Inflammation, Animation

By Adem Lewis / in , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , /

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.

8 thoughts on “Inflammation, Animation

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