Exposure to high levels of estrogen and progesterone may help curb proinflammatory cytokine and chemokine expression associated with HIV-1.
A new study published in PLoS One demonstrated that the pretreatment of monocyte derived macrophages (MDMs) with high concentrations of estrogen and progesterone results in the downmodulation of proinflammatory cytokine and chemokine expression as well as the downregulation of HIV-1 replication.
“[Our] data implies that the inhibitory effect of estrogen and progesterone may be mediated through the engagement of estrogen and progesterone receptors,” according to study investigator Indira Hewlett, PhD, et al. “A probable mechanism for the regulatory effect exerted by estrogen and progesterone could be due to modulation of chemokine receptors that serve as co-receptors for HIV-1 entry.”
Investigators of this study sought to determine the molecular mechanisms of HIV-1 replication downregulation and associated antiviral responses following exposure to estrogen and progesterone treatment. After leukapheresis, the researchers isolated human monocytes from peripheral blood mononuclear cells of male and female donors who were seronegative for HIV-1.
All primary MDMs were cultured for a total of 5 days and subsequently infected with HIV-1 Ba-L, isolates of HIV-1 subtype B-NSI, and HIV-1 subtype C-NSI. Infected MDMs were pretreated with 0.6 nM mifepristone or 5 μM tamoxifen and then exposed to 110 nM estrogen or 64 nM progesterone. The researchers also used varying concentrations of the 2 hormones to determine the effect of low versus high concentrations on replication/modulation.