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PubMed1990

Analysis of factors which determine the existence of Yersinia pseudotuberculosis in a saprophytic phase.

Data are presented on the effects of a variety of abiotic and biotic environmental factors on the existence and changes in the numbers of Y. pseudotuberculosis. Experiments with sterile soil showed that Y. pseudotuberculosis populations were resistant over a wide range of major abiotic factors: temperature (0-30 degrees C), humidity (15-50%), pH (5.9-9.0). Although exerting some effect on the duration of different growth phases, the above abiotic factors did not influence, within the tested range, the general nature of populational dynamics of the microbe. Comparative experiments carried out in sterile and natural soil specimens using an RNA-polymerase mutant warranted the conclusion that the numbers of Y. pseudotuberculosis in soil (water) are largely controlled by the biotic components of ecosystems, including microflora and microfauna. Y. pseudotuberculosis was shown to exist in the environment (vegetable storehouses and substrate of rodent nests) in association with bacteria belonging to the family Enterobacteriaceae as well as the genera Acinetobacter and Pseudomonas. Endosymbiotic relationships are described between Y. pseudotuberculosis and the free-living infusorian Tetrahymena pyriformis which sustains microbial populations in the soil (water).

Animals↗

PubMed1997

Selective cytotoxicity of dermaseptin S3 toward intraerythrocytic Plasmodium falciparum and the underlying molecular basis.

The antimicrobial activity of various naturally occurring microbicidal peptides was reported to result from their interaction with microbial membrane. In this study, we investigated the cytotoxicity of the hemolytic peptide dermaseptin S4 (DS4) and the nonhemolytic peptide dermaseptin S3 (DS3) toward human erythrocytes infected by the malaria parasite Plasmodium falciparum. Both DS4 and DS3 inhibited the parasite's ability to incorporate [3H]hypoxanthine. However, while DS4 was toxic toward both the parasite and the host erythrocyte, DS3 was toxic only toward the intraerythrocytic parasite. To gain insight into the mechanism of this selective cytotoxicity, we labeled the peptides with fluorescent probes and investigated their organization in solution and in membranes. In Plasmodium-infected cells, rhodamine-labeled peptides interacted directly with the intracellular parasite, in contrast to noninfected cells, where the peptides remained bound to the erythrocyte plasma membrane. Binding experiments to phospholipid membranes revealed that DS3 and DS4 had similar binding characteristics. Membrane permeation studies indicated that the peptides were equally potent in permeating phosphatidylserine/phosphatidylcholine vesicles, whereas DS4 was more permeative with phosphatidylcholine vesicles. In aqueous solutions, DS4 was found to be in a higher aggregation state. Nevertheless, both DS3 and DS4 spontaneously dissociated to monomers upon interaction with vesicles, albeit with different kinetics. In light of these results, we propose a mechanism by which dermaseptins permeate cells and affect intraerythrocytic parasites.

Amino Acid Sequence↗

PubMed2005

Biosynthesis, processing, and sorting of human myeloperoxidase.

Exclusively synthesized by normal neutrophil and monocyte precursor cells, myeloperoxidase (MPO) functions not only in host defense by mediating efficient microbial killing but also can contribute to progressive tissue damage in chronic inflammatory states such as atherosclerosis. The biosynthetic precursor, apoproMPO, is processed slowly in the ER, undergoing cotranslational N-glycosylation, transient interactions with the molecular chaperones calreticulin and calnexin, and heme incorporation to generate enzymatically active proMPO that is competent for export into the Golgi. After exiting the Golgi the propeptide is removed prior to final proteolytic processing in azurophil granules, resulting in formation of a symmetric MPO homodimer linked by a disulfide bond. Some proMPO escapes granule targeting and becomes constitutively secreted to the extracellular environment. Although the precise mechanism is unknown, the pro-segment is required for normal processing and targeting, as propeptide-deleted MPO precursor is either degraded or constitutively secreted. Characterizing the molecular consequences of naturally occurring mutations that cause inherited MPO deficiency provides unique insight into the structural determinants of MPO involved in biosynthesis, processing and targeting.

