Smooth muscle contraction is the fundamental event in gastrointestinal motion. Inflammation of the human intestine causes increased levels of smooth muscle-specific actin, which in turn promotes the thickening of the smooth muscle layers. The increased smooth muscle actin may affect force production and further demonstrates the plasticity of HCoSMC in the inflamed intestine. Studies also show that human intestinal smooth muscle cells respond to IL-1beta and TNF-alpha stimulation by releasing IL-6. It may significantly contribute to the overall systemic inflammatory response. Human colonic smooth muscle cells (HCoSMC) possess a different subtype of somatostatin receptor from gastric smooth muscle cells. HCoSMC makes it more feasible to study the contractile and proliferative responses of human colonic smooth muscle.