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At least 631 records · Page 35Linked to original sources
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↗
PubMed1984

Changing patterns of resistance to new beta-lactam antibiotics. In vitro efficacy of cefoperazone against bacterial pathogens.

No evidence for significant increase in resistance to cefoperazone was detected in susceptibility test surveillance programs or in the literature through 1983, but rare endemic resistance to cefoperazone and some other newer beta-lactams was found. Medical centers contemplating the use of a third-generation drug for cost-containment should be aware of the susceptibility of isolates in their hospitals, and the drug's ability to withstand beta-lactamase hydrolysis by local pathogens. The possible dangers of inducible cephalosporins in certain Enterobacteriaceae and strains of Pseudomonas aeruginosa are discussed in the light of the physical and chemical characteristics of the newer antimicrobial agents. Criteria for judging the values of investigational beta-lactams are presented. These focus on the interaction of antimicrobial agents with host defense mechanisms and circulating blood elements.

Anti-Bacterial Agents↗
PubMed1996

The role of iron in plant host-pathogen interactions.

Iron is unlikely to be readily available in plant tissues for invading microorganisms. Soft rot, caused by Erwinia chrysanthemi strain 3937 on African violets, is a valuable model for studying the role of iron and its ligands in plant-pathogen interactions. These studies could lead to the development of new control strategies against microbial infections of plants.

Carbohydrate Sequence↗
PubMed1990

A rapid [3H]glycerol radioassay for determination of monocyte-mediated growth inhibition of Mycobacterium avium.

[3H]glycerol was used to radiolabel Mycobacterium avium (MA) bacteria after interaction with human monocytes in a rapid in vitro assay for determination of the growth inhibition of the mycobacteria by monocytes. Monocytes and MA were co-cultured in 96-well microtiter plates for 1-5 days, and [3H]glycerol was added for an additional 3 days of incubation to radiolabel residual bacteria. The results indicate that monocytes inhibited mycobacterial growth within 24 h of co-culture, an activity which increased during incubation until optimal growth inhibition was noted by 3-4 days. A comparison with conventional plate counting methodology demonstrated similar responses between the two assays except that the conventional assay required 2-3 weeks of culture before visible MA colonies could be detected and enumerated. Thus, the development of a rapid radiolabel assay to quantitate the interaction between monocytes and MA will facilitate the investigation of normal host responses to this opportunistic pathogen.

Colony Count, Microbial↗
PubMed2004

Bacterial sensitivity to bacteriophage in the aquatic environment.

There are several unusual features about phage when you first encounter them as a biologist. They are small, but conform to one of a few morphological types. Next their genomes can be composed of DNA or RNA and be single or double stranded. Finally they are numerically more abundant than prokaryotes and a significant proportion of them form an association in their microbial host populations termed lysogeny. The latter findings indicate that they are numerically significant in microbial populations. Since bacterial and phage abundance or lack of it is related in environments, this implies that the phage populations 'titrate' their hosts, and more probably the host's physiological status. Microbial populations wax and wane with nutritional inputs and there is a dynamic relationship between phage population sizes and host numbers and physiology. Overlay this with the different phage life cycle strategies, exemplified at the extremes by phage lambda (temperate) and phage T4 (virulent), then it becomes apparent that phage are a component in nutrient cycling in ecology. But their contribution does not stop there. Many are capable of transduction, moving DNA from one cell into another. So they can also aid the evolutionary progress of microbial populations by allowing them to share genes, just as gene exchange via plasmids and transformation does. Our perception of bacteria has been derived from pure culture studies and we are just being able to appreciate how subtle their ecological interactions are. This is no less true of the studies on bacteriophage, which are almost all based on laboratory experimentation, where the hosts are physiologically stressed by growing in 'high nutritional and optimum conditions'. The natural environment is naturally discontinuous and life evolved in this. Thus our perceptions of bacteriophage and their life cycle patterns derived from laboratory experimentation may be a little off the mark when we come to understand how they and their hosts interact in the niches available to them. It is worth just considering this as you read the article, as I suspect phage behaviours are more intimately involved in, and moderated by the physiological stresses in the life cycle of bacteria than we currently believe.

Bacteria↗
PubMed1994

Integration of antimicrobial host defenses: role of the bactericidal/permeability-increasing protein.

