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At least 217 records · Page 12Linked to original sources
PubMed2026

Friends or foes: Unraveling the tsetse fly-Spiroplasma symbiosis.

Tsetse flies (Glossina spp.) transmit African trypanosomes, the causative agents of human African and African animal trypanosomiases (HAT and AAT, respectively). These neglected tropical diseases impose significant public health and economic burdens across sub-Saharan Africa. Trypanosome transmission by tsetse flies is influenced by multiple factors, including host genetic background, ecological factors, and interactions with heritable microbial endosymbionts. Spiroplasma glossinidia has recently emerged as an important modulator of tsetse reproductive fitness and vector competence, making it a potential target for symbiont-based vector control strategies. In this review, we summarize the current knowledge of the tsetse-Spiroplasma symbiosis. We detail Spiroplasma's spatial and temporal infection dynamics in laboratory-reared and natural populations. Additionally, we highlight key aspects of the bacterium's genomics, phylogenetics, and physiological interactions with its tsetse host, including influences on host gene expression reproductive physiology, and vector competence. Finally, we discuss how the tsetse-Spiroplasma symbiosis could be harnessed to develop innovative, biological-based vector control and trypanosome transmission-blocking strategies, and we identify critical gaps that must be addressed to translate these findings into effective disease control interventions.

Animals↗
PubMed2004

Microbial-gut interactions in health and disease. Epithelial cell responses.

Intestinal epithelial cells are unique in that they represent the only host cells that are constantly interacting with a very large bacterial population in the lumen. The single monolayer of epithelial cells consists of subpopulations with distinct functions that include protection against luminal microorganisms. Although the microbial flora remains to be fully characterized, its normal relationship with the host intestinal epithelial cells appears to be predominantly symbiotic or commensal. The molecular complexity of the epithelial-microbial relationship has been shown in studies that have examined the establishment of the resident bacteria in germ-free mice. Recent work has also demonstrated the ability of resident bacteria to enhance epithelial protective responses. The mechanisms by which epithelial cells may avoid pro-inflammatory responses to resident microorganisms, while retaining the capacity to respond to pathogens, are also being characterized.

Enterobacteriaceae↗
PubMed2004

Microbes and their products--physiological effects upon mammalian mucosa.

A dynamic array of interactions occurs between pathogens and host mucosal surfaces. The signature molecules unique to microbial pathogens allow the mammalian immune system to recognize them as non-self. This recognition, mediated by the toll-like receptor proteins, results in innate immune responses targeted against the invading organism. Pathogens also elaborate a variety of proteins that actively engage host signaling pathways and subvert them to facilitate their growth and dispersal. These interactions, developed over a long evolutionary period, have been specialized to exquisite detail. These proteins and toxins are either secreted into the medium or directly delivered into host cells by specialized secretion systems. An array of host function alterations is mediated by microbial pathogens including inflammatory responses, secretory responses, alteration of host cytoskeleton, disruption of epithelial tight junctions and apoptosis. The signaling axes involved in these interactions are potential targets for therapeutic strategies against infectious microbes.

Animals↗
PubMed2006

Bacteriophage migration via nematode vectors: host-parasite-consumer interactions in laboratory microcosms.

Pathogens vectored by nematodes pose serious agricultural, economic, and health threats; however, little is known of the ecological and evolutionary aspects of pathogen transmission by nematodes. Here we describe a novel model system with two trophic levels, bacteriophages and nematodes, each of which competes for bacteria. We demonstrate for the first time that nematodes are capable of transmitting phages between spatially distinct patches of bacteria. This model system has considerable advantages, including the ease of maintenance and manipulation at the laboratory bench, the ability to observe many generations in short periods, and the capacity to freeze evolved strains for later comparison to their ancestors. More generally, experimental studies of complex multispecies interactions, host-pathogen coevolution, disease dynamics, and the evolution of virulence may benefit from this model system because current models (e.g., chickens, mosquitoes, and malaria parasites) are costly to maintain, are difficult to manipulate, and require considerable space. Our initial explorations centered on independently assessing the impacts of nematode, bacterium, and phage population densities on virus migration between host patches. Our results indicated that virus transmission increases with worm density and host bacterial abundance; however, transmission decreases with initial phage abundance, perhaps because viruses eliminate available hosts before migration can occur. We discuss the microbial growth dynamics that underlie these results, suggest mechanistic explanations for nematode transmission of phages, and propose intriguing possibilities for future research.

