Role Of Toxins In Pathogenesis Research Articles

CbpA: a novel surface exposed adhesin ofClostridium difficiletargeting human collagen

Clostridium difficile is the leading cause of antibiotic-associated diarrhoea and pseudomembranous colitis. While the role of toxins in pathogenesis has been extensively described, the contribution of surface determinants to intestinal colonization is still poorly understood. We focused our study on a novel member of the MSCRAMM family, named CbpA (Collagen binding protein A), for its adhesive properties towards collagen. We demonstrate that CbpA, which carries an LPXTG-like cell wall anchoring domain, is expressed on the bacterial surface of C. difficile and that the recombinant protein binds at high affinity to collagens I and V (apparent Kd in the order of 10(-9 ) M). These findings were validated by confocal microscopy studies showing the colocalization of the protein with type I and V collagen fibres produced by human fibroblasts and mouse intestinal tissues. However, the collagen binding activity of the wild-type C. difficile 630 strain was indistinguishable to the cbpA knock-out strain. To overcome this apparent clostridial adherence redundancy, we engineered a Lactococcus lactis strain for the heterologous expression of CbpA. When exposed on the surface of L. lactis, CbpA significantly enhances the ability of the bacterium to interact with collagen and to adhere to ECM-producing cells. The binding activity of L. lactis-CbpA strain was prevented by an antiserum raised against CbpA, demonstrating the specificity of the interaction. These results suggest that CbpA is a newsurface-exposed adhesin contributing to the C. difficile interaction with the host.

Histopathology of spot blotch disease of wheat caused byBipolaris sorokiniana(Teleomorph:Cochliobolus sativus)

Bipolaris sorokiniana (Sacc.) Shoemaker (Teleomorph: Cochliobolus sativus (Ito and Kuribayashi) Drechs. Ex. Dastur) is a serious necrotrophic pathogen of wheat and barley in several countries. In this paper we report on mechanism of resistance and histopathological changes that occur on pathogen attack in resistant and susceptible genotypes. Callose deposition was observed in the epidermal cell wall of resistant genotype, Pusa T3336 at 2DAI. Lignin deposition around mesophyll tissues was also strongly observed by Phloroglucinol-HCl test in Pusa T3336. Four days after inoculation (4DAI), the pathogen colonized the leaf tissues showing inter and intracellular hyphae in susceptible genotype, Agralocal. In resistant genotype, no colonization was observed. The host tissue in susceptible genotype showed degeneration away from the site of colonization and also showed loss of structural integrity thereby indicating the role of toxin in pathogenesis. Separation of plasmalemma from the cell wall was observed due to loss of electrolytes and degradation of chloroplast at 5 DAI in the susceptible genotypes was prominently seen through light microscopy.

The use of entomogenous fungi for pest control and the role of toxins in pathogenesis

AbstractFungi have been suggested as agents for the biological control of insects for over a century, but their use remains extremely limited. This paper examines the biology of entomogenous fungi, highlighting their need for moisture, and reviews studies on the Entomophthoraceae, Beauveria bassiana, Beauveria brongniartii, Metarhizium anisopliae and Verticillium lecanii. It is suggested that current studies should be directed towards the control of pests living in humid micro‐climates and that moisture‐retaining formulations should be developed to reduce the reliance of fungi on moisture.Many entomogenous fungi produce insecticidal toxins in submerged culture and these compounds are of interest as a source of new toxophores. The most extensively studied toxins are the cyclic depsipeptides from M. anisopliae, termed destruxins, and their possible role in pathogenesis is discussed. Beauveria bassiana also produces the cyclic peptides termed beauvericin, beauverolides, and bassianolide. Toxins produced by V. lecanii, and the Entomophthoraceae are also described.

Studies on host-specific AF-toxins produced by Alternaria alternata strawberry pathotype causing alternaria black spot of strawberry. 2. Role of toxins in pathogenesis.

The role of AF-toxins in the interaction of A. alternata strawberry pathotype and its hosts, strawberry cv. Morioka-16 and Japanese pear cv. Nijisseiki, was investigated at the early stage of infection. Time course study of the production of AF-toxins from germinating spores elucidated that all three AF-toxins (I, II and III) were detectable early after inoculation and increased in quantity with incubation time. The leaves inoculated with pathogen were allowed to leak electrolytes by AF-toxin produced during the germination of spores. The electrolyte leakage was shown to have two peaks at different stages of the infection behaviors of the spores; the first was detected before the establishment of infection and the second was detected after the establishment of infection. The first peak suggests that the AF-toxins from germinating spores prior to fungal invasion could change the physiological potential related to the membrane system of the host cells to be desirable to the pathogen. The effect of AF-toxins on the establishment of infection by pathogenic spore was investigated by treating the leaves both the high molecular weight fraction “inducer” in germination fluids of spores and AF-toxins. The treatment with “inducer” rendered the susceptible leaves relatively resistant to the pathogen, while, the treatment with AF-toxins rendered the leaves susceptible even to non-pathogenic A. alternata. Concomitant treatment with the “inducer” and AF-toxins resulted in the suppression of the induction of host resistance. These data suggest that pathogenic spores of A. alternata strawberry pathotype produce AF-toxins during their germination, and thereby may suppress the resistance response through the disturbance of membrane integrity of the host cells, and consequently succeed in establishing infection.

Host damage from bacterial toxins

Bacterial infection often involves toxin-mediated damage to the host. This can occur at mucosal epithelial surfaces, in subepithelial tissues (involving connective tissue, blood vessels and host defence cells), or at organ or tissue sites distant from the focus of infection. This paper deals with host damage at each of these levels and examples have been selected of toxins that have a well defined role in pathogenesis and for which evidence is less clear cut. Current views of mechanisms of host damage are presented along with summaries of mode of action at the molecular level where this is known. Certain unifying features of mechanisms of toxin action on host cells are emphasised. Modern genetic methods and gene cloning techniques should help in the assessment of the role of individual toxic factors where pathogenesis is multifactorial, and preliminary examples of this approach are mentioned. The search for new toxins continues and this is illustrated with reference to the toxins involved in the staphylococcal scalded skin syndrome and staphylococcal toxic shock syndrome. This overview is intended to convey an impression of the rapid development that has taken place in knowledge of the role of toxins in pathogenesis.