Gene Expression Regulation, Enzymologic↗

PubMed2005

Mycobacterium tuberculosis as viewed through a computer.

Mathematical models are emerging as important tools in the study of microbiology. As an illustrative example, we present results from several models each generated to study the interaction of Mycobacterium tuberculosis and the immune system. Different mathematical models were formulated on the basis of assumptions regarding system-component interactions, enabling us to explore specific aspects at diverse biological scales (e.g. intracellular, cell-cell interactions, and cell population dynamics). In addition, we were able to examine both temporal and spatial aspects. At each scale, there were consistent themes that emerged as determinative in infection outcome. Factors we identified include both host and microbial characteristics. The use of the models lies in generating hypotheses that can then be tested experimentally. Here, we outline the primary host and bacterial factors that we have identified as key mechanisms that contribute to the success of M. tuberculosis as a human pathogen. Our goal is to stimulate experimentation and foster collaborations between theoretical and experimental scientists.

Animals↗

PubMed2004

The glycan-rich outer layer of the cell wall of Mycobacterium tuberculosis acts as an antiphagocytic capsule limiting the association of the bacterium with macrophages.

Mycobacterium tuberculosis, the causative agent of tuberculosis, is a facultative intracellular pathogen that infects macrophages and other host cells. We show that sonication of M. tuberculosis results in the removal of material from the surface capsule-like layer of the bacteria, resulting in an enhanced propensity of the bacteria to bind to macrophages. This effect is observed with disparate murine and human macrophage populations though, interestingly, not with freshly explanted alveolar macrophages. Enhanced binding to macrophages following sonication is significantly greater within members of the M. tuberculosis family (pathogens) than within the Mycobacterium avium complex (opportunistic pathogens) or for Mycobacterium smegmatis (saprophyte). Sonication does not affect the viability or the surface hydrophobicity of M. tuberculosis but does result in changes in surface charge and in the binding of mannose-specific lectins to the bacterial surface. The increased binding of sonicated M. tuberculosis was not mediated through complement receptor 3. These results provide evidence that the surface capsule on members of the M. tuberculosis family may be an important virulence factor involved in the survival of M. tuberculosis in the mammalian host. They also question the view that M. tuberculosis is readily ingested by any macrophage it encounters and support the contention that M. tuberculosis, like many other microbial pathogens, has an antiphagocytic capsule that limits and controls the interaction of the bacterium with macrophages.

Animals↗

PubMed2004

Salivary statherin peptide-binding epitopes of commensal and potentially infectious Actinomyces spp. delineated by a hybrid peptide construct.

Adhesion of microorganisms to host receptor molecules such as salivary statherin molecules is a common event in oral microbial colonization. Here we used a hybrid peptide construct (with both a hydroxyapatite-binding portion and a test peptide portion) to map the interaction of Actinomyces species (and Candida albicans) with statherin. Adhesion to hybrid peptides and truncated statherin variants revealed three binding types, types I to III. (i) Type I strains of rat, hamster, and human infection origins bound C-terminal-derived QQYTF and PYQPQY peptides. The QQYTF peptide inhibited statherin binding for some strains but not for others. (ii) Type II strains of human and monkey tooth origins bound middle-region-derived YQPVPE and QPLYPQ peptides. Neither strain was inhibited by soluble peptides. (iii) Type III strains of human infection origins (and C. albicans) did not bind to either statherin-derived peptides or truncated statherin. Moreover, the type I strains inhibited by QQYTF were also inhibited by TF and QAATF peptides and were detached from statherin by the same peptides. In conclusion, it is suggested that commensal and potentially infectious microorganisms bind middle or C-terminal statherin differently and that other microbes might require discontinuous epitopes.

Actinomyces↗

PubMed2006

Dendritic cells in pathogen recognition and induction of immune responses: a functional genomics approach.

