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Capsaicin inhibitory effects on Vibrio cholerae toxin genes expression.

ABSTRACT: Objective:Cholera is an acute secretory diarrhea caused by the Gram-negative bacterium, Vibrio cholerae mostly through production of cholera toxin (CT) and zonula occludens toxin (Zot). Isolates of V. cholerae have acquired resistance elements during the last decade. One of the most promising ways to treat resistant strains is to use antivirulence agents instead of killing the causative agent with conventional antibiotics. In this study, we examined whether different concentrations of capsaicin - the pungent fraction of red chili- can act as an antivirulence agent and inhibit V. cholerae toxin production. Materials and Methods:Two standard strains namely, V. cholerae ATCC 14035 and V. cholerae PTCC 1611 were used in this study. Minimum Inhibitory Concentration (MIC) of capsaicin was determined by broth microdilution method. Based on MIC results, the bacteria were cultured in the presence of sub-MIC concentrations of capsaicin and a negative control without capsaicin. Real-time PCR (RT-PCR) was carried out to determine the expression level of V. cholerae toxin genes at each concentration. Results:MIC test showed that 200 mg/mL of capsaicin in 2% dimethyl sulfoxide (DMSO) could inhibit the growth of the two standard strains of V. cholerae. The expression of V. cholerae toxin genes was significantly reduced following treatment with sub-MIC concentrations of capsaicin as assessed by RT-PCR. Conclusion:Capsaicin showed great inhibitory effect against cholera toxin and reduced Zot production in the tested strains of V. cholerae. The results showed promising insights into antivirulence effects of capsaicin.

SUBMITTER: Erfanimanesh S

PROVIDER: S-EPMC6526041 | biostudies-literature | 2019 May-Jun

REPOSITORIES: biostudies-literature

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Capsaicin inhibitory effects on <i>Vibrio cholerae</i> toxin genes expression.

Erfanimanesh Soroor S Eslami Gita G Taherpour Arezou A Hashemi Ali A

Avicenna journal of phytomedicine 20190501 3

<h4>Objective</h4>Cholera is an acute secretory diarrhea caused by the Gram-negative bacterium, <i>Vibrio cholerae</i> mostly through production of cholera toxin (CT) and zonula occludens toxin (Zot)<i>.</i> Isolates of <i>V. cholerae</i> have acquired resistance elements during the last decade. One of the most promising ways to treat resistant strains is to use antivirulence agents instead of killing the causative agent with conventional antibiotics. In this study, we examined whether different ...[more]

PMID: 31143687

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Project description:A non-O1 non-O139 Vibrio cholerae strain, 10259, belonging to the serogroup O53 was shown to harbor genes related to the vibrio pathogenicity island (VPI) and a cholera toxin (CT) genetic element called CTX. While the nucleotide sequence of the strain 10259 tcpA gene differed significantly (26 and 28%) from those of O1 classical and El Tor biotype strains, respectively, partial sequence analysis data of certain other VPI-associated genes (aldA, tagA, tcpP/H, toxT, acfB/C, and int) and intergenic regions (tcpF to toxT and tcpH to tcpA) of the strain showed only minor variations (0.4 to 4.8%) from corresponding sequences in O1 strains. Strain 10259 also contained CTX element-associated toxin genes with sequences almost identical to those of O1 strains. Growth of the organism in Luria broth (LB) under ToxR inducing conditions (30 degrees C and pH 6.5) led to transcriptional activation of tcpP/H, toxR, toxT, and tcpA genes, but not of ctxA, as determined by reverse transcription-PCR (RT-PCR). Subsequent analysis revealed that strain 10259 possessed only two copies (instead of three or more copies found in epidemic-causing O1 or O139 strains) of the heptanucleotide (TTTTGAT) repeats in the intergenic region upstream of ctxAB. Therefore, a strain 10259 mutant was generated by replacement of this region with a homologous region (1.4 kb) derived from a V. cholerae O1 classical biotype strain (O395) that contained seven such repeats. The resultant recombinant strain (10259R) was found to be capable of coordinately regulated expression of toxT, ctxA, and tcpA when grown under the ToxR inducing conditions. Serological studies also demonstrated that the recombinant strain produced TcpA and a significantly ( approximately 1,000-fold) higher level of CT in vitro compared to that of the parent strain. Virulence gene expression in two other non-O1 non-O139 strains (serogroup O37) containing VPI and the CTX element was studied by RT-PCR and serological assay. One strain (S7, which was involved in an epidemic in Sudan in 1968) showed coordinately regulated expression of virulence genes leading to the production of both CT and TcpA in LB medium. However, the other strain, V2, produced RT-PCR-detectable transcripts of toxT, ctxA, or tcpA genes in the early phase (6 h), but not in the late phase (16 h) of growth in LB medium. These results are consistent with the low levels of production of CT and TcpA by the strain that were serologically detectable. The significance of these results is discussed in relation to the role of virulence genes and their expression to the pathogenic potential of V. cholerae strains belonging to non-O1 serogroups.

Project description:CsrA is a posttranscriptional global regulator in Vibrio cholerae Although CsrA is critical for V. cholerae survival within the mammalian host, the regulatory targets of CsrA remain mostly unknown. To identify pathways controlled by CsrA, RNA-seq transcriptome analysis was carried out by comparing the wild type and the csrA mutant grown to early exponential, mid-exponential, and stationary phases of growth. This enabled us to identify the global effects of CsrA-mediated regulation throughout the V. cholerae growth cycle. We found that CsrA regulates 22% of the V. cholerae transcriptome, with significant regulation within the gene ontology (GO) processes that involve amino acid transport and metabolism, central carbon metabolism, lipid metabolism, iron uptake, and flagellum-dependent motility. Through CsrA-RNA coimmunoprecipitation experiments, we found that CsrA binds to multiple mRNAs that encode regulatory proteins. These include transcripts encoding the major sigma factors RpoS and RpoE, which may explain how CsrA regulation affects such a large proportion of the V. cholerae transcriptome. Other direct targets include flrC, encoding a central regulator in flagellar gene expression, and aphA, encoding the virulence gene transcription factor AphA. We found that CsrA binds to the aphA mRNA both in vivo and in vitro, and CsrA significantly increases AphA protein synthesis. The increase in AphA was due to increased translation, not transcription, in the presence of CsrA, consistent with CsrA binding to the aphA transcript and enhancing its translation. CsrA is required for the virulence of V. cholerae and this study illustrates the central role of CsrA in virulence gene regulation.IMPORTANCE Vibrio cholerae, a Gram-negative bacterium, is a natural inhabitant of the aqueous environment. However, once ingested, this bacterium can colonize the human host and cause the disease cholera. In order to successfully transition between its aqueous habitat and the human host, the bacterium must sense changes in its environment and rapidly alter gene expression. Global regulators, including CsrA, play an integral role in altering the expression of a large number of genes to promote adaptation and survival, which is required for intestinal colonization. We used transcriptomics and a directed CsrA-RNA coimmunoprecipitation to characterize the CsrA regulon and found that CsrA alters the expression of more than 800 transcripts in V. cholerae Processes regulated by CsrA include motility, the rugose phenotype, and virulence pathways. CsrA directly binds to the aphA transcript and positively regulates the production of the virulence regulator AphA. Thus, CsrA regulates multiple processes that have been linked to pathogenesis.

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Capsaicin inhibitory effects on Vibrio cholerae toxin genes expression.

Publications

Capsaicin inhibitory effects on <i>Vibrio cholerae</i> toxin genes expression.

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