The Regulation of Inflammatory Pathways and Infectious Disease of the Cervix by Seminal Fluid
Figure 1
A cartoon highlighting the role of seminal plasma and seminal plasma prostaglandins (PG) such as PGE2 in regulating inflammatory and tumorigenic pathways in cervical cancer cells. Seminal plasma PGE2, or PGE2 endogenously produced by COX enzymes in response to inflammation or HIV infection via the induction of COX-2, binds to PG receptors on the surface of the cell to activate intracellular signal transduction pathways and target gene transcription and biosynthesis. Target genes which are known to be regulated in this manner include HIV chemokine receptors like CXCR4 as well as growth factors, angiogenic factors, chemokines, and cytokines. These latter factors all act in an autocrine/paracrine manner in the tumour microenvironment to facilitate local changes in tissue architecture, inflammation and enhance tumorigenesis. Elevated expression of HIV receptors could enhance virus entry into cells and enhance susceptibility to infection. HIV is also known to enhance inflammation by inducing COX-2 expression. The activity of COX-2 and subsequent inflammation can be inhibited by nonsteroidal anti-inflammatory drugs (NSAIDs). The activity of specific PG receptors can also be inhibited with selective receptor antagonists to inhibit subsequent activation of signal transduction pathways.
