Inflammation
is the response of an organism against pathogens and mechanical alteration in
the network, in the form of a series of reactions that occur at the site of tissue
injury, such as burns, or infected.
Inflammation
or inflammation is one of the main response of the immune system against
infection and irritation. Inflammation is stimulated by
chemical factors (histamine, bradykinin, serotonin, leukotrienes, and prostaglandins)
are released by cells that act as inflammatory mediators in the immune system
to protect surrounding tissue from the spread of infection.
Inflammation
is the signal-mediated cellular response to insults by infectious agents,
toxins, and physical pressure. While acute inflammation is
essential for the immune response, chronic inflammation that may cause tissue
damage (autoimmune, neurodegenerative, cardiovascular disease).
Symptoms
and signs of inflammation varies with fever (pyrogenesis), redness (rubor),
pain swelling (turgor), (dolor), and tissue / organ dysfunction (functio
laesa).
Inflammation is the sequence of events:
■ stimulation by trauma or acute phase reaction pathogens →
■ platelet adhesion, vasoconstriction of the efferent vessels
■ cytokine-induced vascular dilation of the afferent (vasodilatation causes increased blood flow (redness, local heat) for infected / damaged area
■ activation of the complement system, coagulation, fibrinolytic system, and kinin systems
■ endothelial leukocyte adhesion cascade gap increases the permeability of blood vessels and allow extravasation of serum proteins (exudate) and leukocytes (neutrophils → → → lymphocytes macrophages) with resulting tissue swelling
■ phagocytosis of foreign material with the formation of pus
Inflammation is the sequence of events:
■ stimulation by trauma or acute phase reaction pathogens →
■ platelet adhesion, vasoconstriction of the efferent vessels
■ cytokine-induced vascular dilation of the afferent (vasodilatation causes increased blood flow (redness, local heat) for infected / damaged area
■ activation of the complement system, coagulation, fibrinolytic system, and kinin systems
■ endothelial leukocyte adhesion cascade gap increases the permeability of blood vessels and allow extravasation of serum proteins (exudate) and leukocytes (neutrophils → → → lymphocytes macrophages) with resulting tissue swelling
■ phagocytosis of foreign material with the formation of pus
The
inflammatory response is part of the innate immune response, and employs mobile
agents and plasma-derived (path):
Complement system ● ● ● complementary system of interferons (IFN) ● interferon (IFN) ● cytokines, lymphokines, monokines ● cytokines, lymphokines, monokines
● prostaglandins and leukotrienes - arachidonic acid derivatives ● prostaglandins and leukotrienes - arachidonic acid derivatives
● platelet activating factor (PAF) ● platelet activating factor (PAF)
Histamine histamine ● ● ● kinins (bradykinin → pain) ● kinins (bradykinin → pain)
Complement system ● ● ● complementary system of interferons (IFN) ● interferon (IFN) ● cytokines, lymphokines, monokines ● cytokines, lymphokines, monokines
● prostaglandins and leukotrienes - arachidonic acid derivatives ● prostaglandins and leukotrienes - arachidonic acid derivatives
● platelet activating factor (PAF) ● platelet activating factor (PAF)
Histamine histamine ● ● ● kinins (bradykinin → pain) ● kinins (bradykinin → pain)
Pain
evokes proinflammatory mediators, including cytokines, chemokines, protons,
nerve growth factor, and prostaglandin, which is produced by attacking
leukocytes or local cell.
§ Acute phase proteins fluctuate
in response to tissue injury and infection. They synthesized (by hepatocytes) respond to pro-inflammatory
cytokines and include: ● C-reactive protein (CRP), mannose-binding protein,
complement factors, ● alpha-1 acid glycoprotein, alpha 1-antitrypsin ●, alpha
1-antichymotrypsin, ● alpha 2-macroglobulin, alpha 2-macroglobulin ●, ● serum
amyloid P component (SAP, amyloid), haptoglobins (alpha-2-globulins),
ceruloplasmin, complement components C3, C4, coagulation factors (fibrinogen,
prothrombin, factor VIII, factor von Willebrand factor, plasminogen) ● ferritin
§ Pro-inflammatory cytokines including IL-1,
IL-6, IL-8, TNF-α (alpha tumor necrosis factor), and TNF-β (lymphotoxin α, LT). In response to infection, macrophages secrete IL-1 and TNFs, the
broad spectrum of cytokines that stimulate the inflammatory response of
neutrophils, fibroblasts, and endothelial cells.Fibroblasts and endothelial
cells respond to IL-1 and TNF to recruit more immune cells to sites of
inflammation.