Our understanding of the complex and integrated host-defense systems against microbial infection has progressed rapidly with the characterization of individual components. However, the various factors must be studied not only in isolation, but also in a closer approximation to the in vivo situation, where these factors interact. This is well illustrated in recent studies of the role of the bactericidal/permeability-increasing protein.

Animals↗
PubMed2003

Molecular basis of phosphorylation-induced activation of the NADPH oxidase.

The multi-subunit NADPH oxidase complex plays a crucial role in host defense against microbial infection through the production of reactive oxygen species. Activation of the NADPH oxidase requires the targeting of a cytoplasmic p40-p47-p67(phox) complex to the membrane bound heterodimeric p22-gp91(phox) flavocytochrome. This interaction is prevented in the resting state due to an auto-inhibited conformation of p47(phox). The X-ray structure of the auto-inhibited form of p47(phox) reveals that tandem SH3 domains function together to maintain the cytoplasmic complex in an inactive form. Further structural and biochemical data show that phosphorylation of p47(phox) activates a molecular switch that relieves the inhibitory intramolecular interaction. This permits p47(phox) to interact with the cytoplasmic tail of p22(phox) and initiate formation of the active, membrane bound enzyme complex.

Amino Acid Sequence↗
PubMed2006

Defending against parasites: fungus-growing ants combine specialized behaviours and microbial symbionts to protect their fungus gardens.

Parasites influence host biology and population structure, and thus shape the evolution of their hosts. Parasites often accelerate the evolution of host defences, including direct defences such as evasion and sanitation and indirect defences such as the management of beneficial microbes that aid in the suppression or removal of pathogens. Fungus-growing ants are doubly burdened by parasites, needing to protect their crops as well as themselves from infection. We show that parasite removal from fungus gardens is more complex than previously realized. In response to infection of their fungal gardens by a specialized virulent parasite, ants gather and compress parasitic spores and hyphae in their infrabuccal pockets, then deposit the resulting pellet in piles near their gardens. We reveal that the ants' infrabuccal pocket functions as a specialized sterilization device, killing spores of the garden parasite Escovopsis. This is apparently achieved through a symbiotic association with actinomycetous bacteria in the infrabuccal pocket that produce antibiotics which inhibit Escovopsis. The use of the infrabuccal pocket as a receptacle to sequester Escovopsis, and as a location for antibiotic administration by the ants' bacterial mutualist, illustrates how the combination of behaviour and microbial symbionts can be a successful defence strategy for hosts.

Actinobacteria↗
PubMed1978

Ultrastructural basis for the assay of topical acne treatments. Transmission and scanning electron microscopy of untreated comedones.

After two decades of using systemic antibiotics as a main treatment for acne, emphasis is again being placed on topical agents. Thus, it is highly desirable to have a procedure whereby the activity of the various compounds can be evaluated by direct visualization. Scanning electron microscopy combined with transmission electron microscopy provide the tools for such in assay. This study describes the ultrastructure of untreated comedones and provides the baseline or control data necessary for testing topical treatments. Comedones obtained by punch biopsies or comedo extractors were processed for electron microscopy and studied with an ETEC Autoscan Scanning Electron Microscope and with Philips EM 300 and EM 301 Transmission Electron Microscopes. Microorganisms, keratinized cells, sebum, and hairs interact with each other to form the comedonal mass. Corynebacterium acnes and Pityrosporum ovale proliferate abundantly in close association with sebum and penetrate the keratinized cells. Fine structural details of bacteria and yeasts as well as features of host-microbial relationship have been elucidated.

Acne Vulgaris↗
PubMed2006

Campylobacter jejuni induces maturation and cytokine production in human dendritic cells.

