Professional Documents
Culture Documents
Inflammation:
Understanding Its Role In
Acute And Chronic Disease
History
Inflammation has been recognized as a component of the
bodys response to injury from the time of the Egyptians
Celsus of Rome documented the four cardinal signs of
inflammation.
It became clear that inflammation is an integral part of a
persons innate immunity: mechanism of nonspecific first
response to pathogens, toxins, pollutants, and inhalants.
Evidence showed that chronic inflammation exists and that it
can play a significant role in cardiovascular disease and
Alzheimers Dementia (among others).
Inflammation is also a component in injuries from
environmental hazards.
What is Inflammation?
It is the bodys local vascular and cellular response to
injury caused by factors that invade and injure the body
from the outside (exogenous factors) or factors within the
body (endogenous factors) that result in cellular or tissue
injury.
It is part of an innate immune response: requires no
previous exposure to the insult.
Response is rapid
Acute Inflammation
Warmth
Redness in area of injury
Pain (throbbing)
Localized swelling
Loss of function in the site of injury
Vascular Response
Clinical signs of acute inflammation are due to an initial
vascular response localized to the area of injury
The increased blood flow and dilation of vessels
(increased permeability) is caused by relaxation of
vascular smooth muscle.
Stimulation is immediate in response to direct injury or
IgE-mediated effects on tissue mast cells - cause cells to
release Histamine.
Histamine is the predominate stimulus to vascular
response, but there are also other mediators that come
from plasma.
Phagocytosis
Matter is engulfed within a vacuole, which then fuses
with a lysosome to form phagolysosome. Bacteria is then
killed by lysosomal and protease enzymes.
Opsonins: factors that coat particulate matter to enhance
phagocytosis.
- i.e. matter is associated with ligands that can bind to
receptors on the surface of neutrophils.
Phagocytosis can occur in anaerobic environment,
however, the microbicidal activity of neutrophils is much
greater in presence of oxygen.
Monocytes - in circulation.
Macrophages - in tissue.
Are phagocytic (ameboid motion).
Contain the same receptors for Toll-ligands and opsonins
that are expressed on neutrophils.
- Toll-like receptors bind common antigens, such as LPS
in walls of gram negative bacteria.
- Binding activate leukocytes and stimulates release of
proinflammatory cytokines.
Monocytes:
- circulate in blood and differentiate into macrophages in the
tissue.
- 2nd wave of cells at sites of injury in acute inflammation.
Exudate
Suppurative (pus)
It is the accumulation of protein-rich fluid exudate
(neutrophils and necrotic tissue).
Recognized hallmark of infection.
Other exudates are named by their major component:
- Serous (edema fluid)
- Fibrinous (fibrin)
- Hemorrhagic (blood)
Ulcer:
- localized site of inflammation and necrosis at the surface of skin or
the inner surface of an organ.
- Sufficient damage causes gap/hole in tissue surface.
- Non-removed infectious agents can penetrate deeper into tissue
and cause systemic infection.
Fever:
- Results from stimulation of the hypothalmic
thermoregulatory center by cytokines released from
activated macrophages and other cells.
3.
Chronic Inflammation
Occurs when inciting stimuli (chronic infections,
tissue irritants, or altered proteins) for inflammation
cannot be removed from the body.
Prolonged activation of the inflammatory response.
Lymphocytes and macrophages predominate.
Macrophage chemo-attractant production favors
migration of lymphocytes to injury area, rather than
neutrophils (acute).
Ongoing tissue injury incites an ongoing effort to heal
- causes a progressive increase in the accumulation
of collagen and scar formation in the tissue.
Sarcoidosis
Fungal infections
Parasitic infections
Inorganic substances