Airway smooth muscle: immunomodulatory cells that modulate airway remodeling?
Although the pathogenesis of asthma remains unclear, substantial progress has been made over the past decades in the characterization of airway inflammation as a pathogenetic mechanism in asthma. New evidence suggests that airway smooth muscle (ASM), the most important cell modulating bronchomotor tone, plays an important immunomodulatory role in the orchestration and perpetuation of airway inflammation. Evidence now suggests that the signaling pathways that modulate leukocyte function may be disparate from those found in resident effector cells such as ASM, fibroblasts and epithelial cells. Further investigation and understanding of the critical signaling pathways that modulate ASM cell release, secretion of chemokines/cytokines and expression of cell adhesion molecules (CAMs) may offer new therapeutic approaches in the treatment of asthma.
D000222:Adaptation, Physiological; D000276:Adjuvants, Immunologic / Q000378:metabolism*; D000818:Animals; D001249:Asthma / Q000473:pathology* / Q000503:physiopathology*; D015815:Cell Adhesion Molecules / Q000378:metabolism*; D002455:Cell Division / Q000502:physiology; D018925:Chemokines / Q000378:metabolism; D016207:Cytokines / Q000378:metabolism; D005109:Extracellular Matrix / Q000378:metabolism*; D006801:Humans; D009130:Muscle, Smooth / Q000378:metabolism / Q000473:pathology*; D032389:Myocytes, Smooth Muscle / Q000166:cytology / Q000378:metabolism*; D015398:Signal Transduction; D014132:Trachea / Q000473:pathology / Q000503:physiopathology
D000276:Adjuvants, Immunologic; D015815:Cell Adhesion Molecules; D018925:Chemokines; D016207:Cytokines