ABSTRACT
Studies of hyper-responsiveness of bronchial smooth muscle in asthma provide the best known systems of the complexities of inflammatory mediators and muscle pathophysiology. Despite considerable evidence that intestinal motility is markedly altered in inflammatory conditions of the small and large intestine, there is a paucity of information about the mechanisms underlying these abnormalities in muscle function. To study the inflammation-induced alterations in intestinal smooth muscle function, an obvious strategy is to undertake a detailed histological and ultrastructural evaluation to determine if any abnormalities in structure or cellular composition are evident. Intestinal smooth muscle is composed of the muscle cells themselves, the vasculature, extensive neural networks, connective tissue matrix, and various interstitial cells, including fibroblasts and mast cells. Inflammation of muscle occurs in many conditions and can involve neutrophils, eosinophils, mast cells and lympho-mononuclear cells. The contributions of smooth muscle cells themselves to adaptations in function that arise with inflammatory states must be explored.