At the 38th Annual Meeting of the Society for Leukocyte Biology held in Oxford this year, the biology of dendritic cells (DCs) and macrophages was discussed. In particular, functional genomics approaches were presented to investigate transcriptional changes during microbe and phagocytes interactions. Here, we report functional genomics studies likely to be of interest to the Journal of Leukocyte Biology readers with a particular emphasis on DC biology. DCs are professional antigen-presenting cells, which are essential for the initiation and regulation of natural killer, T, and T regulatory cell responses. Immature DCs, resident in peripheral sites, are specialized in antigen capture and continually sample soluble and particulate antigens in their local environment. DCs express receptors for cytokines, chemokines, endogenous danger signals, and microbial structures. The interactions between DCs and microorganism are complex, but progress in the past few years has shed light on several aspects of these processes. Infectious disease is the result of an intimate relationship between pathogens and hosts. Thus, understanding the cross-talk between host and pathogen is essential to improve our knowledge of infectious disease. Functional genomics and proteomics applied to DCs and macrophage biology are now providing powerful tools to dissect, at the molecular level, host-pathogen interactions.

Animals↗

PubMedDate not supplied

Are biological antagonists an alternative to synthetic fungicides for preventing postharvest diseases of fruits and vegetables?

In recent years, both the public and health authorities have become increasingly concerned about the presence of pesticides in our food supply and the environment. As a direct result of this mounting concern, research efforts for the development of alternative methods for the control of postharvest diseases of fruits and vegetables have been intensified. Considerable attention has been placed on assessing the potential of the use of biological antagonists as a viable alternative to the use of synthetic fungicides. Naturally occurring microbial antagonists have been shown to control several rot pathogens on diverse commodities. Such antagonists have various modes of action: antibiosis or competition for nutrients and space or both, induction of resistance in the host tissue, and direct interaction with the pathogen. The commercialization of certain antagonists to control postharvest decay of fruits and vegetables appears to be feasible and may present an alternative to synthetic pesticides.

Agriculture↗

PubMed2002

Genetically modified Streptococcus mutans for the prevention of dental caries.

There are many examples of positive and negative interactions between different species of bacteria inhabiting the same ecosystem. This observation provides the basis for a novel approach to preventing microbial diseases called replacement therapy. In this approach, a harmless effector strain is permanently implanted in the host's microflora. Once established, the presence of the effector strain prevents the colonization or outgrowth of a particular pathogen. In the case of dental caries, replacement therapy has involved construction of an effector strain called BCS3-L1, which was derived from a clinical Streptococcus mutans isolate. Recombinant DNA technology was used to delete the gene encoding lactate dehydrogenase in BCS3-L1 making it entirely deficient in lactic acid production. This effector strain was also designed to produce elevated amounts of a novel peptide antibiotic called mutacin 1140 that gives it a strong selective advantage over most other strains of S. mutans. In laboratory and rodent model studies, BCS3-L1 was found to be genetically stable and to produce no apparent deleterious side effects during prolonged colonization. BCS3-L1 was significantly less cariogenic than wild-type S. mutans in gnotobiotic rats, and it did not contribute at all to the cariogenic potential of the indigenous flora of conventional Sprague-Dawley rats. And, its strong colonization properties indicated that a single application of the BCS3-L1 effector strain to human subjects should result in its permanent implantation and displacement over time of indigenous, disease-causing S. mutans strains. Thus, BCS3-L1 replacement therapy for the prevention of dental caries is an example of biofilm engineering that offers the potential for a highly efficient, cost effective augmentation of conventional prevention strategies. It is hoped that the eventual success of replacement therapy for the prevention of dental caries will stimulate the use of this approach in the prevention of other bacterial diseases.

Dental Caries↗

PubMed2006

Brucella spp noncanonical LPS: structure, biosynthesis, and interaction with host immune system.

