Abstract
BACKGROUND: Inflammation-induced changes in smooth muscle may be the consequence of changes in the properties of smooth muscle itself, in the control by nerves and hormones, in the microenvironment, or in the balance of constitutive or induced mediators. A general concept is that the specific characteristics and effects of inflammation can be linked to the nature of the infiltrate and the associated mediators, which are dictated predominantly by the immune environment. Inflammatory mediators may regulate smooth muscle function by directly acting on smooth muscle cells or, indirectly, through stimulation of the release of mediators from other cells. In addition, smooth muscle is not a passive bystander during inflammation and our knowledge of molecular signaling pathways that control smooth muscle function, and the contribution of the immune mechanisms to smooth muscle homeostasis, has expanded greatly in the last decade. Recent studies also demonstrated the relevance of extracellular proteases, of endogenous or exogenous origin, redox imbalance, or epigenetic mechanisms, to gastrointestinal dismotility and inflammation in the context of functional and organic disorders. PURPOSE: In this review we discuss the various types of inflammation and the established and emerging mechansims of inflammation-induced changes in smooth muscle morphology and function.