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10.1371/journal.pone.0137529 http://scihub22266oqcxt.onion/10.1371/journal.pone.0137529 C4567338!4567338 !26361388     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=26361388 &cmd=llinks): Failed to open stream: HTTP request failed! 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Suppression of Virulence of Toxigenic Vibrio cholerae by Anethole through the Cyclic AMP (cAMP)-cAMP Receptor Protein Signaling System |pdf=|usr=}}{{26361388 }} gab.com Text Suppression of Virulence of Toxigenic Vibrio cholerae by Anethole through the Cyclic AMP (cAMP)-cAMP Receptor Protein Signaling System JO: PLoS One http://www.kidney.de/pget.php?&tw=1&pmid=26361388 #FOAvip Use of natural compounds as antivirulence drugs could be an alternative therapeutic approach to modify the outcome of bacterial infections, particularly in view of growing resistance to available antimicrobials. Here, we show that sub-bactericidal concentration of anethole, a component of sweet fennel seed, could suppress virulence potential in O1 El Tor biotype strains of toxigenic Vibrio cholerae, the causative agent of the ongoing 7th cholera pandemic. The expression of cholera toxin (CT) and toxin coregulated pilus (TCP), the major virulence factors of V. cholerae, is controlled through a regulatory cascade involving activation of ToxT with synergistic coupling interaction of ToxR/ToxS with TcpP/TcpH. We present evidence that anethole inhibits in vitro expression of CT and TCP in a toxT-dependent but toxR/toxS-independent manner and through repression of tcpP/tcpH, by using bead-ELISA, western blotting and quantitative real-time RT-PCR assays. The cyclic AMP (cAMP)-cAMP receptor protein (CRP) is a well-studied global signaling system in bacterial pathogens, and this complex is known to suppress expression of tcpP/tcpH in V. cholerae. We find that anethole influences the virulence regulatory cascade by over-expressing cyaA and crp genes. Moreover, suppression of toxigenic V. cholerae-mediated fluid accumulation in ligated ileum of rabbit by anethole demonstrates its potentiality as an antivirulence drug candidate against the diseases caused by toxigenic V. cholerae. Taken altogether, these results revealing a mechanism of virulence inhibition in V. cholerae by the natural compound anethole, may have relevance in designing antivirulence compounds, particularly against multiple antibiotic resistant bacterial pathogens. Twit Text FOAVip Suppression of Virulence of Toxigenic Vibrio cholerae by Anethole through the Cyclic AMP (cAMP)-cAMP Receptor Protein Signaling System ????PLoS One http://www.kidney.de/pget.php?&tw=1&pmid=26361388 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=26361388 #FOAvip English Wikipedia <ref>{{Cite pmid|26361388 }}</ref> Suppression of Virulence of Toxigenic Vibrio cholerae by Anethole through the Cyclic AMP (cAMP)-cAMP Receptor Protein Signaling System #MMPMID26361388 Zahid MS ; Awasthi SP ; Asakura M ; Chatterjee S ; Hinenoya A ; Faruque SM ; Yamasaki S PLoS One 2015[]; 10 (9 ): e0137529 PMID26361388 show ga Use of natural compounds as antivirulence drugs could be an alternative therapeutic approach to modify the outcome of bacterial infections, particularly in view of growing resistance to available antimicrobials. Here, we show that sub-bactericidal concentration of anethole, a component of sweet fennel seed, could suppress virulence potential in O1 El Tor biotype strains of toxigenic Vibrio cholerae, the causative agent of the ongoing 7th cholera pandemic. The expression of cholera toxin (CT) and toxin coregulated pilus (TCP), the major virulence factors of V. cholerae, is controlled through a regulatory cascade involving activation of ToxT with synergistic coupling interaction of ToxR/ToxS with TcpP/TcpH. We present evidence that anethole inhibits in vitro expression of CT and TCP in a toxT-dependent but toxR/toxS-independent manner and through repression of tcpP/tcpH, by using bead-ELISA, western blotting and quantitative real-time RT-PCR assays. The cyclic AMP (cAMP)-cAMP receptor protein (CRP) is a well-studied global signaling system in bacterial pathogens, and this complex is known to suppress expression of tcpP/tcpH in V. cholerae. We find that anethole influences the virulence regulatory cascade by over-expressing cyaA and crp genes. Moreover, suppression of toxigenic V. cholerae-mediated fluid accumulation in ligated ileum of rabbit by anethole demonstrates its potentiality as an antivirulence drug candidate against the diseases caused by toxigenic V. cholerae. Taken altogether, these results revealing a mechanism of virulence inhibition in V. cholerae by the natural compound anethole, may have relevance in designing antivirulence compounds, particularly against multiple antibiotic resistant bacterial pathogens. |*Second Messenger Systems [MESH] |Allylbenzene Derivatives [MESH] |Animals [MESH] |Anisoles/*pharmacology [MESH] |Anti-Bacterial Agents/*pharmacology [MESH] |Bacterial Proteins/metabolism [MESH] |Cholera Toxin/genetics/metabolism [MESH] |Cyclic AMP Receptor Protein/*metabolism [MESH] |Cyclic AMP/metabolism [MESH] |DNA-Binding Proteins/metabolism [MESH] |Fimbriae Proteins/metabolism [MESH] |Ileum/microbiology [MESH] |Membrane Proteins/metabolism [MESH] |Rabbits [MESH] |Transcription Factors/metabolism [MESH] |Vibrio cholerae/*drug effects/metabolism/pathogenicity [MESH]Suppression of Virulence of Toxigenic Vibrio cholerae by Anethole thro(epmc).pdf DeepDyve Pubget Overpricing