Pain: When
tissue destroyed or attacked by leukocytes in inflammation, many mediators are
delivered by circulation and / or released from the population and migrated
cells on the site. Mediator Proalgesic including
proinflammatory cytokines, chemokines, protons, nerve growth factor, and
prostaglandin, which is produced by attacking leukocytes or cell population. Mediator analgesic, against pain, also produced in inflamed
tissues.These include anti-inflammatory cytokines and opioid peptides. Interactions between leukocyte-derived opioid peptides and opioid
receptors may cause potent, clinically relevant inhibition of pain (analgesic).
Opioid receptors are present on the tip of the peripheral sensory neurons. Opioid peptides are synthesized in circulating leukocytes, which migrate to inflamed tissues directed by chemokines and adhesion molecules.Under conditions of stress or in response to releasing agent (eg, corticotropin-releasing factor, cytokine, noradrenaline), leukocytes can secrete opioid. They activate peripheral opioid receptors and produces analgesia by inhibiting sensory nerve stimulation and / or release of excitatory neuropeptides. The concept of pain generation by mediators released from leukocytes and analgesia by immune-derived opioids.
Opioid receptors are present on the tip of the peripheral sensory neurons. Opioid peptides are synthesized in circulating leukocytes, which migrate to inflamed tissues directed by chemokines and adhesion molecules.Under conditions of stress or in response to releasing agent (eg, corticotropin-releasing factor, cytokine, noradrenaline), leukocytes can secrete opioid. They activate peripheral opioid receptors and produces analgesia by inhibiting sensory nerve stimulation and / or release of excitatory neuropeptides. The concept of pain generation by mediators released from leukocytes and analgesia by immune-derived opioids.
Inflammation
has three important role in resistance to infection:
§ allows the addition of effector molecules
and cells to the site of infection to improve the performance of macrophages
§ provides a barrier to prevent the spread
of infection
§ sparked the repair process for damaged
tissue.
Inflammatory
response can be recognized from the pain, skin bruising, fever, etc., caused by
changes in blood vessels in the area of infection:
§ enlargement of the diameter of blood
vessels, accompanied by an increase in blood flow in the area of infection. It can cause skin looks bruising redness and decreased blood
pressure, especially in small vessels.
§ activation of adhesion molecules to glue
endotelia with blood vessels.
§ the combination of the decline in blood
pressure and activation of adhesion molecules, will allow white blood cells to
the endothelium and migrate into the tissue. This process is known as extravasation.
Parts
of the body become inflamed have the following signs
§ Rubor (redness) occurred because the blood
flow into the local microsomal on where inflammation.
§ Calor (heat) because more blood is
supplied to the place inflammation of the channeled into the normal area.
§ Dolor (pain) due to swelling of the
tissues resulting in increased local pressure and also because there are
expenses substance histamine and other bioactive chemicals.
§ Tumor (swelling) expenditure ciran-fluid
into the interstitial tissue.
§ Functio laesa (change function) is the
disruption of the function of organs
Mechanisms
of Inflammation can be divided into two phases:
§ Vascular changes
Vascular response at the site of injury is a fundamental for acute inflammatory reaction. These changes include changes in blood flow and vascular permeability. Changes in blood flow due to local arterial dilatation resulting in the increase of blood flow (hypermia) followed by slowing blood flow. As a result, the part becomes red and hot. White blood cells will be gathered along the walls of blood vessels by sticking. Vessel walls become loose arrangement allowing white blood cells out through the vessel wall.White blood cells act as a defense system against attacks for foreign objects.
