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2 Inflammation Hedwig S 2 Inflammation Hedwig S. Murphy FPO FPO FPO FPO Overview Of Inflammation Leukocyte Recruitment In Acute Inflammation Acute Inflammation: Vascular Events Leukocyte Adhesion Plasma-Derived Mediators Of Inflammation Chemotactic Molecules Hageman Factor Leukocytes Traverse the Endothelial Cell Barrier to Gain Kinins Access to the Tissue Complement System and the Membrane Attack Leukoctye Functions In Acute Inflammation Complex (MAC) Phagocytosis Cell-Derived Mediators Of Inflammation Neutrophil Enzymes Arachidonic Acid and Platelet-Activating Factor Oxidative and Nonoxidative Bactericidal Activity Prostanoids, Leukotrienes, and Lipoxins Outcomes Of Acute Inflammation Cytokines Chronic Inflammation Reactive Oxygen Species (ROS) Cells From Both the Circulation and Affected Tissue Cells Of Inflammation Play a Role in Chronic Inflammation Neutrophils Injury And Repair In Chronic Inflammation Endothelial Cells Granulomatous Inflammation Monocyte/Macrophages Systemic Manifestations Of Inflammation Mast Cells and Basophils Acute Phase Response Eosinophils Fever Platelets Shock Inflammation is the response to injury of a tissue the second century AD. These features correspond to and its microcirculation and is characterized by elab- inflammatory events of vasodilation, edema, and tis- oration of inflammatory mediators as well as move- sue damage. A fifth sign functio laesa (loss of func- ment of fluid and leukocytes from the blood into ex- tion) was added in the 19th century by Rudolf travascular tissues. Inflammation localizes and Virchow, who recognized inflammation as a response eliminates microorganisms, damaged cells, and foreign to tissue injury. particles, paving the way for a return to normal struc- ture and function. The clinical signs of inflammation, recognized in Overview Of Inflammation Egyptian medical texts before 1000 BC, were codified Inflammation is best viewed as an ongoing process that can as the four cardinal signs of inflammation: rubor be divided into phases. (redness), calor (heat), tumor (swelling), and dolor • Initiation results in a stereotypic, immediate response (pain) by the Roman encyclopedist Aulus Celsus in termed acute inflammation. The acute response is 2323 24 Essentials of Rubin’s Pathology Acute inflammation with densely packed polymor- FIGURE 2-1. Chronic inflammation. phonuclear neutrophils (PMNs) with multilobed nu- FIGURE 2-2. Lymphocytes, plasma cells clei (arrows). (arrows), and a few macrophages are present. characterized by the rapid flooding of the injured tissue with fluid, coagulation factors, cytokines, chemokines, platelets and inflammatory cells, and neutrophils in par- Acute Inflammation: Vascular Events ticular (Fig. 2-1). Among the earliest responses to tissue injury are alterations • Amplification depends upon the extent of injury and in the anatomy and function of the microvasculature, activation of mediators such as kinins and complement which may promote edema (see Figs. 2-3 and 2-4). These re- components. Additional leukocytes and macrophages sponses include: are recruited to the area. • Destruction of the inciting agent by phagocytosis and 1. Transient vasoconstriction of arterioles at the site of enzymatic or nonenzymatic processes reduces or elimi- injury is the earliest vascular response to mild skin in- nates foreign material or infectious organisms. At the jury. This process is mediated by both neurogenic and same time, damaged tissue components are also re- chemical mediator systems and usually resolves within moved, paving the way for repair to begin (see Chapter 3). seconds to minutes. • Termination of the inflammatory response is mediated 2. Vasodilation of precapillary arterioles then increases by intrinsic anti-inflammatory mechanisms that limit blood flow to the tissue, a condition known as hyper- tissue damage and allow for either restoration of tis- emia. Vasodilation is caused by release of specific medi- sue, with return to normal physiological function, or ators and is responsible for redness and warmth at sites repair and the development of scar in place of normal of tissue injury. tissue. 