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Inflammation
- a response of vascularized tissues to
infections and damaged tissues that brings
cells and molecules of host defense from the
circulation to the sites where they are needed
in order to eliminate the offending agents
- a protective response that rids the host cells of
both the initial cause of cell injury (microbes,
toxins) and the consequences of such injury
(necrotic cells and tissues)
Steps in a typical inflammatory response:
1. The offending agent (located in extravascular
tissues) is recognized by host cells and
molecules (macrophages, dendritic cells, mast Fundamental Properties of the Inflammatory
cells)
Response: A Review
2. Recruitment of leukocytes from circulation to
Components of the Inflammatory Response
site of injury leukocytes engulf and destroy
- Major participants:
bacteria, tissue, debris, and other particulate
blood vessels (vascular response), and
material
leukocytes (cellular response)
3. Leukocytes and proteins (chemical mediators)
are activated and work together to destroy
Harmful consequences of inflammation
and eliminate the offending substance
- Often accompanied by local tissue damage
(through proteolytic degradation).
and its associated signs and symptoms (pain
4. The reaction is controlled and terminated.
and functional impairment)
5. The damaged tissue is repaired/restored to its
- Typically, these harmful consequences are
normal structure and function. Limited by:
self-limited and resolve as the inflammation
extent
of
tissue
abates.
degradation, and
- There are many diseases in which the
regenerative capacity
inflammatory reaction is misdirected, for
of specific tissue
example:
- OR Autoimmune diseases against self
5 Rs of the inflammatory response
tissues
1. Recognition of the injurious agent
Allergies against normally harmless
2. Recruitment of leukocytes
environmental substances
3. Removal of the agent
Where inflammatory reaction is
4. Regulation (control) of the response
inadequately controlled
5. Resolution (repair/restoration)
- Anti-inflammatory drugs control the
harmful sequelae of inflammation yet not
interfere with its beneficial effects
confined
Systemic
to
Widespread;
sepsis
systemic
systemic
inflammatory
manifestations
(e.g.,
fever in bacterial/viral
response
Tissue injury
(SIRS)
pharyngitis)
Mediators of inflammation
-
and
and
self-
severe
progressive
Prominent
Less
systemic signs
Type of host
Innate
Adaptive
defense
immunity
immunity
and
Termination
of
inflammation
Often
limited
Local
syndrome
Usually mild
and
fluid
and
destruction,
Cellular
Mainly
Causes of Inflammation
proliferation of
Infection and microbial toxins
blood vessels,
- Bacterial, viral, fungal, parasitic
and deposition
- Inflammatory
responses
vary
of connective
depending on the type of pathogen and
tissue
the characteristics of the host
Monocytes or
infiltrate
neutrophils
macrophages
(polymorpho
and
-nuclear
lymphocytes
plasma
proteins
(edema) and
emigration
of leukocytes
leukocytes or
PMN)
Tissue necrosis
-
Includes:
Foreign bodies
- Splinters, dirt, sutures
- They cause traumatic injury or carry
microbes
- Endogenous substances (in large
amounts):
Urate crystals (gout)
Cholesterol
crystals
(atherosclerosis)
Lipids
(obesity-associated
metabolic syndrome)
Immune reactions
-
induces
the
The
vascular
reactions
of
acute
inflammation consist of changes in the:
1. Flow of blood
2. Permeability of vessels
Both are designed to maximize
the movement of plasma
proteins and leukocytes out of
the circulation and into the site
of infection/injury.
Circulating proteins
-
Exudate
- an extravascular fluid that has a high
protein concentration and contains
cellular debris
- its presence implies that there is an
increase in the permeability of small
blood vessels triggered by some sort of
tissue
injury
and
an
ongoing
inflammatory reaction
Transudate
microbes
ACUTE INFLAMMATION
3 major components:
1. Dilation of small vessels leading to an
increase in blood flow
2. Increased
permeability
of
the
microvasculature enabling
plasma
proteins and leukocytes to leave the
circulation, and
3. Emigration of the leukocytes from the
microcirculation, their accumulation in
the focus of injury, and their activation
to eliminate the offending agent
Reactions
of
Inflammation
Blood
Vessels
in
Acute
Edema
- Denotes an excess of fluid in interstitial
tissue or serous cavities
- It can either be an exudate or a
transudate.
Pus
- A purulent exudate an inflammatory
exudate rich in leukocytes (mostly
neutrophils), the debris of dead cells,
and in many cases, microbes.
and
the
leukocytes,
principally
neutrophils,
accumulate
along
vascular
endothelium
the
Increased
vascular
(vascular leakage)
-
permeability
Mechanisms
responsible
for
the
increased permeability of postcapillary
venules: