Cholera and Related Diseases: Grasping Bacterial ‘Friending’ Paves the Way to Disrupt

The Silent Role of Biofilms in Chronic Disease Forums Biofilm Community The Human Ecosystem Cholera and Related Diseases: Grasping Bacterial ‘Friending’ Paves the Way to Disrupt

This topic contains 0 replies, has 1 voice, and was last updated by  Harrison 9 years, 1 month ago.

  • Author
    Posts
  • #2821 Score: 0

    Harrison
    Keymaster
      2 pts

      ScienceDaily (Feb. 12, 2010) — Finding a biological mechanism much like an online social network, scientists have identified the bacterial protein VpsT as the master regulator in Vibrio, the cause of cholera and other enteric diseases. This discovery, now published in the journal Science, provides a major tool to combat enteric disease.

      For decades, it has been observed that bacteria engage in biofilm formation in nature and the lab. Like the online social network Facebook, free-swimming bacteria ditch the solitary lifestyle to form a biofilm community, but only after they’ve signaled their intention to do so to others. The protein VpsT receives the invitation and accepts it by starting a cellular program facilitating the process. “We have the parts list now,” said Holger Sondermann, professor at Cornell University’s College of Veterinary Medicine. “The next step will be to develop a clear understanding of the triggers and processes that regulate biofilm formation. With this data, we can find opportunities to disrupt the process and find entry points for therapeutic interventions.”

      Thus, bacteria hunker down with millions of other bacteria to form a biofilm community powerful enough to fog your contacts, rot your teeth, corrode metal and cause a host of human and animal diseases. Biofilms have been implicated in numerous chronic infections including cystic fibrosis, otitis media and prostatitis. Through interactions within a biofilm, the resident population of bacteria is likely to benefit from increased metabolic efficiency, substrate accessibility, enhanced resistance to environmental stress and antibiotics and an increased ability to cause infection and disease, says Sondermann.

      In addition to Sondermann, it was also authored by Petya Krasteva, first author, a graduate student in biochemistry, molecular and cellular biology, and by Marcos V. A. S. Navarro, a postdoctoral fellow in the Sondermann group. The work is a close collaboration with Fitnat H. Yildiz’s laboratory at the University of California at Santa Cruz, and her a postdoctoral fellow Jiunn C. N. Fong, and her graduate students Nicholas J. Shikuma and Sinem Beyhan.

      The project was funded by grants from the National Institutes of Health and the Pew Foundation

    You must be logged in to reply to this topic.