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inflammation
pathology

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Written and fact-checked by The Editors of Encyclopaedia Britannica

Last Updated: Mar 11, 2024 • Article History

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Summary

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Inflammation, a response triggered by damage to living tissues. The

inflammatory response is a defense mechanism that evolved in higher organisms
to protect them from infection and injury. Its purpose is to localize and eliminate
the injurious agent and to remove damaged tissue components so that the body
can begin to heal. The response consists of changes in blood flow, an increase in
permeability of blood vessels, and the migration of fluid, proteins, and white
blood cells (leukocytes) from the circulation to the site of tissue damage. An
inflammatory response that lasts only a few days is called acute inflammation,
while a response of longer duration is referred to as chronic inflammation.
Although acute inflammation is usually
beneficial, it often causes unpleasant
sensations, such as the pain of a sore throat or
the itching of an insect bite. Discomfort is
usually temporary and disappears when the
zoom_in
inflammatory response has done its job. But in
some instances inflammation can cause harm.
Tissue destruction can occur when the pathways of complement
activation
regulatory mechanisms of the inflammatory
response are defective or the ability to clear See all media

damaged tissue and foreign substances is

impaired. In other cases an inappropriate
immune response may give rise to a prolonged
and damaging inflammatory response.
Examples include allergic, or hypersensitivity,
reactions, in which an environmental agent
Category: Science & Tech
Key People: Aulus Cornelius Celsus •
Julius Friedrich Cohnheim
Related Topics: sepsis • rheumatoid
arthritis • Bright disease • acute
inflammation • chronic inflammation

such as pollen, which normally poses no threat

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to the individual, stimulates inflammation,
and autoimmune reactions, in which chronic
inflammation is triggered by the body’s
immune response against its own tissues.

Causes
The factors that can stimulate inflammation include microorganisms, physical
agents, chemicals, inappropriate immunological responses, and tissue death.
Infectious agents such as viruses and bacteria are some of the most common
stimuli of inflammation. Viruses give rise to inflammation by entering and
destroying cells of the body; bacteria release substances called endotoxins that
can initiate inflammation. Physical trauma, burns, radiation injury, and frostbite
can damage tissues and also bring about inflammation, as can corrosive
chemicals such as acids, alkalis, and oxidizing agents. As mentioned above,
malfunctioning immunological responses can incite an inappropriate and
damaging inflammatory response. Inflammation can also result when tissues die
from a lack of oxygen or nutrients, a situation that often is caused by loss of blood
flow to the area.

Signs
The four cardinal signs of inflammation—redness (Latin rubor), heat (calor),
swelling (tumor), and pain (dolor)—were described in the 1st century AD by the
Roman medical writer Aulus Cornelius Celsus. Redness is caused by the dilation of
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small blood vessels in the area of injury. Heat results from increased blood flow
through the area and is experienced only in peripheral parts of the body such as
the skin. Fever is brought about by chemical mediators of inflammation and
contributes to the rise in temperature at the injury. Swelling, called edema, is
caused primarily by the accumulation of fluid outside the blood vessels. The pain
associated with inflammation results in part from the distortion of tissues caused
by edema, and it also is induced by certain chemical mediators of inflammation,
such as bradykinin, serotonin, and the prostaglandins.

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A fifth consequence of inflammation is the loss of function of the inflamed area, a

feature noted by German pathologist Rudolf Virchow in the 19th century. Loss of
function may result from pain that inhibits mobility or from severe swelling that
prevents movement in the area.

The acute inflammatory response

Vascular changes
When tissue is first injured, the small blood vessels in the damaged area constrict
momentarily, a process called vasoconstriction. Following this transient event,
which is believed to be of little importance to the inflammatory response, the
blood vessels dilate (vasodilation), increasing blood flow into the area.
Vasodilation may last from 15 minutes to several hours.

