The effect of cortisol on glycogen and fructose-1,6-bisphosphatase in baby hamster kidney cells infected with Chlamydia trachomatis.
This study was designed to assay changes in glycogen synthesis which may occur as a result of cortisol treatment of chlamydial-infected cells. Monolayers of baby hamster kidney (BHK) cells, unlabeled and prelabeled with [6-14C]glucose, were treated with various concentrations of cortisol before (pretreated) or during (post-treated) infection with Chlamydia trachomatis. At designated times after absorption, the cells were harvested and assayed for total glycogen and 14C accumulation in glycogen. The total amount of glycogen accumulated in cells during the period of greatest chlamydial glycogen synthesis (36 h) was not affected by cortisol treatment. Cortisol treatment appeared to have retarded the accumulation of glycogen in treated infected cells until 30 h after infection. Treated infected cells prelabeled with [6-14C]glucose accumulated a greater amount of 14C in glycogen than untreated infected cells. All cortisol-treated, infected cells exhibited elevated levels of fructose-1,6-bisphosphatase activity, whereas untreated infected cells did not. The hypothesis that cortisol affects chlamydia multiplication by altering the intracellular environment of the host cell is compatible with the results obtained.
D002478:Cells, Cultured; D002692:Chlamydia trachomatis / Q000254:growth & development* / Q000378:metabolism; D006597:Fructose-Bisphosphatase / Q000378:metabolism*; D006003:Glycogen / Q000096:biosynthesis*; D006854:Hydrocortisone / Q000494:pharmacology*; D007668:Kidney
D006003:Glycogen; D006597:Fructose-Bisphosphatase; D006854:Hydrocortisone