RT Book, Section A1 Levi, Marcel A2 Kaushansky, Kenneth A2 Prchal, Josef T. A2 Burns, Linda J. A2 Lichtman, Marshall A. A2 Levi, Marcel A2 Linch, David C. SR Print(0) ID 1180477591 T1 The Inflammatory Response T2 Williams Hematology, 10e YR 2021 FD 2021 PB McGraw-Hill Education PP New York, NY SN 9781260464122 LK accessmedicine.mhmedical.com/content.aspx?aid=1180477591 RD 2024/03/29 AB SUMMARYThe acute inflammatory response is characterized by a rapid localized increase in blood flow, an increase in microvascular permeability, and the sequential recruitment of different types of leukocytes. Acute inflammation may be followed by “chronic” inflammation and a superimposed series of reparative processes (eg, angiogenesis, production of extracellular matrix, parenchymal regeneration, and scar formation). The early hemodynamic changes at a site of inflammation establish low shear conditions that enable marginated leukocytes to engage in low-affinity selectin-mediated rolling interactions with activated endothelial cells. In response to locally produced soluble and cell-surface mediators, endothelial cells and rolling leukocytes sequentially express several sets of complementary adhesion molecules that include selectins, integrins, and members of the immunoglobulin superfamily. Leukocyte and endothelial cell adhesion molecules mediate the high-affinity adhesive interactions necessary for leukocyte emigration from the vascular space along chemotactic gradients. Analogous, temporally regulated, soluble mediators and cellular adhesion molecules also orchestrate succeeding monocyte- and lymphocyte-rich chronic inflammatory responses. This paradigm is modulated by a vast network of surface-active and soluble inflammatory mediators. Recruited leukocytes and cells indigenous to the anatomic site of inflammation both play critical roles in host defense, resolution of inflammation, and tissue repair.