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Next, the walls of the blood vessels, which normally allow only water and salts to
pass through easily, become more permeable. Protein-rich fluid, called exudate, is
now able to exit into the tissues. Substances in the exudate include clotting
factors, which help prevent the spread of infectious agents throughout the body.
Other proteins include antibodies that help destroy invading microorganisms.
As fluid and other substances leak out of the blood vessels, blood flow becomes
more sluggish and white blood cells begin to fall out of the axial stream in the
centre of the vessel to flow nearer the vessel wall. The white blood cells then
adhere to the blood vessel wall, the first step in their emigration into the
extravascular space of the tissue.

Cellular changes

The most important feature of inflammation is the accumulation of white blood

cells at the site of injury. Most of these cells are phagocytes, certain “cell-eating”
leukocytes that ingest bacteria and other foreign particles and also clean up
cellular debris caused by the injury. The main phagocytes involved in acute
inflammation are the neutrophils, a type of white blood cell that contains
granules of cell-destroying enzymes and proteins. When tissue damage is slight,
an adequate supply of these cells can be obtained from those already circulating
in the blood. But, when damage is extensive, stores of neutrophils—some in
immature form—are released from the bone marrow, where they are generated.

To perform their tasks, not only must neutrophils exit through the blood vessel
wall but they must actively move from the blood vessel toward the area of tissue
damage. This movement is made possible by chemical substances that diffuse
from the area of tissue damage and create a concentration gradient followed by
the neutrophils. The substances that create the gradient are called chemotactic
factors, and the one-way migration of cells along the gradient is called
chemotaxis.

Large numbers of neutrophils reach the site of injury first, sometimes within an
hour after injury or infection. After the neutrophils, often 24 to 28 hours after
inflammation begins, there comes another group of white blood cells, the
monocytes, which eventually mature into cell-eating macrophages. Macrophages
usually become more prevalent at the site of injury only after days or weeks and
are a cellular hallmark of chronic inflammation.

Chemical mediators of inflammation

Although injury starts the inflammatory response, chemical factors released upon
this stimulation bring about the vascular and cellular changes outlined above.
The chemicals originate primarily from blood plasma, white blood cells
(basophils, neutrophils, monocytes, and macrophages), platelets, mast cells,
endothelial cells lining the blood vessels, and damaged tissue cells.
One of the best-known chemical mediators released from cells during
inflammation is histamine, which triggers vasodilation and increases vascular
permeability. Stored in granules of circulating basophils and mast cells, histamine
is released immediately when these cells are injured. Other substances involved
in increasing vascular permeability are lysosomal compounds, which are
released from neutrophils, and certain small proteins in the complement system,
namely C3a and C5a. Many cytokines secreted by cells involved in inflammation
also have vasoactive and chemotactic properties.

The prostaglandins are a group of fatty acids produced by many types of cells.
Some prostaglandins increase the effects of other substances that promote
vascular permeability. Others affect the aggregation of platelets, which is part of
the clotting process. Prostaglandins are associated with the pain and fever of
inflammation. Anti-inflammatory drugs, such as aspirin, are effective in part
because they inhibit an enzyme involved in prostaglandin synthesis.
Prostaglandins are synthesized from arachidonic acid, as are the leukotrienes,
another group of chemical mediators that have vasoactive properties.

The plasma contains four interrelated systems of proteins—complement, the

kinins, coagulation factors, and the fibrinolytic system—that generate various
mediators of inflammation. Activated complement proteins serve as chemotactic
factors for neutrophils, increase vascular permeability, and stimulate the release
of histamine from mast cells. They also adhere to the surface of bacteria, making
them easier targets for phagocytes. The kinin system, which is activated by
coagulation factor XII, produces substances that increase vascular permeability.
The most important of the kinins is bradykinin, which is responsible for much of
the pain and itching experienced with inflammation. The coagulation system
converts the plasma protein fibrinogen into fibrin, which is a major component of
the fluid exudate. The fibrinolytic system contributes to inflammation primarily
through the formation of plasmin, which breaks down fibrin into products that
affect vascular permeability.

Events following acute inflammation

Once acute inflammation has begun, a number of outcomes may follow. These
include healing and repair, suppuration, and chronic inflammation. The outcome
depends on the type of tissue involved and the amount of tissue destruction that
has occurred, which are in turn related to the cause of the injury.
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