The Foundations of Inflammation

Inflammation is a natural, normal response with three objectives: detoxification, repair and protection. It is an essential function mediated by the immune system. It is also a highly complex process which initiates a series of events that, as far as possible, heal and reconstitute the damaged tissue. Repair begins during the early phases of inflammation but reaches completion usually after the injury or influence has been neutralized.

Inflammation rids the body of both the initial cause of the cell injury (e.g. microbes, toxins, oxidation) and the consequences (e.g. necrotic tissue). Without inflammation, infections would go unchecked, wounds would never heal, and injured organs would fail.

However, inflammation may be harmful. Inflammatory reactions underlie life-threatening hypersensitivity reactions to insect bites, drugs and toxins. It also drives a fever. Common chronic diseases involving inflammation are rheumatoid arthritis, heart disease and cancer.

The inflammatory response occurs in the plasma, circulating cells, blood vessels and cellular and extracellular constituents of connective tissue. The circulating cells include neutrophils, monocytes, eosinophils, lymphocytes, basophils and platelets. The connective tissue cells are mast cells, which contain histamine, and fibroblasts.

Inflammation has two patterns, acute and chronic. Acute reactions last up to a few days and their main characteristics are the exudation of fluid and plasma proteins (edema) and the emigration of leukocytes and antibodies to the site. Chronic reactions are associated with the emigration of lymphocytes and macrophages, the proliferation of blood vessels, fibrosis and tissue necrosis. Both responses are mediated by chemical factors derived from the plasma or cells and triggered by inflammatory stimuli.

Essentially there are two pathways of inflammation commonly utilized by our bodies. Whenever there is a factor that involves either a functional or metabolic stress, there will always be an increased rate of cellular respiration in the area. The cells under stress speed up their rate of metabolism. This causes more toxic by-products from metabolism. These must be neutralized and eliminated by the body to prevent cellular damage in the area. Mediation is by cytotoxic antibody and complements.

Once the area is detoxified, the repair of injured tissues in the area takes place. When the primary pathway of inflammation is efficient, there are few symptoms of pain, swelling, redness or heat in the area. This pathway is utilized either in the early stages of a problem, or ongoing when it remains efficient and effective at managing the stress in the area.

There are various reasons why the primary pathway of inflammation may prove inefficient. The first is a compromised immune system, which is unable to drive the necessary detoxification and repair pathway. The second reason is that the level of functional or metabolic stress in the area is beyond the capabilities of the primary pathway. When this happens, there will be an added level of toxification of the tissues (areas under this type of stress serve as free-radical magnets, free radicals being electrically unstable particles that are responsible for damaging tissue). A higher degree of damage may then follow. This is where the secondary pathway of inflammation come into play.

The defense against microbes and antigens is both innate (non-antigen specific) and adaptive (antigen specific). Immune complex inflammation is mediated by antigen-antibody complex and complements. This is most common in allergy. Cytotoxic inflammation is mediated by cytotoxic antibody and complements.

Secondary, or chronic, inflammation, is the pathway that takes over when the primary pathway fails to manage the problem. It is mediated by T-cells and cytokines. This pathway is concerned with protection of cells from rapid destruction and it also works to allow the tissues to adapt and compensate for the ongoing problem. Secondary inflammation prevents the tissue assault from spiraling out of control.

Lipids

When cells are activated by stimuli, their membrane lipids are rapidly remodeled to generate biologically active lipid mediators that serve as intracellular and extracellular signals. The metabolic products of the lipid aracadonic acid affect inflammation. These lipid signals, prostaglandins, act as short range hormones which are rapidly formed, act and rapidly decay. Two enzymes, COX1 and 2, mediate the conversion of aracadonic acid to the prostaglandins. The class of drugs known as non-steroidal anti-inflammatories (NSAIDs) inhibit this conversion. Prostaglandins have multiple involvement in inflammation, as fever, and pain.

The inflammatory process is of immense complexity with considerable overlap and multiple responses. Long-term chronic inflammation has both local and systemic effects. Cellular and immune response is altered. The inflammatory focus may be unresolved and the system unable to restore normal function. Remaining dysfunction may be slight or grow out of control. It is a matter of degrees where the strength of the lesion and the strength of the inflammatory/immune response are engaged. The outcome depends on this relative state and the success of medical and healing intervention.