*3.1. Monocytes*

In vitro studies also suggest that prostacyclin decreased cytokine secretion by human monocytes. Beraprost, iloprost, and treprostinil dose-dependently suppressed TNF-α expression, and iloprost was the most efficient of the three analogs based on the concentration needed to achieve a partial reduction in cytokine production [13]. These results provide a potential role for prostacyclin in helping to control the symptoms of asthma that may be due to increased TNF-α levels. The effects of prostacyclin in restraining cytokine production in monocytes may not be IP-dependent, as is the case in studies in which DCs were used. For example, in a study that analyzed the effects of prostacyclin analogs on both Th1 and Th2 cytokines in human monocytes, prostacyclin analogs suppressed Th1-related chemokine expression via PPAR-γ [23]. Additionally, the same study reported that iloprost and treprostinil suppressed IP-10, a Th1-related chemokine protein, via the IP-receptor-cAMP pathway [23]. Overall, these studies reflect the importance of better understanding the multiple pathways by which prostacyclin acts, as they can provide several avenues in which to study prostacyclin analog efficacy.
