Abstract
The spirochete Borrelia burgdorferi survives in its tick vector, Ixodes scapularis, or within various hosts. To transition between and survive in these distinct niches, B. burgdorferi changes its gene expression in response to environmental cues, both biochemical and physiological. Exposure of B. burgdorferi to weak monocarboxylic organic acids, including those detected in the blood meal of fed ticks, decreased the cytoplasmic pH of B. burgdorferi in vitro. A decrease in the cytoplasmic pH induced the expression of genes encoding enzymes that have been shown to restore pH homeostasis in other bacteria. These include putative coupled proton/cation exchangers, a putative Na+/H+ antiporter, a neutralizing buffer transporter, an amino acid deaminase and a proton exporting vacuolar-type VoV1 ATPase. Data presented in this report suggested that the acid stress response triggered the expression of RpoN- and RpoS-dependent genes including important virulence factors such as outer surface protein C (OspC), BBA66, and some BosR (Borrelia oxidative stress regulator)-dependent genes. Because the expression of virulence factors, like OspC, are so tightly connected by RpoS to general cellular stress responses and cell physiology, it is difficult to separate transmission-promoting conditions in what is clearly a multifactorial and complex regulatory web.
Highlights
Pathogens disseminated by arthropod vectors are responsible for many emerging and reemerging infectious diseases that impose a significant burden on public health worldwide
Since acetate-induced expression of outer surface protein C (OspC) and RpoS was independent of Ac-P concentration, it seemed likely that this “acetate effect” might result from acetate directly decreasing pHi
The effects of acid stress have been best characterized in enteric bacteria exposed to drastic changes in extracellular pH as they pass from the gastric stomach into the lower digestive tract
Summary
Pathogens disseminated by arthropod vectors are responsible for many emerging and reemerging infectious diseases that impose a significant burden on public health worldwide. Bacterial pathogens sense, respond, and adapt to host environments during vector– host–vector (infectious cycle) transitions These adaptations ensure that the appropriate changes in gene expression occur at the time suitable for successful colonization of these habitable hosts. Transmission from ticks and establishment of infection in a host requires an atypical signaling cascade, the Rrp2–RpoN–RpoS cascade, to direct key changes in gene expression (Yang et al, 2003; Fisher et al, 2005; Dunham-Ems et al, 2012). This signaling cascade consists of the cytoplasmic response regulator protein-2 (Rrp2) and two alternative sigma factors, RpoN and RpoS. Activation of Rrp promotes RpoNdirected transcription of rpoS and subsequent RpoS-directed transcription of genes encoding proteins required for survival and key virulence factors (Hübner et al, 2001; Clifton et al, 2006; Burtnick et al, 2007; Caimano et al, 2007; Samuels, 2011)
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