The variable inclusion morphology and lower infection

rate within chlamydiae-infected buy Foretinib monocytes and DCs as opposed to in HeLa indicated that replication cycle of C. trachomatis was somewhat restricted in these two immune cell types. Attempts to recover infectious particles from the monocytes and DCs infected with the chlamydia serovars led to an interesting observation. Monocytes infected with serovars Ba and D when passaged to HeLa cells could not produce any inclusions, which is in accordance with earlier studies demonstrating inability of serovar K to productively infect monocytes [23,24]. In contrast to earlier observations [48] where mononuclear cells were considered to be microbicidal for all C. trachomatis serovars our results revealed that serovar L2 could productively infect monocytes. A similar trend was observed in DCs, where serovar Ba and serovar D showed abortive infection with no typical inclusions. Infectious particles could only be recovered from serovar L2 infected DCs as has been reported previously by Selumetinib order Gervassi et al. [31]. However Gervassi et al. showed that serovar E passaged in DCs could be further propagated in HeLa cell whereas in our study serovar D, member of the same biovariant could not be propagated in HeLa cells. The differences between

these findings can be caused by effects of genetic human host polymorphism (source of DCs are different), differences in culture condition (10% FCS vs 10% autologous serum), or use of selleck different MOIs 10 vs 3). In conjunction with the reinfection data, high expression levels of 16S rRNA within monocytes infected with serovars Ba, D and L2 indicated that C. trachomatis

serovars were viable throughout the infection period, even though infectious progeny could only be recovered from L2 infected monocytes. This phenomenon of viability without producing infectious bodies is known as chlamydial persistence [18,49]. Serovar K infection of monocytes resulted in attenuation of new EB production although genes involved in chlamydial DNA replication were expressed during persistence [20]. Nevertheless our study establishes that this is a general phenomenon occurring in monocytes for several serovars of C. trachomatis biovariants. Contrasting observations are provided by DCs infected with the chlamydial serovars. The absence of recovered infectious Aprepitant progeny along with the negligible expression of 16S rRNA in serovars Ba and D in infected DCs 2 days p.i. suggest the loss of metabolic activity of C. trachomatis serovars within DCs. This loss of metabolic activity of C. trachomatis serovars within DCs indicated towards a probable degradation of chlamydiae. Serovar L2 could however, produce inclusions during reinfection studies and express 16S rRNA 2 days p.i. in DCs but suffered rapid decline in viability 3 days p.i.. DCs have shown the ability to degrade Chlamydia psittaci and C. trachomatis MoPn [29] but other DC- C.