The Inflammatory Process

What is inflammation? Isn’t this the process that is supposed to be good for our bodies? How can it now be something that causes harm to so many different aspects of the body? As we learn more about the biological mechanisms of inflammation, it becomes clear that this process is more complicated than was once thought.

Inflammation is the body’s response to cellular injury. Despite the fact that the press has emphasized the harmful effects of inflammation, the fact remains that without this process, our bodies could not survive. Inflammation represents a protective response designed to rid the body of the initial cause of cell injury and the consequences of that injury. Cell injury may occur due to trauma, genetic defects, physical and chemical agents, tissue necrosis, foreign bodies, immune reactions and infections.

Inflammation is a local reactive change that involves the release of antibacterial agents from nearby cells that defend the host against infection. It also facilitates early tissue healing and repair. It contains—or “walls off”—the infectious or injurious agent and serves as a defense mechanism that the body can use to restore itself to a normal morphological form and function.

The inflammatory response consists of a vascular and a cellular reaction. These reactions are mediated by chemical factors derived from plasma proteins or cells. The classic signs of inflammation are redness, swelling, heat, pain and loss of function. The physiologic explanations for these signs appear in Table I. Other signs of inflammation include fever, leukocytosis or an increase in the number of circulating white blood cells, the presence of acute-phase proteins including C-reactive proteins (CRP), fibrinogen and serum amyloid A protein (SAA), and sepsis.

There are two types of inflammation: acute and chronic. Acute inflammation is characterized by a rapid onset and short duration. It manifests with exudation of fluid and plasma proteins, and emigration of leukocytes, most notably neutrophils. Chronic inflammation is of prolonged duration and manifests histologically by the presence of lymphocytes and macrophages and results in fibrosis and tissue necrosis. When inflammation continues for prolonged periods of time, it can be thought of as the healing process in overdrive, and deleterious changes can occur to localized tissues as well as the entire body.

In appreciating the inflammatory process, it is important to understand the role of chemical mediators. These are the substances that tend to direct the inflammatory response. These inflammatory mediators come from plasma proteins or cells including mast cells, platelets, neutrophils and monocytes/macrophages. They are triggered by bacterial products or host proteins. Chemical mediators bind to specific receptors on target cells and can increase vascular permeability and neutrophil chemotaxis, stimulate smooth muscle contraction, have direct enzymatic activity, induce pain or mediate oxidative damage. Most mediators are short-lived but cause harmful effects.1 Examples of chemical mediators include vasoactive amines (histamine, serotonin), arachadonic acids (prostaglandins, leukotrienes) and cytokines (tumor necrosis factor and interleukin–1).

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