Animals↗
PubMed2003

Characterization of mediators of microbial virulence and innate immunity using the Caenorhabditis elegans host-pathogen model.

The soil-borne nematode, Caenorhabditis elegans, is emerging as a versatile model in which to study host-pathogen interactions. The worm model has shown to be particularly effective in elucidating both microbial and animal genes involved in toxin-mediated killing. In addition, recent work on worm infection by a variety of bacterial pathogens has shown that a number of virulence regulatory genes mediate worm susceptibility. Many of these regulatory genes, including the PhoP/Q two-component regulators in Salmonella and LasR in Pseudomonas aeruginosa, have also been implicated in mammalian models suggesting that findings in the worm model will be relevant to other systems. In keeping with this concept, experiments aimed at identifying host innate immunity genes have also implicated pathways that have been suggested to play a role in plants and animals, such as the p38 MAP kinase pathway. Despite rapid forward progress using this model, much work remains to be done including the design of more sensitive methods to find effector molecules and further characterization of the exact interaction between invading pathogens and C. elegans' cellular components.

Animals↗
PubMed1995

Entry of microbes into the host: using M cells to break the mucosal barrier.

Enteric microbial pathogens interact with the gut epithelium to establish infection. Recently, it has become clear that many microorganisms that colonize or traverse the intestinal mucosa do so via the specialized M cells. Recent work has shown that Shigella flexneri and Salmonella typhimurium specifically target M cells to initiate infection of the host.

Animals↗
PubMed1995

Direct antimicrobial activity of T cells.

T cells are generally thought to contribute to antimicrobial activity either by releasing lymphokines, which recruit and activate other cell types, or by major histocompatibility complex (MHC)-restricted lysis of infected host cells. Recently, it has become apparent that T cells can also mediate antimicrobial activity by direct interaction with microbial targets. Such interactions, which can be either antigen specific or nonspecific, occur in the apparent absence of MHC restriction and do not require the presence of other host cells. Microbial targets recognized by T cells include fungi, parasites and bacteria. Here, Stuart Levitz, Herbert Mathews and Juneann Murphy discuss the direct antimicrobial activity of T cells and speculate on its in vivo relevance.

Animals↗
PubMed1994

Bacterial symbionts induce host organ morphogenesis during early postembryonic development of the squid Euprymna scolopes.

The mutualistic association between the squid Euprymna scolopes and the bacterium Vibrio fischeri is an emerging experimental system for the study of the influence of bacteria on animal development. Taking advantage of the ability to raise both this host and its microbial partner independently under laboratory conditions, we describe the effects of bacterial interactions on morphogenesis of the juvenile host symbiotic organ. Our results show that bacteria are essential for normal postembryonic development of the symbiotic organ, which involves changes in both the surface epithelium and the epithelial tissue within the organ where the bacterial culture will take up residence. Cell death induced by exposure to symbiotic V. fischeri results in the regression of a complex ciliated surface epithelium, a tissue that apparently functions to facilitate inoculation of the juvenile organ with the appropriate specific bacterial species. Regression of this tissue begins within hours of exposure to symbiosis-competent bacteria and progresses over the next 5 days, at which time full regression is complete, resulting in a symbiotic organ whose epithelial surface resembles that of the fully mature organ. Moreover, symbiosis-competent bacteria induce modification of the epithelial cells of the crypts that will house these symbionts; these cells undergo significant changes in shape and size in response to interactions with symbiotic V. fischeri. In contrast, we find that when these tissues are not exposed to the proper bacterial symbionts they remain in a state of arrested morphogenesis, a condition that can be rescued by interactions with symbionts. The results of these studies are the first experimental data demonstrating that a specific bacterial symbiont can play an inductive role in animal development.

Animals↗
PubMed2006

Host-pathogen systems biology.

Unlike traditional biological research that focuses on a small set of components, systems biology studies the complex interactions between a large number of genes, proteins and other elements of biological networks and systems. Host-pathogen systems biology examines the interactions between the components of two distinct organisms, either a microbial or viral pathogen and its animal host or two different microbial species in a community. With the availability of complete genomic sequences of various hosts and pathogens, together with breakthroughs in proteomics, metabolomics and other experimental areas, the investigation of host-pathogen systems on a multitude of levels of detail has come within reach.