Brucella spp. are facultative intracellular pathogens that have the ability to survive and multiply in professional and non-professional phagocytes, and cause abortion in domestic animals and undulant fever in humans. Several species are recognized within the genus Brucella and this classification is mainly based on the difference in pathogenicity and in host preference. Brucella strains may occur as either smooth or rough, expressing smooth LPS (S-LPS) or rough LPS (R-LPS) as major surface antigen. This bacterium possesses an unconventional non-endotoxic lipopolysaccharide that confers resistance to anti-microbial attacks and modulates the host immune response. The strains that are pathogenic for humans (B. abortus, B. suis, B. melitensis) carry a smooth LPS involved in the virulence of these bacteria. The LPS O-chain protects the bacteria from cellular cationic peptides, oxygen metabolites and complement-mediated lysis and it is a key molecule for Brucella survival and replication in the host. Here, we review i) Brucella LPS structure; ii) Brucella genome, iii) genes involved in LPS biosynthesis; iv) the interaction between LPS and innate immunity.

Journal Article↗

PubMed1998

Bacterial arthritis due to beta-hemolytic streptococci of serogroups A, B, C, F, and G. Analysis of 23 cases and a review of the literature.

The clinical features, essential laboratory findings, management, and outcome of all 23 cases of septic arthritis caused by different serogroups of beta-hemolytic streptococcus (BHS) seen at the Stanford Medical Center, Stanford, CA, from July 1, 1985, through October 31, 1996, were reviewed and compared to those found in the literature. Group A streptococci (GAS) accounted for 9 (40%) of our cases; group B (GBS), for 7 (30%); and Group G (GGS), for 7 (30%). No cases were caused by Group C (GCS) or F (GFS) during this period. During the same period, GAS accounted for 66 (33%) of 200 cases of bacteremia due to BHS, GBS, for 98 (49%); GCS, for 12 (6%); GFS, for 4 (2%); and GGS, for 20 (10%). A review of potential risk factors revealed that, with the exception of GGS, male and female patients were almost equally distributed among each of the serogroups. Patients aged 50 years and older comprised 56%-77% of each group. Associated conditions and risk factors were present among most patients (19/23, 83%); autoimmune diseases and a chronic skin wound or trauma were notably present among patients with GAS, while diabetes mellitus and malignancy were more common among patients with GBS. Infected prosthetic implants were present in 7 patients, including 4/7 patients with GGS. All patients had positive cultures of synovial fluid, and 11/23 (49%) had positive blood cultures (GAS, 5/9; GBS, 6/7; and GGS, 0/7). The clinical presentation and hospital course of patients infected with the different serogroups varied. Patients infected with GAS had the most severe disease and those with GGS the least severe. Necrotizing fascitis, shock, DIC, and admission to the intensive care unit were found only among patients infected with GAS. Despite aggressive management with antimicrobial therapy and surgery, 4/23 patients died (3 patients with GAS; 1 with GBS). The isolates from our patients were not available for study; investigations by others of the biology of BHS suggest that the production of 1 or more of the streptococcal pyrogenic exotoxins by isolates of GAS may account for the differences in the severity of disease among our patients with septic arthritis caused by different serogroups of BHS. Although septic arthritis due to BHS is uncommon, such patients provide a valuable model to study features of the host-parasite interaction that may contribute to the observed differences in severity of disease.

Adult↗

PubMed1992

Considerations in dosage selection for third generation cephalosporins.

Pharmacokinetic parameters of third generation cephalosporins vary widely, requiring different dosage regimens and adjustment methods for each agent. Although their antibacterial spectrum favours their usage in infections caused by aerobic Gram-negative organisms, due to their limited post-antibiotic effect against these organisms, dosage regimens should ensure that free drug concentrations at the site of infection remain above the minimum inhibitory concentration for as much of the dosage interval as possible in patients with normal host defence mechanisms and for the entire dosage interval in immunocompromised patients. Altered protein binding encountered in various disease states can affect both microbiological and pharmacokinetic properties especially for drugs with high protein binding. Since the concentrations at the site of action are often different from those in serum, a higher or lower range of dosages needs to be selected depending on the target site. Decreased renal function affects the elimination of most third generation cephalosporins, whereas the presence of hepatic disease does not generally necessitate dosage adjustment. Because of the complex age-related physiological changes in paediatric and elderly patients, dosage should be adjusted on the basis of the reported pharmacokinetic data in these populations. The usual recommended dose may or may not be optimal in a given condition depending on the complex interactions between pharmacokinetic, microbiological and other host factors.

