(A) ECC-1 cells grown in normal FCS supplemented cell culture. Typical RB forms are present at 24 hours post infection (B) No

hormone supplemented stripped FCS media. Once again normal RB morphology was observed under this condition; RBs appeared similar to normal FCS supplemented cell culture. (C) Estradiol supplemented, RBs were distinctly different, appearing as large aberrant form. Estradiol supplementation of infected cells, resulting in BIIB057 cost smaller inclusions containing enlarged, atypical RB forms (arrows). (D) Progesterone supplemented, shape and morphology of RBs were normal including binary fission. Morphological examination of progesterone exposed cultures with TEM did not show any evidence of aberrant, persistent forms. Magnification: × 20K, marker represent 200 nm. Progesterone exposure induces an up-regulated energy utilising chlamydial response Overall, 85 chlamydial genes were observed to have two-fold or greater up-regulated gene expression levels in the presence of progesterone. The five top genes that were observed with this mRNA expression profile encode for proton or sodium-glutamate symport Selleckchem A1155463 protein (gltT) [33.4 fold], the putative glycerol-3-phosphate acyltransferase

(plsX) [16.17 fold], glucose inhibited division protein (lplA_2) [11.9 fold], NADH-quinone reductase complex (nqr2) [10.95 fold] and polynucleotide adenylyltransferase (pcnB_1) [10.75 fold]. In addition to these 85 genes, 135 chlamydial genes were observed to have a reduced gene expression profile in response to the presence of progesterone. The five top down AZD5363 order regulated Histamine H2 receptor genes include

exoribonuclease II (vacB) [67.96 fold], isopentenylpyrophosphate transferase (miaA) [33.91 fold], cysteinyl-tRNA synthetase (cysS) [33.64 fold], thioredoxin reductase (trxB) [33.44fold], and ribonucleotide-diphosphate reductase subunit alpha (nrdA) [29.25 fold]. 103 genes had unknown annotated functions (hypothetical genes). By comparison to the estradiol response, which resulted in a down-regulation of fatty acid and nucleotide metabolism pathways, progesterone exposure had no or little effect on these pathways but did result in a significant up-regulation of the TCA cycle and glycolysis pathways (Table 3). In some aspects the progesterone response was opposite or counter-balancing to the estradiol response. Progesterone resulted in a general up-regulation of carbohydrate metabolism pathways as well as an up-regulation of amino acid metabolism pathways. The progesterone-mediated response mounted by Chlamydia reflects the host’s flux of metabolites. Progesterone has been reported to have a suppressive effect in general on estradiol [25], and after prolonged exposure, it appears that Chlamydia is diverting specific pathways to compensate.