Animals↗
PubMed2006

The anti-microbial peptide LL-37 inhibits the activation of dendritic cells by TLR ligands.

The endogenous anti-microbial peptide LL-37/hCAP-18 is an effector molecule of the innate host defense system at surfaces of the body. Besides its direct anti-microbial activity, the peptide interacts with different cell types. Dendritic cells (DCs) play a central role in mucosal host defense. It was the aim of the study to determine whether LL-37 modulates the response of DCs to pathogen-associated molecular patterns. Monocyte-derived DCs were stimulated with the Toll-like receptors (TLRs) ligands LPS, lipoteichoic acid and flagellin. We measured classical markers of DC maturation and assayed the ability of the DCs to activate T cell responses. Co-incubation with LL-37 resulted in suppressed activation of DCs. Levels of released IL-6, IL-12p70 and TNF-alpha and surface expression of HLA-DR, CD80, CD83, CD86 and the chemokine receptor CCR7 were decreased. Exposure of DCs to LL-37 during LPS exposure induced co-cultured naive T cells to produce less IL-2 and IFN-gamma and decreased their proliferation. The response of memory T cells to a recall antigen was also decreased. In conclusion, we demonstrate that the anti-microbial peptide LL-37 inhibits the activation of DCs by TLR ligands. We propose that LL-37 is a regulator of host defense responses at the intersection of innate and adaptive immune systems.

Amino Acid Sequence↗
PubMed1998

Homoserine lactone-mediated gene regulation in plant-associated bacteria.

Many plant-associated bacteria produce and utilize diffusible N-acyl-homoserine lactones (AHLs) to regulate the expression of specific bacterial genes and operons. AHL-mediated regulation utilizes two genes that encode proteins similar to the LuxI/LuxR system originally studied in the marine symbiont Vibrio fischeri. The LuxI-type proteins are AHL synthases that assemble the diffusible AHL signal. The LuxR-type proteins are AHL-responsive transcriptional regulatory proteins. LuxR proteins control the transcription of specific bacterial genes in response to the levels of AHL signal. To date, AHL-mediated gene regulation has been identified in a broad range of gram-negative bacteria, most of which are host-associated. However, it seems unlikely that such a widely conserved regulatory mechanism would be limited only to host-microbe interactions. These signals probably play central roles in ecological interactions among organisms in microbial communities by affecting communication among bacterial populations as well as between bacterial populations and their eukaryotic hosts.

Journal Article↗
PubMed1985

The urethral catheter--a review of its implication in urinary-tract infection.

The research into acquisition of urinary-tract infection over the last few decades has established three ways in which organisms may gain access to the urinary tract of the catheterized patients: Firstly, during the process of passing the catheter into the bladder should complete asepsis not be observed; secondly by travelling along the urethra in the small, fluid-filled cavity between catheter and mucosa; Thirdly following contamination of the drainage system, along the inside of the catheter directly into the bladder. The relative importance of each route is not clear and is still the subject of much controversy but it would seem that all these routes have a part to play in allowing infection to develop. The risk of catheterized patients acquiring urinary-tract infection is so great that where possible catheterization should be avoided. The most important preventive measure which may be taken is to limit the duration of indwelling catheterization. In addition, a considerable amount of research has attempted to distinguish other factors which might affect the rate at which urinary-tract infection in the catheterized patient becomes established so that high-risk patients may be identified. The evidence indicates that the risk increases with duration of catheterization, age, length of hospital stay, immunosuppressant treatment, that it is greater in female than male patients and that a patient with a serious or fatal underlying disease is also more likely to develop bacteriuria. Finally, properties of the urine and the host defence mechanisms may affect the susceptibility of the individual to urinary-tract infection. Identification of the routes of infection and patients at risk is only part of the problem. The next stage is to formulate criteria for the care of catheterized patients which reduce the risk of infection to the absolute minimum and will hopefully go some way towards diminishing the unsatisfactory high levels of urinary-tract infection that are currently associated with indwelling catheterization.

Age Factors↗
PubMed1989

The beige mouse model for Mycobacterium avium complex (MAC) disease: optimal conditions for the host and parasite.

