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Inflammation is the body’s protective response against infections or injuries. Inflammation mobilizes defensive cells to the site of injury, limits the spread of pathogens, eliminates them, and initiates tissue repair. Inflammation can occur in any organ, but is most common, and also most easily observable in the skin and underlying tissues. Typical signs include redness, heat, swelling and pain.
Inflammation is an important defense mechanism, but it can be a double-edged sword when things go wrong. An autoimmune disease may result when inflammation targets and destroys the body’s own cells. An acute inflammation that fails to stop after the original insult is cleared, can become chronic and damaging to healthy tissues.
Acute inflammation is initiated when tissue-resident immune cells, such as macrophages, encounter an inflammatory stimulus. This stimulus can be a pathogen, a toxin, or an injured host cell. Binding of the stimulus to its receptor on the immune cell triggers a signaling cascade that activates production of cytokines and other inflammatory mediators.
Inflammatory chemicals dilate blood vessels, increasing blood flow and enhancing vessel permeability, allowing plasma fluid and more immune cells to seep through and accumulate in the inflamed tissue. This vasodilation is responsible for clinical signs of inflammation such as redness, heat and swelling.
The infiltration of blood components into the injured tissue occurs in 3 phases. The first phase is the exudation of plasma fluid containing various antimicrobial mediators, platelets and blood clotting factors. These factors can destroy microbes and stop any bleeding that may have occurred.
The second phase is the infiltration of neutrophils – the major phagocytes involved in first-line defense. Once activated by inflammatory mediators, endothelial cells of blood vessels become adhesive, they attach to neutrophils in blood flow, slowing them down, before getting them to squeeze through the vessel wall. Chemical cues guide neutrophils to the battle field, where they engulf bacteria and destroy them with enzymes or toxic peroxides. Neutrophils may also release highly reactive oxygen species in a phenomenon known as oxidative burst, which kills pathogens faster and more efficiently. The pathogen-laden neutrophils then die via apoptosis.
In the third phase arrive monocytes. Monocytes differentiate into macrophages, which then remove pathogens, injured cells and dying neutrophils by phagocytosis. Macrophages that have completed their mission are cleared from the tissue by the lymphatic system. Accumulation of fluid increases pressure on lymphatic capillaries, forcing open their one-way valves, facilitating lymphatic drainage. Lymph containing debris-laden macrophages passes through a number of lymph nodes and is filtered clean before it returns to the bloodstream.
Once the site is cleared from the original insult, immune cells stop producing pro-inflammatory chemicals and, instead, start producing anti-inflammatory mediators, which actively drive the termination of inflammation. Many of these anti-inflammatory molecules are lipids, some of which are synthesized from dietary omega-3 fatty acids. This step is essential in ensuring the favorable outcome of inflammation. Failure to resolve inflammation leads to development of chronic inflammation which continuously deals damage to healthy tissues. Chronic inflammation is a known contributing factor to pathogenesis of a wide variety of conditions including cardiovascular diseases, asthma, diabetes, arthritis, and even cancer.
