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Bacterial Virulence Factors (bacterial + virulence_factor)
Selected AbstractsImmunization of mice with Lactobacillus casei expressing intimin fragments produces antibodies able to inhibit the adhesion of enteropathogenic Escherichia coli to cultivated epithelial cellsFEMS IMMUNOLOGY & MEDICAL MICROBIOLOGY, Issue 2 2008Patrícia C.D. Ferreira Abstract Enteropathogenic Escherichia coli (EPEC) are frequently isolated as a cause of infantile diarrhea in developing countries. Its pathogenicity is distinguished by histopathological alterations at the site of infection, known as attaching and effacing (A/E) lesions, in which bacterial virulence factors and host proteins participate. Intimin, a bacterial adhesin expressed by all EPEC described to date, is responsible for the intimate adherence of the bacteria to host cells and is essential for the formation of A/E lesions. Mucosal vaccination may represent an efficacious intervention to prevent EPEC infection and lower morbidity and mortality rates. Strategies for mucosal vaccinations that use lactic acid bacteria for the delivery of heterologous antigens rely on their safety profile and ability to stimulate the immune system. In the present work, we have constructed Lactobacillus casei strains expressing different fragments of intimin ,, a subtype that is frequently expressed by EPEC strains. Mucosal immunization of mice with L. casei expressing intimin fragments induced specific systemic and mucosal antibodies. These antibodies were able to recognize native intimin on the surface of EPEC and to inhibit in vitro EPEC binding to epithelial cells. [source] Pathogenesis of Helicobacter pylori InfectionHELICOBACTER, Issue 2005Céu Figueiredo ABSTRACT As with many infectious diseases, only a fraction of people infected with Helicobacter pylori develop clinical disease, and host genetics, host immune response, and bacterial virulence factors appear to play critical roles. There has been considerable interest in putative bacterial virulence factors and, while several have been identified, it is not clear whether they act independently or in concert. Disease associations have been proposed for the cag pathogenicity island (PAI), vacA, and genes encoding outer membrane proteins (OMPs). Numerous studies published in the last year have provided new insights into the function of these putative virulence factors in gastroduodenal pathogenesis. This article will review the recent novel findings (from April 2004) for the roles of the putative disease-associated virulence factors as well as their interaction with host. [source] Mucosal Production of Antigastric Autoantibodies in Helicobacter pylori GastritisHELICOBACTER, Issue 3 2000Gerhard Faller Background. Apart form bacterial virulence factors of Helicobacter pylori, certain host factors influence the pathogenesis of H. pylori gastritis. In particular, antigastric autoantibodies that are detectable in the sera of a substantial proportion of H. pylori were shown to correlate with the development of gastric atrophy. The aim of this study was to analyze the possible antigastric autoimmune response in H. pylori gastritis at the site where the action is, i.e., in the gastric mucosa. Material and Methods. Gastric biopsy specimens from antrum and corpus mucosa of 24 H. pylori,infected and of 33 noninfected patients were cultured for 3 days, and tissue culture supernatants were analyzed for the amount of locally produced IgA and IgG. Antigastric autoantibodies were screened in the sera and in the supernatants by means of immunohistochemistry. Results. The infected patients had significantly higher concentrations of locally produced IgA, whereas the IgG concentrations were virtually the same in infected and noninfected patients. IgG or IgA antigastric autoantibodies, or both, were detectable only in the sera (38%) and supernatants (17%) of infected patients. Interestingly, the patient with the strongest local autoimmune response showed body-predominant H. pylori gastritis, with destruction of gastric glands and atrophy of the body mucosa. Conclusions. These results demonstrate that antigastric autoimmune reactions are detectable at the site of the disease and might be relevant for the pathogenesis of gastric mucosa atrophy in H. pylori gastritis. [source] Effects of glucose on formation of cytotoxic end-products and proteolytic activity of Prevotella intermedia, Prevotella nigrescens and Porphyromonas gingivalisJOURNAL OF PERIODONTAL RESEARCH, Issue 6 2001Kaoru Saito Black-pigmented bacteria which produce cytotoxic metabolic end-products and cell membrane-associated proteases have been reported to play an important role in the pathogenesis of periodontal diseases. These bacterial virulence factors can be modified by the environmental conditions including nutrients supplied variously into the oral cavity. Although glucose is one of the most essential nutrients for oral bacteria, the exogenous supply of glucose may be discontinuous and the glucose concentration in a periodontal pocket may be influenced by the depth of the periodontal pocket. Therefore, effects of glucose as an environmental factor on the virulence factors of Prevotella intermedia, Prevotella nigrescens and Porphyromonas gingivalis were studied. When grown in the presence of glucose, both P. intermedia and P. nigrescens markedly decreased the production of cytotoxic end-products including succinate, isobutyrate, isovalerate and ammonia, although their growth was increased. Furthermore, the proteolytic activities such as immunoglobulin-, albumin- and casein-degrading activities of these bacteria were decreased in the presence of glucose. On the other hand, no effect of glucose on the metabolic activity of P. gingivalis was observed. These results suggest that pathogenicity of P. intermedia and P. nigrescens may be decreased by the presence of glucose. [source] Host,pathogen interplay and the evolution of bacterial effectorsCELLULAR MICROBIOLOGY, Issue 2 2008John Stavrinides Summary Many bacterial pathogens require a type III secretion system (T3SS) and suite of type III secreted effectors (T3SEs) to successfully colonize their hosts, extract nutrients and consequently cause disease. T3SEs, in particular, are key components of the bacterial arsenal, as they function directly inside the host to disrupt or suppress critical components of the defence network. The development of host defence and surveillance systems imposes intense selective pressures on these bacterial virulence factors, resulting in a host,pathogen co-evolutionary arms race. This arms race leaves its genetic signature in the pattern and structure of natural genetic variation found in T3SEs, thereby permitting us to infer the specific evolutionary processes and pressures driving these interactions. In this review, we summarize our current knowledge of T3SS-mediated host,pathogen co-evolution. We examine the evolution of the T3SS and the T3SEs that traverse it, in both plant and animal pathosystems, and discuss the processes that maintain these important pathogenicity determinants within pathogen populations. We go on to examine the possible origins of T3SEs, the mechanisms that give rise to new T3SEs and the processes that underlie their evolution. [source] Dynamics of gonococcal type IV pili during infectionCHEMPHYSCHEM, Issue 9-10 2009Dirk Opitz Abstract Keep that motor running: Type IV pili are among the strongest molecular motors characterized to date. Herein it is reported that pilus motors of the human pathogen Neisseria gonorrhoeae are very active for at least one day post-infection of epithelial cells. They generate force in the range on 70 pN and retract at a higher velocity as compared to abiotic environments (see picture). Type IV pili are important bacterial virulence factors that mediate attachment to mammalian host cells and elicit downstream signals. When adhered to abiotic surfaces, the human pathogen Neisseria gonorrhoeae generates force by retracting these polymeric cell appendages. We recently found that single pili generate stalling forces that exceed 100 pN, but it is unclear whether bacteria generate force once they adhere to their human host cells. Here, we report that pili retract very actively during infection of human epithelial cells. The retraction velocity is bimodal and the high velocity mode persisted at higher forces in contrast to an abiotic environment. Bacteria generate considerable force during infection, but the maximum force is reduced from 120±40 pN on abiotic surfaces to 70±20 pN on epithelial cells, most likely due to elastic effects. Velocity and maximum force of pilus retraction are largely independent of the infection period within 1 h and 24 h post-infection. Thus, the force generated by type IV pili during infection is high enough to induce cytoskeletal rearrangements in the host cell. [source] | ||||||||||