We extended our earlier studies to establish the beige (C57B1/6/bgJ/bgJ) mouse model for experimental acute infections with Mycobacterium avium complex (MAC). Optimal conditions of the host and the parasites have been determined. Mice bred at our center showed similar responses to those obtained from Jackson Laboratories, the original supplier. Both male and female mice showed similar responses, but older mice in both sexes showed less susceptibility than younger mice. Strain 101 of MAC showed remarkable consistency in its pathogenicity to beige mice, as evidenced by the distribution of colony forming unit (CFU) counts at various time points after intravenous challenge, in several experiments. CFU counts showed an association with the dose of challenge, and histopathological observations.

Animals↗
PubMed1988

Antigenicity and immunogenicity of Hypoderma lineatum soluble proteins in the bovine host.

Protein species found in soluble crude extracts of Hypoderma lineatum (common cattle grub) 1st-instar larvae (HL1) were separated by non-denaturing and denaturing polyacrylamide gel electrophoresis (PAGE) and analyzed for antigenicity by Western blotting using serum from H. lineatum-infested and vaccinated cattle. All HL1 proteins resolved by non-denaturing PAGE were found to be antigenic in the infested bovine host. Treatment of the proteins with sodium dodecyl sulfate and 2-mercaptoethanol destroyed the ability of hypodermin B and the Peak 2 proteins from DEAE-ion exchange HPLC to be bound by antibody. The principal proteins, hypodermin A and hypodermin C (collagenase), appear to be the most immunogenic of the larval proteins. Although having similar amino acid composition, hypodermin A did not appear to share an antigenic epitope with the most prevalent protein, hypodermin C. These results may allow for the selection of proteins to be used in vaccine trials and studies of protective immunological mechanisms associated with acquired resistance to H. lineatum infestation in the bovine host.

Animals↗
PubMed1994

Binding and internalization of microorganisms by integrin receptors.

Many microbial pathogens bind host-cell integrin receptors. These interactions are promoted either by a host protein binding the microorganism or by a surface-localized ligand encoded by the pathogen. Attachment facilitates extracellular adhesion of the microorganism or internalization by the host cell.

Amino Acid Sequence↗
PubMed2002

The role of parasites in sympatric and allopatric host diversification.

Exploiters (parasites and predators) are thought to play a significant role in diversification, and ultimately speciation, of their hosts or prey. Exploiters may drive sympatric (within-population) diversification if there are a variety of exploiter-resistance strategies or fitness costs associated with exploiter resistance. Exploiters may also drive allopatric (between-population) diversification by creating different selection pressures and increasing the rate of random divergence. We examined the effect of a virulent viral parasite (phage) on the diversification of the bacterium Pseudomonas fluorescens in spatially structured microcosms. Here we show that in the absence of phages, bacteria rapidly diversified into spatial niche specialists with similar patterns of diversity across replicate populations. In the presence of phages, sympatric diversity was greatly reduced, as a result of phage-imposed reductions in host density decreasing competition for resources. In contrast, allopatric diversity was greatly increased as a result of phage-imposed selection for resistance, which caused populations to follow divergent evolutionary trajectories. These results show that exploiters can drive diversification between populations, but may inhibit diversification within populations by opposing diversifying selection that arises from resource competition.

Animals↗
PubMed1997

Inactivation of Streptococcus pyogenes extracellular cysteine protease significantly decreases mouse lethality of serotype M3 and M49 strains.

Cysteine proteases have been implicated as important virulence factors in a wide range of prokaryotic and eukaryotic pathogens, but little direct evidence has been presented to support this notion. Virtually all strains of the human bacterial pathogen Streptococcus pyogenes express a highly conserved extracellular cysteine protease known as streptococcal pyrogenic exotoxin B (SpeB). Two sets of isogenic strains deficient in SpeB cysteine protease activity were constructed by integrational mutagenesis using nonreplicating recombinant plasmids containing a truncated segment of the speB gene. Immunoblot analyses and enzyme assays confirmed that the mutant derivatives were deficient in expression of enzymatically active SpeB cysteine protease. To test the hypothesis that the cysteine protease participates in host mortality, we assessed the ability of serotype M3 and M49 wild-type strains and isogenic protease-negative mutants to cause death in outbred mice after intraperitoneal inoculation. Compared to wild-type parental organisms, the serotype M3 speB mutant lost virtually all ability to cause mouse death (P < 0.00001), and similarly, the virulence of the M49 mutant was detrimentally altered (P < 0.005). The data unambiguously demonstrate that the streptococcal enzyme is a virulence factor, and thereby provide additional evidence that microbial cysteine proteases are critical in host-pathogen interactions.

Animals↗