Campylobacter jejuni is a leading bacterial cause of human diarrheal disease in both developed and developing nations. Colonic mucosal invasion and the resulting host inflammatory responses are thought to be the key contributing factors to the dysenteric form of this disease. Dendritic cells (DCs) play an important role in both the innate and adaptive immune responses to microbial infection. In this study, the interaction between human monocyte-derived dendritic cells and C. jejuni was studied. We found that C. jejuni was readily internalized by DCs over a 2-h period. However, after a prolonged infection period (24 or 48 h) with C. jejuni, only a few viable bacteria remained intracellularly. Minimal cytotoxicity of C. jejuni to dendritic cells was observed. C. jejuni induced the maturation of dendritic cells over 24 h, as indicated by up-regulation of cell surface marker proteins CD40, CD80, and CD86. In addition, Campylobacter-infected DCs triggered activation of NF-kappaB and significantly stimulated production of interleukin-1beta (IL-1beta), IL-6, IL-8, IL-10, IL-12, gamma interferon, and tumor necrosis factor alpha (TNF-alpha) compared to uninfected DCs. Active bacterial invasion of DCs was not necessary for the induction of these cytokines, as heat-killed C. jejuni stimulated similar levels of cytokine production as live bacteria. Purified lipooligosaccharide of C. jejuni appears to be the major stimulant for the increased production of cytokines by DCs. Taken together, these data indicate that during infection, Campylobacter triggers an innate inflammatory response through increased production of IL-1beta, IL-6, IL-8, and TNF-alpha and initiates a Th1-polarized adaptive immune response as predicted from the high level of production of IL-12.

Campylobacter jejuni↗
PubMed2004

Regulatory cells and infectious agents: detentes cordiale and contraire.

This brief review describes the types of interactions that occur between CD4(+)CD25(+) regulatory T cells (Treg) and microbial pathogens. These interactions range from one of mutual benefit (détente cordiale) such as occurs in Leishmania major infection of resistant mouse strains, to instances where the Treg response appears to mainly favor the pathogen and be detrimental to the host (détente contraire). Examples of the latter include chronic persistent infections with retroviruses, perhaps including HIV, and hepatitis C virus. The Treg response also hampers the effectiveness of immunity against some acute virus infections such as HSV. Evidence is also discussed showing that Treg can play a benevolent role to limit the severity of bystander tissue damage in circumstances where the immune response to pathogens is immunopathological. Finally, emerging approaches are discussed that either blunt or activate Treg and that could be used practically to manage host-pathogen interaction.

Animals↗
PubMed2003

Anti-microbial activities of mannose-binding lectin.

Mannose-binding lectin (MBL; also known as mannan-binding lectin) is involved in first-line defence by binding to bacteria, viruses, protozoa and helminths through a pattern-recognition mode of detection and then initiating a range of host responses. Currently, we have been unable to extrapolate from what we know of the biochemistry of MBL binding to predict accurately the interaction of MBL with individual micro-organisms; even subtle surface alterations have been shown to have an extensive impact on MBL-mediated recognition of pathogens. MBL has a major protective effect through activation of the complement system via MBL-associated serine proteases (MASPs). This can cause the lysis of Gram-negative bacteria and also opsonize a wide spectrum of potential pathogens for phagocytosis. MBL may also influence phagocytosis in the absence of complement activation through an interaction with one or more collectin receptors. This may also be the basis for a direct effect of the protein on inflammatory responses. MBL can alter the function of microbial structures, such as gp120 of HIV, to prevent infection. The protein may also interact with the components of other cascade systems such as the clotting system, which will have a role in microbial pathogenesis. An understanding of these basic mechanisms will be vital if we are to use purified or recombinant MBL in therapeutic applications.

Bacterial Capsules↗
PubMed1998

Lactoferrin and interleukin-6 interaction in amniotic infection.

Lactoferrin (Lf) has been found in most biological fluids including amniotic fluid and cervical mucoids in pregnant women, and released from neutrophils in response to the inflammation. As Lf possesses antimicrobial properties, it is widely considered to be an important component of the host defence against microbial infections. It is known that premature labor is caused by amniotic infection with the increase of prostaglandin production. High concentration of the inflammatory cytokines: interleukin-1 beta (IL-1 beta), interleukin-6 (IL-6), tumor necrosis factor-alpha (TNF-alpha) in the amniotic fluid has been known. However, changes of Lf in amniotic fluid with infection has not been reported. In the present study, Lf concentrations in amniotic fluid were measured under the intra-uterine infections state and the biological significance of Lf was investigated. The effects of Lf on the IL-6 and IL-6mRNA production in cultured amnion cells were also investigated. The concentrations of Lf and IL-6 in amniotic fluid with CAM were 8.76 +/- 0.65 micrograms/ml and 6.92 +/- 4.88 ng/ml (n = 28) respectively and both were significantly higher (p < 0.01) than those without CAM [0.86 +/- 0.81 microgram/ml and 0.34 +/- 0.25 ng/ml (n = 31)]. Significant positive correlation (r = 0.91, p < 0.01) between Lf and IL-6 levels in amniotic fluid was found. IL-6 production induced by lipopolysaccharide (LPS) (100 ng/ml) in cultured amnion cells was significantly inhibited (p < 0.05) under the physiological concentration of Lf in amnion. Total RNA was extracted from the amniotic cells by guianizine solution. RT-PCR procedure and product analysis were performed from one microgram aliquote of total RNA. beta-actin was used as an international standard and c-DNA samples were followed by 30 cycles of PCR. RT-PCR product of IL-6 mRNA was detected by Southern hybridization. Expression of IL-6 mRNA was inhibited by the addition of Lf. From the results, the possibility that Lf might suppress amniotic IL-6 production under the condition of amniotic infection is suggested. It is also suggested that Lf might act as self defence mechanism from intra-uterine infection.

