Interactions between fibroblast growth factor 2 and distinct asthma mediators enhance bronchial smooth muscle cell proliferation
Increased bulk of smooth muscle mass around the airways is a typical feature of asthma. Several mediators act in concert or antagonistically to regulate airway smooth muscle (ASM) cell proliferation. This thesis focuses on fibroblast growth factor (FGF)2 and transforming growth factor (TGF)[béta]1 which are known to be sequentially upregulated in the lung following allergic challenge and have recently been shown to synergize together in ASM cell proliferation. Emphasis is put toward the conflicting studies documenting the mitogenic effect of TGF[béta]1 in vitro and to its seemingly potent effect in vivo. Thereafter, different asthma mediators, such as IL-4 and IL-13, are introduced and how their mitogenic potential toward ASM cells could be altered by FGF2 is presented. Finally, how the controversial issue between in vitro and in vivo data regarding the mitogenic effect of leukotrienes could be reconciliated and how it could be related to FGF2 and TGF[béta]1 proliferative synergism is discussed.