OspC facilitates Borrelia burgdorferi invasion of Ixodes scapularis salivary glands

Abstract

Outer surface protein C (OspC) is a differentially expressed major surface lipoprotein of Borrelia burgdorferi. ospC is swiftly upregulated when spirochetes leave the Ixodes scapularis tick gut, migrate to the salivary gland, and exit the arthropod vector. Here we show that OspC strongly binds to the tick salivary gland, suggesting a role for OspC in spirochete adherence to this tissue. In vivo studies using a murine model of Lyme borreliosis showed that while OspC F(ab) 2 fragments did not influence either the viability of spirochetes or ospC gene expression, they did interfere with B. burgdorferi invasion of tick salivary glands. We then generated ospC knockout spirochetes in an infectious clone of B. burgdorferi and examined them within the vector. OspC-deficient or wild-type spirochetes persisted equally within the gut of unfed ticks and multiplied during the tick engorgement; however, unlike wild-type B. burgdorferi, the mutants were unable to invade salivary glands. Salivary gland colonization of OspC-deficient spirochetes was completely restored when this mutant was complemented in trans with a plasmid harboring the wild-type ospC gene. These studies conclusively demonstrate the importance of OspC in the invasion of tick salivary glands by B. burgdorferi, a critical step in the transmission of spirochetes from the arthropod vector to the mammalian host.

bptA(bbe16) is essential for the persistence of the Lyme disease spirochete,Borrelia burgdorferi, in its natural tick vector

“…Whereas many of these differentially regulated genes likely represent physiological ''housekeeping'' genes typically not thought of as virulenceassociated, others have been noted in separate studies to encode virulence factors essential for Bb's infection of or survival within its arthropod or mammalian hosts (6,7,33,(43)(44)(45). Nevertheless, the testing of Koch's molecular postulates to ascertain whether a gene encodes a virulence trait (46) has been hindered greatly by a paucity of systems for genetically manipulating virulent Bb (13,14).…”

“…Most notable is the reciprocal expression patterns of the two plasmid-encoded outer surface lipoproteins (Osp)A and OspC as Bb migrates from the tick midgut to a mammalian host (2)(3)(4)(5). OspA has been shown to be essential for tick colonization (6), and OspC is crucial for events associated with the migration of Bb from tick midguts to salivary glands and subsequent transmission into the mammalian host (7).…”

The Fur homologue BosR requires Arg39 to activate rpoS transcription in Borrelia burgdorferi and thereby direct spirochaete infection in mice

“…Transcription of ospC is known to require RpoS (Radolf et al, 2012). In vivo, OspC is expressed on the surface of the spirochaete at the point when the spirochaete moves from the gut of the tick into the haemolymph just prior to invading a mammalian host (Grimm et al, 2004;Pal et al, 2004;Tilly et al, 2006). Therefore, although genes other than rpoS may have had a role in making the BosRR39K-expressing spirochaetes non-infectious, failure to upregulate rpoS appears to have been a major cause.…”

Biology of Infection with Borrelia burgdorferi

“…The OspC product has been shown to be required for an early stage of mammalian infection [113][114][115][116] and conflicting data have been presented regarding its importance in tick transmission [113,114,119,120]. OspC production begins in feeding ticks (or immediately after needle inoculation, Fig.…”