IL6 and inflammatory bowel disease: Whereas the pathogenesis of IBD is generally believed to be the result of immune dysregulation due to the interaction of genetic and microbial factors, this stimulus will also accelerate cellular senescence and promote increased production of inflammatory factors such as tumor necrosis factor (TNF) α, interleukin (IL)-1, IL-6, IL-18, IL-12 and IL-23 [30–32].