Charles Wan

Molecular Evidence to Support the Expansion of the Hostrange of Chlamydophila pneumoniae to Include Reptiles as Well as Humans, Horses, Koalas and Amphibians

The Chlamydiales are a family of unique intracellular pathogens that cause significant disease in humans, birds and a wide range of animal hosts. Of the currently recognized species, Chlamydophila (previously Chlamydia) pneumoniae, unlike the other chlamydial species, has been previously considered to be solely a pathogen of humans, causing significant respiratory disease and has also been strongly connected with cardiovascular disease. Here we report the finding that strains of C. pneumoniae are widespread in the environment, being detected by molecular methods in a range of reptiles (snakes, iguanas, chameleons) and amphibians (frogs, turtles). Of particular interest was the finding that genotyping of the chlamydial major outer membrane protein gene in these newly identified C. pneumoniae strains showed that many were genetically very similar, if not identical to the human respiratory strains. Whether these reptilian and amphibian strains of C. pneumoniae are still capable of infecting humans, or crossed the host barrier some time ago, remains to be determined but may provide further insights into the relationship of this common respiratory infection with its human host.

Progesterone activates multiple innate immune pathways in Chlamydia trachomatis-infected endocervical cells.

Susceptibility to Chlamydia trachomatis infection is increased by oral contraceptives and modulated by sex hormones. We therefore sought to determine the effects of female sex hormones on the innate immune response to C. trachomatis infection.

Modulation of the Chlamydia trachomatis in vitro transcriptome response by the sex hormones estradiol and progesterone.

BackgroundChlamydia trachomatis is a major cause of sexually transmitted disease in humans. Previous studies in both humans and animal models of chlamydial genital tract infection have suggested that the hormonal status of the genital tract epithelium at the time of exposure can influence the outcome of the chlamydial infection. We performed a whole genome transcriptional profiling study of C. trachomatis infection in ECC-1 cells under progesterone or estradiol treatment.ResultsBoth hormone treatments caused a significant shift in the sub-set of genes expressed (25% of the transcriptome altered by more than 2-fold). Overall, estradiol treatment resulted in the down-regulation of 151 genes, including those associated with lipid and nucleotide metabolism. Of particular interest was the up-regulation in estradiol-supplemented cultures of six genes (omcB, trpB, cydA, cydB, pyk and yggV), which suggest a stress response similar to that reported previously in other models of chlamydial persistence. We also observed morphological changes consistent with a persistence response. By comparison, progesterone supplementation resulted in a general up-regulation of an energy utilising response.ConclusionOur data shows for the first time, that the treatment of chlamydial host cells with key reproductive hormones such as progesterone and estradiol, results in significantly altered chlamydial gene expression profiles. It is likely that these chlamydial expression patterns are survival responses, evolved by the pathogen to enable it to overcome the hosts innate immune response. The induction of chlamydial persistence is probably a key component of this survival response.