Apparent Role for Borrelia burgdorferi LuxS during Mammalian Infection
The Lyme disease spirochete,Borrelia burgdorferi, controls protein expression patterns during its tick-mammal infection cycle. Earlier studies demonstrated thatB. burgdorferisynthesizes 4,5-dihydroxy-2,3-pentanedione (autoinducer-2 [AI-2]) and responds to AI-2 by measurably changing production of several infection-associated proteins.luxSmutants, which are unable to produce AI-2, exhibit altered production of several proteins.B. burgdorfericannot utilize the other product of LuxS, homocysteine, indicating that phenotypes ofluxSmutants are not due to the absence of that molecule. Although a previous study found that aluxSmutant 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 andluxSstrains, and bacterial numbers were assessed using quantitative PCR. The wild-type bacteria substantially outcompeted the mutants, suggesting that LuxS performs a significant function during mammalian infection. These data also provide further evidence that nonquantitative infection studies do not necessarily provide conclusive results and that regulatory factors may not make all-or-none, black-or-white contributions to infectivity.