Vascular response at the site of injury is a fundamental for acute inflammatory reaction. These changes include changes in blood flow and vascular permeability. Changes in blood flow due to local arterial dilatation resulting in the increase of blood flow (hypermia) followed by slowing blood flow. As a result, the part becomes red and hot. White blood cells will be gathered along the walls of blood vessels by sticking. Vessel walls become loose arrangement allowing white blood cells out through the vessel wall.White blood cells act as a defense system against attacks for foreign objects.
§ The formation of inflammatory fluid
Increased vascular permeability is accompanied by the release of white blood cells and plasma proteins in the network is called exudation. Fluids are the basis for the swelling. Swelling causes stress and pressure on the nerve cells, causing pain (Mansjoer, 1999).
The cause of inflammation may be caused by mechanical (puncture), Chemical (histamine causes alerti, excess stomach acid can cause irritation), thermal (temperature), and Microbe (infectious disease.
Increased vascular permeability is accompanied by the release of white blood cells and plasma proteins in the network is called exudation. Fluids are the basis for the swelling. Swelling causes stress and pressure on the nerve cells, causing pain (Mansjoer, 1999).
The cause of inflammation may be caused by mechanical (puncture), Chemical (histamine causes alerti, excess stomach acid can cause irritation), thermal (temperature), and Microbe (infectious disease.
Stages
3-phase inflammatory
1. Changes in the cells and circulatory
system, there are injuries on the body of
the narrowing of the blood vessels to control bleeding, so terlepaslah
histamine use to increase blood flow to the injured area. At the same time dikelurkan quinine to increase capillary
permeability which would facilitate the entry of protein, fluid, and leukocytes
to supply the injured area. After sufficient local blood
flow decreased to maintain leukocytes to remain in the area of injury.
2. release of exudates, occurs
after eating bakteri2 leukocytes in the area of injury, then exudate removed.
3. regeneration, the
recovery phase of tissue repair or the formation of new tissue.
Inflammatory
Response
During
the early stages of infection, cytokines produced when the immune defenses
bawaandiaktifkan. Rapid release of cytokines in
the infection start a new response with far-reaching consequences that include
inflammation.
One of
the earliest produced cytokines tumor necrosis factor alpha (TNF-α), which is
synthesized by activated monocytes and macrophages. These cytokines alter capillary nearby so that the circulation of
white blood cells can easily be brought to the site of infection. TNF-α can also bind to receptors on infected cells and stimulate
antiviral response. Within seconds, a series of
signals initiated that leads to cell death, an attempt to prevent the spread of
infection.
There
are four typical signs of inflammation: erythema (redness), heat, swelling, and
pain. This is a consequence of
increased blood flow and capillary permeability, the influx of phagocytic
cells, and tissue damage. Increased blood flow is caused
by a narrowing of the capillaries that carry blood from the infected area, and
causes swelling of the capillary network. Erythema and increased
capillary constriction accompany tissue temperature. In addition, increased capillary permeability, cells and fluids
that allow to leave and enter the surrounding tissue. This fluid has a higher protein content than is usually found in
the tissue fluid, causing swelling.
Another
feature is the presence of inflammatory immune cells, mononuclear phagocytes
mostly, who are interested in the infected area by cytokines. Neutrophils are one of the earliest types of phagocytic cells that
go to the site of infection, and the classic signs of inflammatory response
(illustration). These cells are abundant in the
blood, and usually absent from the network. Together
with infected cells, dendritic cells, and macrophages, they produce cytokines
that can be formed in response to infection, and also modulate adaptive
response can follow.
The
precise nature of the inflammatory response depends on the virus and infected
tissue. The virus does not kill cells -
noncytopathic virus - does not cause a strong inflammatory response. Because the cells and proteins of the inflammatory response is
derived from the blood stream, network with access to blood does not have
destruction associated with inflammation. However, the result of an
infection such 'special' sites - the brain, for example - may be very different
compared to other tissues.
One important component is the
'inflammasome' - a very large cytoplasmic structures with properties and initiator
receptor signaling patterns (eg, MDA-5 and RIG-I). Recent experimental findings indicate that the inflammasome is
very important in the innate immune response against influenza virus infection,
and pulmonary pathology moderator on influenza pneumonia.
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