th2-promoting DC, selectively express elevated levels of the inflammatory chemokines CCL2/MCP-1, CCL3/MIP-1alpha, CCL4/MIP-1beta and CCL5/RANTES, as well as the homeostatic chemokine CCL19/MIP-3beta. CCL21/6Ckine is preferentially expressed by Th2-promoting DC. Production of the Th1-attracting chemokines, CXCL9/Mig, CXCL10/IP-10 and CXCL11/I-TAC, is restricted to Th1-promoting DC. In contrast, expression of Th2-associated chemokines does not strictly correlate with the Th2-promoting DC phenotype, except for CCL22/MDC, which is preferentially expressed by Th2-promoting DC. Because inflammatory chemokines and Th1-associated chemokines are constitutively expressed by mature Th1-promoting DC and CCL22/MDC is constitutively expressed by mature Th2-promoting DC, we propose a novel role for mature DC present in inflamed peripheral tissues in orchestrating the immune response by recruiting appropriate leucocyte populations to the site of pathogen entry.

Cell Movement↗
PubMed2003

Helicobacter pylori activates Toll-like receptor 4 expression in gastrointestinal epithelial cells.

Helicobacter pylori activates the transcription factor NF-kappaB, leading to proinflammatory cytokine production by gastric epithelial cells. However, the receptors for the initial bacterial interaction with host cells which activate downstream signaling events have not been completely defined. Recently, it has been shown that microbial components activate Toll-like receptors (TLRs), thereby leading to AP-1- and NF-kappaB-dependent transcription and resulting in the production of proinflammatory cytokines. The aim of this study was to determine whether H. pylori activates TLR4. Reverse transcription-PCR showed that both type I and type II H. pylori clinical isolates induced TLR4 mRNA expression in AGS cells compared with that by uninfected controls. H. pylori upregulated TLR4 protein expression in two gastric epithelial cell lines (AGS and MKN45) and one intestinal epithelial cell line (T84). Monoclonal TLR4 antibody inhibited lipopolysaccharide-induced interleukin-8 secretion from THP-1 macrophages but not from gastric epithelial cells infected with H. pylori. H. pylori demonstrated increased adherence to CHO TLR4-transfected cells compared with that to both CHO TLR2-transfected and nontransfected CHO cells (P < 0.01). These results indicate that H. pylori activates TLR4 expression in epithelial cells and that TLR4 can serve as a receptor for H. pylori binding.

Animals↗
PubMed2003

Plant-nematode interactions.

Root-knot nematodes and cyst nematodes are obligate, biotrophic pathogens of numerous plant species. These organisms cause dramatic changes in the morphology and physiology of their hosts. The molecular characterization of induced plant genes has provided insight into the plant processes that are usurped by nematodes as they establish their specialized feeding cells. Recently, several gene products have been identified that are secreted by the nematode during parasitism. The corresponding genes have strong similarity to microbial genes or to genes that are found in nematodes that parasitize animals. New information on host resistance genes and nematode virulence genes provides additional insight into this complex interaction.

Animals↗
PubMed1990

Influence of antibiotics on host-parasite interactions with an emphasis on in-vivo studies.

There has been considerable recent interest in the nature and importance of interactions which occur between antibiotics, microorganisms and the various cellular and humoral components of the host. The influence of antibiotics on host defense mechanisms is important because of the increasing number of compromised hosts in whom even a marginal influence on the host response may have a significant effect of the outcome. The influence of antibiotics on host/bacterial interaction reveals subtle effects on the ultrastructure of the bacterial cell, the biosynthesis of various virulence factors, the ability of microorganisms to adhere to epithelial cells and the function of polymorphonuclear leukocytes and the immune-specific response of mononuclear cells. These effects permit the proposal that at least some of the subtle effects of antibiotics on microbial pathogenicity might take place in vivo. If antibiotics can be shown definitely to enhance host-defense mechanisms, especially in compromised hosts, then more effective antibiotic therapy can be provided for these indications. Finally if antibiotics can modify the outcome of host-parasite interactions then perhaps we need to consider testing antibiotics against these parameters.

Animals↗
PubMed2001

Changes in subgingival microflora and humoral immune response following periodontal therapy.

OBJECTIVES: To investigate the effect of scaling and root planing (SRP) on the microflora and humoral immune response in adult periodontitis. MATERIALS & METHODS: Clinical measurements, subgingival plaque samples, gingival crevicular fluid and sera were taken from 4 sites in 28 adult periodontitis patients before and after SRP. Polymerase chain reaction was used to determine the presence of A. actinomycetemcomitans, P. gingivalis, B. forsythus, P. intermedia, and T. denticola. ELISA was used to investigate the systemic and local antibody titres to these organisms, and thiocyanate dissociation for the determination of serum antibody avidity. RESULTS: SRP produced a good clinical improvement. On a subject basis there was little significant change in the microflora. However, on a site basis, there were significant reductions in P. intermedia, B. forsythus and T. denticola. There was little change in systemic and local antibody titres following SRP, although there was a significant reduction in antibody avidity to P. gingivalis and P. intermedia CONCLUSION: Post-therapy clinical improvement was associated with a reduction in bacterial prevalence, but statistical significance was only reached at a site level and this microbial reduction was not significant for all organisms. No significant post-therapy effects on the humoral immune response were noted other than a reduced antibody avidity to P. gingivalis and P. intermedia. The lack of a clear pattern in the humoral immune response may reflect a failure of the host response to produce adequate levels of biologically functional antibodies, and complex interactions between the subgingival flora and the host response.

Adult↗
PubMed2025

The ecology and evolution of microbial immune systems: a look on the wild vibrio side.

Natural populations of vibrio beyond the well-studied pandemic strains of Vibrio cholerae, provide a powerful model for investigating the eco-evolutionary dynamics of microbial immune systems. Their genetic diversity, ecological versatility, ease of culturability and the availability of time-series data enable detailed studies of phage-host interactions in natural contexts. This review synthesizes recent advances in vibriophage research, highlighting key findings and emerging tools. High-throughput assays and genomic tools have offered new perspectives on phage specificity, host range and the evolutionary pressures shaping these interactions. Theoretical frameworks, such as arms race and fluctuating selection dynamics, are informed by empirical data from vibrio-phage systems, with time-series sampling providing crucial insights into their temporal and spatial dynamics. A major finding is the role of mobile genetic elements (MGEs) in encoding bacterial defence systems, which shape phage-host coevolution. Discoveries like the phage satellite PICMI illustrate how MGEs facilitate the transfer of antiviral systems, influencing ecological and evolutionary dynamics. The paradox of generalist vibriophages, rare despite their broad host ranges, is also explored. By integrating experimental approaches with field observations, vibriophage research advances microbial ecology and informs sustainable applications in aquaculture and phage therapy, reinforcing vibrios as a versatile model system.This article is part of the discussion meeting issue 'The ecology and evolution of bacterial immune systems'.

Bacteriophages↗
PubMed2005

Fermented functional foods based on probiotics and their biogenic metabolites.

The claimed health benefits of fermented functional foods are expressed either directly through the interaction of ingested live microorganisms, bacteria or yeast with the host (probiotic effect) or indirectly as a result of ingestion of microbial metabolites produced during the fermentation process (biogenic effect). Although still far from fully understood, several probiotic mechanisms of action have been proposed, including competitive exclusion, competition for nutrients and/or stimulation of an immune response. The biogenic properties of fermented functional foods result from the microbial production of bioactive metabolites such as certain vitamins, bioactive peptides, organic acids or fatty acids during fermentation.

Animals↗
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↗