TY - CHAP M1 - Book, Section TI - Leukocyte Accumulation in Pulmonary Disease A1 - Lukacs, Nicholas W. A1 - Ward, Peter A. A2 - Grippi, Michael A. A2 - Elias, Jack A. A2 - Fishman, Jay A. A2 - Kotloff, Robert M. A2 - Pack, Allan I. A2 - Senior, Robert M. A2 - Siegel, Mark D. PY - 2015 T2 - Fishman's Pulmonary Diseases and Disorders, 5e AB - Mediators produced during inflammatory/immune responses dictate the severity and intensity of pulmonary disease. The profile of inflammatory leukocyte populations accumulating in inflamed tissues is initiated by cytokine-induced expression of adhesion molecules on the vascular endothelium. Endothelial adhesion molecules include intracellular adhesion molecule-1 (ICAM-1), vascular cell adhesion molecule-1 (VCAM-1), as well as E- and P-selectins that initiate, and in some cases, mediate the migration of leukocytes into tissues. Subsequently, leukocyte adherence to the endothelium is followed by leukocyte migration into the inflamed tissue, directed by chemotactic molecules at the site of the inflammatory/immune response. Upregulation of these early response mediators is crucial for the initiation of early events that regulate the inciting agent, whether it is infectious or noninfectious in nature. However, the continuous over-production of these mediators can lead to destructive, pathologic consequences due to the continued recruitment and activation of disease-specific leukocyte populations. In human lung, inflammation-induced damage can be observed in numerous inflammatory diseases, including both acute and chronic disease settings. In this chapter, we will examine the mediators that promote inflammatory diseases in lung and outline how specific leukocyte populations can contribute to pulmonary pathology. SN - PB - McGraw-Hill Education CY - New York, NY Y2 - 2024/04/19 UR - accessmedicine.mhmedical.com/content.aspx?aid=1122356063 ER -