3. An increase in endothelial cell barrier permeability results in edema. Loss of fluid from intravascular com- Certain types of injury trigger a sustained inflammatory partments as blood passes through capillary venules response associated with the inability to clear injured tissue leads to local stasis and plugging of dilated small vessels and foreign agents. Such a persistent response (which often with erythrocytes. These changes are reversible following has an immune component) is termed chronic inflamma- mild injury: within several minutes to hours, the ex- tion. Chronic inflammatory infiltrates are composed largely travascular fluid is cleared through lymphatics. of lymphocytes, plasma cells, and macrophages and often have an immune component (Fig. 2-2). Acute and chronic in- The vascular response to injury is a dynamic event that flammatory infiltrates often coexist. involves sequential physiological and pathological changes. CHAPTER 2: INFLAMMATION 25 A NORMAL VENULE Basement membrane Endothelial cell Tight junction B VASOACTIVE MEDIATOR-INDUCED INJURY Endothelial Time course of change in permeability retraction and gap y t i l n i formation i b e a g e Electrolytes, n m a r h fluid, protein e C p 012345 Hours C DIRECT INJURY TO ENDOTHELIUM Time course of change Denuded in permeability basement membrane y t i Severe l n i i b e a g e Gap formation n m a r h e p C Mild Blebbing 012345 Hours FIGURE 2-3. Responses of the microvasculature to injury. A. The wall of the normal venule is sealed by tight junctions between adjacent endothelial cells. B. During mild vasoactive mediator-induced injury, the endothelial cells separate and permit the passage of the fluid constituents of the blood. C. With severe direct injury, the endothelial cells form blebs (b) and separate from the underlying basement membrane. Areas of denuded basement membrane (arrows) allow a prolonged escape of fluid elements from the microvasculature. Vasoactive mediators, originating from both plasma and Mild direct injury to the endothelium results in a biphasic cellular sources, are generated at sites of tissue injury (see response: an early change in permeability occurs within Fig. 2-4). These mediators bind to specific receptors on vas- 30 minutes after injury, followed by a second increase in cular endothelial and smooth muscle cells, causing vasocon- vascular permeability after 3 to 5 hours. When damage is se- striction or vasodilation. Proximal to capillaries, vasodilation vere, exudation of intravascular fluid into the extravascular of arterioles increases blood flow and can exacerbate fluid compartment increases progressively, peaking 3 to 4 hours leakage into the tissue. Distally, vasoconstriction of postcap- after injury. illary venules increases capillary bed hydrostatic pressure, po- Severe direct injury to the endothelium, such as is tentiating edema formation. By contrast, vasodilation of caused by burns or caustic chemicals, may result in irre- venules decreases capillary hydrostatic pressure and inhibits versible damage. In such cases, the endothelium separates movement of fluid into extravascular spaces. from the basement membrane, resulting in cell blebbing After injury, vasoactive mediators bind specific receptors (blisters or bubbles between the endothelium and the on endothelial cells, causing endothelial cell contraction basement membrane). This leaves areas of basement and gap formation, a reversible process (see Fig. 2-3B). This membrane naked (see Fig. 2-3C), thereby disrupting the break in the endothelial barrier leads to extravasation (leak- barrier between the intravascular and extravascular age) of intravascular fluids into the extravascular space. spaces. 26 Essentials of Rubin’s Pathology SOURCE MEDIATOR Clotting/fibrinolytic Fibrin split system products • Hageman factor PLASMA- activation DERIVED Kallikrein-kinin Kinins system (bradykinin) • Complement system activation C3a, C5a Increased vascular EDEMA permeability • Mast cell/basophil degranulation Histamine • Platelets Serotonin CELL- DERIVED • Platelet- • Inflammatory cells activating factor • Prostaglandins • Leukotrienes • Nitric oxide • Endothelium • Platelet- activating factor • Prostaglandins Inflammatory mediators of FIGURE 2-4. increased vascular permeability. Several definitions are important for understanding the in which the predominant cell type is the polymor- vascular components of inflammation: phonuclear neutrophil (PMN). • Edema is accumulation of fluid within the extravascular compartment and interstitial tissues. • A transudate is edema fluid with low protein content Plasma-Derived Mediators (specific gravity <1.015). Transudates tend to occur in Of Inflammation noninflammatory conditions, where the endothelial bar- rier remains intact and prevents the loss of large mole- Numerous chemical mediators are integral to initiation, cules from the vasculature. amplification, and termination of inflammatory processes • An exudate is edema fluid with a high protein concen- (Fig. 2-4). Cell- and plasma-derived mediators work in con- tration (specific gravity >1.015), which frequently con- cert to activate cells by (1) binding specific receptors, (2) re- tains inflammatory cells. Exudates are observed early in cruiting cells to sites of injury, and (3) stimulating the re- acute inflammatory reactions and are produced by mild lease of additional soluble mediators. These mediators injuries, such as sunburn
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