Infect Immun. 2015 Jan 20. pii: IAI.00032-15. [Epub ahead of print] An apparent role for Borrelia burgdorferi LuxS during mammalian infection. iai.asm.org/content/early/2015/01/14/IAI.00032-15.long Arnold WK1, Savage CR1, Antonicello AD1, Stevenson B2. Author information Abstract The Lyme disease spirochete, Borrelia burgdorferi, controls protein expression patterns during its tick-mammal infection cycle. Earlier studies demonstrated that B. burgdorferi synthesizes 4,5-dihydroxy-2,3-pentanedione (autoinducer-2, AI-2) and responds to AI-2 by measurably changing production of several infection-associated proteins. A luxS mutant, which is unable to produce AI-2, exhibits altered production of several proteins. B. burgdorferi cannot utilize the other product of LuxS, homocysteine, indicating that phenotypes of luxS mutants are not due to absence of that molecule. Although a previous study found that a luxS mutant was capable of infecting mice, a critical caveat to those results is that bacterial loads were not quantified. To more precisely determine whether LuxS serves a role in mammalian infection, mice were simultaneously inoculated with congenic wild-type and luxS strains, then bacterial numbers were assessed using quantitative PCR. The wild type bacteria substantially out-competed the mutant, suggesting that LuxS performs a significant function during mammalian infection. These data also provide further evidence that non-quantitative infection studies do not necessarily provide conclusive results, and that regulatory factors may not make all-or-none, black-or-white contributions to infectivity.
Posted on: Fri, 23 Jan 2015 05:44:58 +0000
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