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      Small-molecule inhibitor of Vibrio cholerae virulence and intestinal colonization.

      Science (New York, N.Y.)
      Animals, Anti-Bacterial Agents, pharmacology, Bacterial Proteins, biosynthesis, drug effects, Butyrates, Cell Line, Cholera, microbiology, Cholera Toxin, Fimbriae, Bacterial, Gene Expression Regulation, Bacterial, Intestine, Small, Mice, Microbial Sensitivity Tests, Naphthalenes, Naphthalimides, Transcription Factors, Vibrio cholerae, pathogenicity, Virulence, Virulence Factors

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          Abstract

          Increasing antibiotic resistance requires the development of new approaches to combating infection. Virulence gene expression in vivo represents a target for antibiotic discovery that has not yet been explored. A high-throughput, phenotypic screen was used to identify a small molecule 4-[N-(1,8-naphthalimide)]-n-butyric acid, virstatin, that inhibits virulence regulation in Vibrio cholerae. By inhibiting the transcriptional regulator ToxT, virstatin prevents expression of two critical V. cholerae virulence factors, cholera toxin and the toxin coregulated pilus. Orogastric administration of virstatin protects infant mice from intestinal colonization by V. cholerae.

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