The conditional role of inflammation in pregnancy and cancer

Abstract

Cancer growth is characterized by proliferation of tumor cells in conjunction with invasion of all different immune cells that also invade healing wounds. This inflammatory response is necessary for cell proliferation but a second purpose of the inflammatory process is so that a low Th1/Th2 ratio is present with overexpression of IL-10, TGF-β and IFN-γ. Down regulation of NO activity also shifts the balance between M1 and M2 macrophages. Both aspects allow the antigenous nature of the tumor to escape anti-tumor effects of the host. Support for this view comes from observations in pregnancy in which the placenta exhibits identical immune responses and downregulation of NO production to allow trophoblast cells to invade the uterine tissues without being rejected. Cell proliferation requires a metabolic set-up in which the organism produces adequate substrate for growth. This also bears the characteristics of a systemic inflammatory response delivering a similar substrate mix required for cancer and fetal growth. This arrangement is clearly beneficial in pregnancy and therefore supports the view that cancer growth is facilitated by the organism: the cancerous tumor elicits an immunological response opposing anti-tumor effects and induces the host to produce building blocks for growth.