Plasmid-Cured Chlamydia caviae Activates TLR2-Dependent Signaling and Retains Virulence in the Guinea Pig Model of Genital Tract Infection
Figure 1
C. caviae CC13 is plasmid-deficient but displays no alteration in plaque size or efficiency.
(A) Equal amounts of template were added to PCR reactions with primers directed against the pgp1 coding sequence expressed by pCpGP1 or the C. caviae genome and amplified products were analyzed on 2% agarose gels. (B) Genomic DNA was isolated from GPIC or CC13, digested with SphI and separated on a 1% agarose gel. The DNA was transferred to a nylon membrane and probed for the presence of pCpGP1 DNA using a ∼1.6 Kb probe directed against a region spanning pGP4-6. Plasmid pCpGP1 was isolated from GPIC and digested with Sph1 to yield a single, linear fragment of ∼7.9 kb which was used as a positive control for hybridization. (C) Plaques formed by CC13 do not differ from those formed by GPIC. C. caviae-infected L929 monolayers were incubated for 5 days at 37 C, 5% CO2, then the media overlay was removed and the plaques visualized using crystal violet.