The genome of Vibrio cholerae contains five flagellin genes that encode proteins (FlaA-E) of 39 -41 kDa with 61-82% identity among them. Although the existing live oral attenuated vaccine strains against cholera are protective in humans, there is an intrinsic residual cytotoxic and inflammatory component associated with these candidate vaccine strains. Bacterial flagellins are known to be potent inducers of proinflammatory molecules via activation of Toll-like receptor 5. Here we found that purified flagella from wild type V. cholerae 395 induced significant release of interleukin (IL)-8 from cultured HT-29 human colonic epithelial cells. Furthermore we found that filtered supernatants of KKV90, a ⌬flaA isogenic strain unable to produce flagella, were still able to activate production of IL-8 albeit to significantly lower levels than the wild type, suggesting that other activators of proinflammatory molecules were still present in these supernatants. Cholera remains a devastating bacterial cause of human morbidity and mortality in some areas of the world (1). The disease is produced by Vibrio cholerae, a Gram-negative curved rod that colonizes the human intestine where it secretes the potent cholera toxin (CT), 1 which ultimately stimulates cellular adenylate cyclase to cause massive intestinal fluid loss leading to profuse watery diarrhea. CT is the major V. cholerae virulence factor, and it is encoded by the ctxA and ctxB genes carried on the transmissible prophage CTX⌽ (2). V. cholerae produces an array of virulence factors, which are coordinately regulated by the transcriptional activator ToxR (3). In turn, ToxR activates ToxT, a second transcriptional regulator that activates the expression of CT and the toxincoregulated pilus (TCP) (4, 5). TCP is considered the most important intestinal colonization factor of V. cholerae (6).In addition to CT, the accessory cholera toxin (Ace) (7) and the zonula occludens toxin (Zot) (7, 8) were reported as potential cytotoxic factors, but these proteins were later demonstrated to be components of a filamentous bacteriophage (2). Several in vitro studies have shown that V. cholerae secretes other cytotoxic factors such as the hemagglutinin/ protease (HAP), hemolysin (Hly), and repeats-in-toxin (RTX) (9 -11). These cytotoxic factors may cause tissue damage by different mechanisms that could contribute to proinflammatory responses. However, only RTX mutants have been demonstrated in a murine pulmonary cholera model to show less severe pathology and decreased serum levels of proinflammatory IL-6 and murine macrophage inflammatory protein-2, suggesting that RTX participates in the severity of acute inflammatory responses (12).Research on cholera vaccines has focused largely on oral formulations that stimulate the mucosal immune system thereby mimicking natural infection (13). Through the years, different formulations of cholera vaccines have been proposed that include formalin or heat-killed bacteria alone or in combination with CT B-subunit. As new putative virulence factors ...
Vibrio cholerae colonizes the human intestine and causes the acute diarrheal disease cholera. Flagellar-mediated chemotaxis contributes to intestinal colonization as well as infectivity. The virulence-regulatory protein ToxT activates transcription of the genes encoding the major virulence factors cholera toxin and toxin coregulated pilus. ToxT additionally activates transcription of two genes, tcpI and acfB, located within the Vibrio Pathogenicity Island predicted to encode methyl-accepting chemoreceptors. We show that disruption of either tcpI or acfB individually does not noticeably affect V. cholerae intestinal colonization within the infant mouse, but disruption of both tcpI and acfB leads to a decrease in intestinal colonization. These results suggest that TcpI and AcfB may have overlapping or redundant chemotactic functions that contribute to V. cholerae intestinal colonization.
Tolerance in isolations of Trichoderma was developed by exposing two strains of T. harzianum and three of T. asperelloides to increasing concentrations of chemical fungicides. This isolation of Trichoderma was exposed to three fungicides: Captan, Thiabendazol and the mixture Captan-Carboxin. Some selected lines of these strains reached tolerance to Captan and partial tolerance to the mixture Captan-Carboxin. The biological and genetic changes in these tolerant lines were monitored by determining the relative growth rate of the fungus, inhibition of Fusarium and by analyzing the genomic changes through UP-PCR. The results show that the tolerance to fungicides can be developed without affecting the parameters of biological activity in these lines of Trichoderma (growth and parasitism against Fusarium). Chemical tolerance to the fungicide was verified by means of changes at the DNA level (UP-PCR), mainly in the lines tolerant to Captan. This suggests that Trichoderma survives in environments with remnants of fungicide molecules.
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