Acute Kidney Injury↗

PubMed1992

Cemented versus cementless hip arthroplasty. A review of prosthetic biocompatibility.

The fibrous interface tissue between hip prostheses and surrounding bone is often morphologically and functionally synovial-like. The fibroblast is the major cell type; but also giant cells and macrophages are present, and their numbers are increased in the occasional adverse-type host reaction to the prosthesis. Adverse lytic reactions are often associated with methylmethacrylate debris, whereas in cementless cases, polyethylene and metallic (titanium) wear debris seem to cause adverse reactions. Osteoblasts, osteoclasts, and mesenchymal collagenase secreted by fibroblasts and macrophages play an important role in the process of prosthetic loosening. Methylmethacrylate is immunologically relatively inert, while it induces inflammatory mononuclear-cell migration. Both cemented and cementless prostheses cause a foreign-body type host response, including adaptive and reactive processes. This response includes the formation of fibroblast-like B-type lining cells, which are able to synthesize and secrete hyaluronate. Material surfaces of hip arthroplasty components also provide a unique environmental niche to which staphylococcal strains adhere and colonize. Antibiotic resistance is related to the material colonized rather than to the presence of an exopolysaccharide barrier; organisms bound to polyethylene and methylmethacrylate are more resistant than organisms that are bound to stainless steel. An understanding of prosthetic biocompatibility requires an appreciation of tissue cell, bacterial cell and host defense-system response to biomaterials. The site of implantation is a stage on which the "players" (bacteria, host cells, and organic moieties) interact and compete, and before which the host is a "responsive audience."

Anti-Bacterial Agents↗

PubMedDate not supplied

[Persistence of pathogenic bacteria: theory and practice].

Persistence of pathogenic bacteria is viewed as a model of the parasite--host system. The variable signs of the pathogen and the host body, responsible for the mutual adaptation of the symbionts, are evaluated. The tactical ways of bacteria, enabling them to defend (isolate) their peptidoglycan from immune recognition by the host and thus ensuring the phenomenon of persistence, are presented. An attempt to assess the relationship between the persistence of bacteria ans their pathogenicity has been made. As noted in this study, the survival of bacteria inside host cells is determined by the expression of genes responsible for the adaptation of microorganisms to novel environmental conditions, ans the life of an infective agent adapted to the host is regarded as a series of steps of gene activation in response to the discrete complex of environmental conditions. Approaches to the solution of applied tasks in medicine, biology and ecology with the use of microbial persistence as the model of the parasite--host system is discussed.

Adaptation, Physiological↗

PubMed2003

Recognition of microbial infection by Toll-like receptors.

The Toll-like receptors (TLRs) of the innate immune system detect host invasion by pathogens and initiate immune responses. All of the TLRs use the adaptor MyD88 to transduce a signal; however, two newly identified signaling molecules, TIRAP and TRIF, interact with a subset of the TLRs, suggesting a signaling specificity that may be relevant to the type of infection. Activation of the TRIF pathway, for example, leads to the production of antiviral gene products via the transcription factor, IRF3. In vivo experiments in TLR-deficient mice underscore the importance of TLRs in overcoming infection.

Adaptor Proteins, Signal Transducing↗

PubMed1998

Plants under attack II.

