Chapter 10 Inflammation
Inflammation is usually classified according to its time course as:
ACUTE INFLAMMATION
Causes of acute inflammation
The principal causes of acute inflammation are:
Essential macroscopic appearances of acute inflammation
Redness (rubor)
An acutely inflamed tissue appears red, for example skin affected by sunburn, cellulitis due to bacterial infection or acute conjunctivitis. This is due to dilatation of small blood vessels within the damaged area (Fig. 10.1).
Heat (calor)
Increase in temperature is seen only in peripheral parts of the body, such as the skin. It is due to increased blood flow (hyperaemia) through the region, resulting in vascular dilatation and the delivery of warm blood to the area. Systemic fever, which results from some of the chemical mediators of inflammation, also contributes to the local temperature.
Swelling (tumor)
Swelling results from oedema—the accumulation of fluid in the extravascular space as part of the fluid exudate—and, to a much lesser extent, from the physical mass of the inflammatory cells migrating into the area (Fig. 10.2). As the inflammation response progresses, formation of new connective tissue contributes to the swelling.
Early stages of acute inflammation
Changes in vessel calibre
The microcirculation consists of the network of small capillaries lying between arterioles, which have a thick muscular wall, and thin-walled venules. Capillaries have no smooth muscle in their walls to control their calibre, and are so narrow that red blood cells must past through them in single file. The smooth muscle of arteriolar walls forms precapillary sphincters which regulate blood flow through the capillary bed. Flow through the capillaries is intermittent, and some form preferential channels for flow while others are usually shut down (Fig. 10.3).
In blood vessels larger than capillaries, blood cells flow mainly in the centre of the lumen (axial flow), while the area near the vessel wall carries only plasma (plasmatic zone). This feature of normal blood flow keeps blood cells away from the vessel wall.
Increased vascular permeability
Small blood vessels are lined by a single layer of endothelial cells. In some tissues, these form a complete layer of uniform thickness around the vessel wall, while in other tissues there are areas of endothelial cell thinning, known as fenestrations. The walls of small blood vessels act as a microfilter, allowing the passage of water and solutes but blocking that of large molecules and cells. Oxygen, carbon dioxide and some nutrients transfer across the wall by diffusion, but the main transfer of fluid and solutes is by ultrafiltration, as described by Starling. The high colloid osmotic pressure inside the vessel, due to plasma proteins, favours fluid return to the vascular compartment. Under normal circumstances, high hydrostatic pressure at the arteriolar end of capillaries forces fluid out into the extravascular space, but this fluid returns into the capillaries at their venous end, where hydrostatic pressure is low (Fig. 10.4). In acute inflammation, however, not only is capillary hydrostatic pressure increased, but there is also escape of plasma proteins into the extravascular space, increasing the colloid osmotic pressure there. Consequently, much more fluid leaves the vessels than is returned to them. The net escape of protein-rich fluid is called exudation; hence, the fluid is called the fluid exudate.
Ultrastructural basis of increased vascular permeability
The ultrastructural basis of increased vascular permeability was originally determined using an experimental model in which histamine, one of the chemical mediators of increased vascular permeability, was injected under the skin. This caused transient leakage of plasma proteins into the extravascular space. Electron microscopic examination of venules and small veins during this period showed that gaps of 0.1–0.4 μm in diameter had appeared between endothelial cells. These gaps allowed the leakage of injected particles, such as carbon, into the tissues. The endothelial cells are not damaged during this process. They contain contractile proteins such as actin, which, when stimulated by the chemical mediators of acute inflammation, cause contraction of the endothelial cells, pulling open the transient pores. The leakage induced by chemical mediators, such as histamine, is confined to venules and small veins. Although fluid is lost by ultrafiltration from capillaries, there is no evidence that they too become more permeable in acute inflammation.
Other causes of increased vascular permeability
In addition to the transient vascular leakage caused by some inflammatory stimuli, certain other stimuli, e.g. heat, cold, ultraviolet light and X-rays, bacterial toxins and corrosive chemicals, cause delayed prolonged leakage. In these circum-stances, there is direct injury to endothelial cells in several types of vessel within the damaged area (Table 10.1).
Table 10.1 Causes of increased vascular permeability
Time course | Mechanisms |
---|---|
Immediate transient | Chemical mediators, e.g. histamine, bradykinin, nitric oxide, C5a, leukotriene B4, platelet activating factor |
Immediate sustained | Severe direct vascular injury, e.g. trauma |
Delayed prolonged | Endothelial cell injury, e.g. X-rays, bacterial toxins |
Formation of the cellular exudate
The accumulation of neutrophil polymorphs within the extracellular space is the diagnostic histological feature of acute inflammation. The stages whereby leukocytes reach the tissues are shown in Figure 10.5.
Adhesion of neutrophils
Endothelial cell expression of selectins, such as endothelial– leukocyte adhesion molecule-1 (ELAM-1), which establishes the first loose contact between leukocytes and endothelium (resulting in ‘rolling’), integrins, and intercellular adhesion molecule-1 (ICAM-1), to which the leukocytes’ surface adhesion molecules bond, is increased by:
Later stages of acute inflammation
Chemical mediators of acute inflammation
Chemical mediators released from cells
5-Hydroxytryptamine (serotonin).
This is present in high concentration in platelets. It is a potent vasoconstrictor.
Plasma factors
Coagulation factor XII (the Hageman factor), once activated by contact with extracellular materials such as basal lamina, and various proteolytic enzymes of bacterial origin, can activate the coagulation, kinin and fibrinolytic systems. The inter-relationships of these systems are shown in Figure 10.6.
Kinin system.
The kinins are peptides of 9–11 amino acids; the most important is bradykinin. The kinin system is activated by coagulation factor XII (Fig. 10.7). Bradykinin is also a chemical mediator of the pain that is a cardinal feature of acute inflammation.
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