Amnion↗
PubMed1988

Dacus oleae microbial symbionts.

Dacus oleae (Gmelin), which is a major insect pest of the olive tree, is closely associated during all developmental stages with a bacterial symbiont. This review describes the localization and transmission of the symbiont, the attempts made to isolate, cultivate and characterize it, and the host-symbiont interactions.

Animals↗
PubMed2005

Intestinal mucosal responses to microbial infection.

Infections of the human intestinal tract with foodborne and waterborne pathogens are among the leading causes of morbidity and death in the world. Upon ingestion, such pathogens commonly pass through the stomach in sufficient numbers to establish infection in the small intestine or colon. The subsequent interactions with the host depend critically on the particular pathogen, ranging from mere presence in the intestinal lumen and minimal interaction with the epithelium to highly mucosal invasive with rapid systemic spread. This article addresses the morphological and molecular changes that occur in the intestinal mucosa after infection with a selected yet representative spectrum of enteric pathogens, ranging from luminally restricted but epithelial adherent, epithelial invasive, to mucosally invasive, with a focus on intestinal epithelial responses.

Animals↗
PubMed2003

Decorin-binding sites in the adhesin DbpA from Borrelia burgdorferi: a synthetic peptide approach.

Lyme disease is caused by the spirochete Borrelia burgdorferi following transmission from infected Ixodes ticks to human hosts. Following colonization of the skin, spirochetes can disseminate throughout the body, resulting in complications that can include ocular, cardiac, neural, and skeletal disease. We have previously shown that B. burgdorferi expresses two closely related decorin-binding adhesins (DbpA and DbpB) of the MSCRAMM (microbial surface component recognizing adhesive matrix molecule) type that can mediate bacterial attachment to extracellular matrices in the host. Furthermore, three Lys residues in DbpA appear to be critical for the binding of DbpA to decorin. We have now characterized the interaction of DbpA and decorin further by using a synthetic peptide approach. We synthesized a panel of peptides that spanned the DbpA sequence and examined their ability to inhibit the binding of intact DbpA to decorin. From these studies, we identified a decorin-binding peptide that lost this activity if the sequence was either scrambled or if a critical Lys residue was chemically modified. A minimal decorin-binding peptide was identified by examining a set of truncated peptides. One peptide is proposed to contain the primary decorin-binding site in DbpA. By comparing the amino acid sequences of 29 different DbpA homologs from different B. burgdorferi sensu lato isolates, we discovered that the identified decorin-binding sequence was quite variable. Therefore, we synthesized a new panel of peptides containing the putative decorin-binding sequence of the different DbpA homologs. All of these peptides were active in our decorin-binding assay, and consensus decorin binding motifs are discussed.

Adhesins, Bacterial↗
PubMedDate not supplied

Mucocutaneous dissemination of acyclovir-resistant herpes simplex virus in a patient with AIDS.

Infections caused by herpes simplex virus (HSV) are a significant source of morbidity in immunocompromised patients. Acyclovir is often used prophylactically and therapeutically in patients with human immunodeficiency virus infection. The emergence of acyclovir-resistant strains of HSV capable of causing disease has been recognized. We report a case in which a thymidine kinase-deficient mutant of HSV caused extensive disease in a patient with AIDS. This case emphasizes that virus recovered from nonhealing lesions should be submitted for further study, which may advance our understanding of the interaction between host defense and drug-resistant strains.

Acquired Immunodeficiency Syndrome↗