In many diseases of plants there is a well defined genetic relationship between host and pathogen, the host possessing resistance genes and the pathogen possessing avirulence genes. Where these are cognate their products interact and trigger a variety of resistance responses, resulting in an incompatible interaction. Where they are not cognate the pathogen is not recognised and invades the host causing a compatible interaction. A few resistance genes and a larger number of avirulence genes have been cloned and this information has afforded us new perspectives of the recognition phenomenon itself and the means by which virulent pathogens avoid being recognised. Mechanisms of resistance range from preformed antimicrobial compounds to a series of components that are induced as a response to microbial challenge. Most of these induced reactions are preceded by and may be triggered by an oxidative burst which results in the cross-linking of cell wall proteins and also causes the death of one to several cells. This localized death of host cells, termed the hypersensitive response, provides an explanation for resistance to obligate parasites which require living host tissue but not for resistance to facultative parasites which colonise dying or dead tissue. However, the hypersensitive response appears to be intimately involved with several other defence responses such as the synthesis and accumulation of phytoalexins, lignification and the production of hydrolase enzymes that attack the invader. Salicylic acid has proved fundamental to the effecting of these defence responses and also to the phenomenon of systemic acquired resistance whereby a previous challenge from a pathogen induces the expression of enhanced resistance to a second challenge by the same or another organism. Despite these sophisticated defences plants still succumb to attack. Two of the weapons to which they are vulnerable and which are produced by many successful pathogens are toxins and enzymes. In some instances an understanding of these has pointed to novel methods of control supplementary to that obtained by conventional breeding for resistance.

Genes, Bacterial↗

PubMed2026

Probiotic Lacticaseibacillus casei 2S-1 Attenuates Escherichia coli-Induced Enteritis via Gut Microbiota Modulation and Host Gene Regulation.

Maintaining gut microbial homeostasis is crucial for host health, whereas infection with Escherichia coli (E. coli) is a major contributor to intestinal inflammation and microbial dysbiosis. Recent research has focused on probiotic strategies for managing enteric inflammatory disorders. Previous studies have shown that beneficial microorganisms show protection through modulating host immune responses, enhancing intestinal epithelial barrier integrity, and inhibiting pathogenic bacteria. To evaluate the prophylactic effectiveness of a recently isolated strain, Lacticaseibacillus casei 2S-1, in a murine model of E. coli-induced enteritis, this study focuses on interactions within the microbiota-intestinal-immune axis, together with host transcriptional responses and pathway enrichment associated with oxidative stress and mitochondrial function. In vitro analysis of probiotic features, including growth dynamics, acidogenic capacity, and tolerance to acidic and bile salt environments, as well as genetic safety profiling, followed the methodical isolation and taxonomic identification of L. casei 2S-1. A preventive intervention protocol was established, and a murine model of enteritis was induced by exposure to E. coli. Histopathological analyses were performed to observe in vivo safety and protective efficacy. Changes in gut microbial structure were characterized by 16S rRNA gene sequencing, while host responses were identified by intestinal immunohistochemistry and transcriptome profiling. L. casei 2S-1 showed probiotic properties. In vitro analyses showed that the strain exhibited tolerance to acidic and bile salt conditions, and its untreated culture supernatant showed antimicrobial activity against pathogenic bacteria. Its safety profile was supported by genomic analysis, which verified the lack of virulence-associated genes and antibiotic resistance factors. In vivo, L. casei 2S-1 pretreatment reduced mortality and intestinal inflammation, modulated gut microbial composition, and preserved intestinal barrier-associated protein expression in infected mice. This study provides experimental evidence supporting the prophylactic effects of L. casei 2S-1 and its associations with gut microbiota modulation and host transcriptional responses, providing a foundation for further investigation of probiotic-based preventive strategies against intestinal infections.

Animals↗

PubMed2005

Interplay of bacterial toxins with host defence: molecular mechanisms of immunomodulatory signalling.

Mucosal surfaces are protected by a first line of defence termed the innate immune system, which controls the resident microflora to effectively prevent microbial diseases. Inflammatory processes are activated as a consequence of a complex interplay between microbes and host target cells. Many bacterial pathogens have developed mechanisms to avoid host recognition. Some are even able to exploit the immune response through sophisticated interactions with the host signalling cascades in order to increase their replication and propagation. While in the past major emphasis on bacterial protein toxins was directed towards their cytotoxic role, it is increasingly evident that toxins can also modulate various cellular functions at non-cytolytic concentrations. Here, we review important aspects on the molecular mechanisms of immunomodulatory interference by bacterial toxins, with emphasis on the signalling induced in the intestinal epithelium.

Animals↗