Researchers
have discovered a link between bacteria metabolism and cell-to-cell
communication, potentially providing a target for new antivirulence and
antibiofilm drugs.
Current
drugs for bacterial infections aim to kill bacteria in large quantities, but
such drugs are often eventually met with antibiotic resistance. Antivirulence
and antibiofilm drugs, on the other hand, block toxic molecules produced by
bacteria or prevent bacteria from forming thin, slimy films called biofilms (a
common example is dental plaque). These mechanisms are controlled by quorum
sensing: the process that allows bacteria populations to communicate and
coordinate group behavior.
For
example, biofilm forming E. coli can
cause urinary tract infections. Thus, disrupting quorum sensing and biofilm
forming in the bacteria could prevent those infections.
Quorum
sensing is facilitated by signaling molecules called autoinducers. One
particular autoinducer, AI-2, is modified by a protein called LsrK so that its
signal can be perceived.
The
findings, which were published in the journal Science Advances, shows that LsrK
forms a complex with HPr, a protein involved in glucose utilization in E. coli.
Posted by Dr. Tim Sandle
