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INNATE IMMUNITY:

ACUTE INFLAMMATION
Inflammation
• Injurious stimuli cause a protective vascular
connective tissue reaction called “inflammation.”

– Dilute
– Destroy
– Isolate
– Initiate repair

• Acute and chronic forms


Inflammation. Response of tissues to the presence of microorganisms or to
injury. Protective mechanisms are focused on a localized region of tissue.

Blood vessel

! !
c h
u
O
Invading organisms
or trauma

injury
Vasoactive Chemotactic
factors factors

Increased
Blood Phagocytes
vascular Neutrophils
vessel permeability macrophages

migration
Antibodies
Edema
and Opsonization
Swelling complement Phagocytosis
Destruction
Pain

The essential features of acute inflammation


ESSENTIAL FEATURES OF ACUTE INFLAMMATION

pathogen-associated
molecular patterns

Mφ, DC and mast cells.


The major structural features of the cell walls of Gram-negative, Gram-
positive, and acid-fast bacteria. These conserved structural molecules
serve as PAMP’s and can bind to pattern-recognition receptors such as
the toll-like receptors.
ACUTE
ACUTE INFLAMMATION

The cardinal signs of acute inflammation


swelling

pain
heat

redness
Serous exudate/subcutaneous edema, photosensitization, skin of the nose and ears, ewe. The nonhaired skin of the nose is covered
by a crust resulting from dehydration of the serous exudate released from injured blood vessels following a short exposure to the
sun. The ears are edematous and droopy.
Catarrhal inflammation. Abomasum, cow. The mucosal epithelium is moderately thickened, covered by a
glistening layer of clear mucus, and has a subtle nodular appearance caused by accumulation of mucinous
secretory products (catarrhal exudate) in the gastric pits.
The principal cellular and vascular responses during the inflammatory response. The majority of leukocyte
transmigration and hemorrhage occurs in the capillaries and postcapillary venules.
Blood pressure and plasma colloid osmotic forces in normal and inflamed microcirculation. Acute inflammation.
Arteriole pressure is increased to 50 mm Hg; the mean capillary pressure is increased because of arteriolar dilation,
and the venous pressure increases to approximately 30 mm Hg. At the same time, osmotic pressure is reduced
(averaging 20 mm Hg) because of protein leakage across the venule. The net result is an excess of extravasated
fluid.
The major local manifestations of
acute inflammation compared with
normal. (1) Vascular dilation (causing
erythema and warmth), (2)
extravasation of plasma fluid and
proteins (edema), and (3) leukocyte
emigration and accumulation in the
site of injury.
How Invaders are Recognized?

1. The innate immunity “senses” that the body is being invaded.

3. The presence of strange material is detected by “sentinel” cells.

5. The sentinel cells are macrophages, dendritic cells and mast cells.

7. These cells have receptor that recognize molecules (PAMPs)


normally found in many microorganisms but not in higher animals
(NAG, NAM, LPS, CHO´s, etc.).
MAST CELL

nucleus

Metachromatic
granules

scrolls
Mast Cells
Mast Cells
Some of the stimuli that make mast cell degranulate.
Normal mast cell Degranulating mast cell
Vascular leakage
Four mechanisms known to cause vascular leakiness

1. Histamines, bradykinins, leukotrienes cause an early, brief (15 – 30


min.) immediate transient response in the form of endothelial cell
contraction that widens intercellular gaps of venules (not arterioles,
capillaries).

Gingival edema. Dog.


VASOACTIVE MOLECULES

HISTAMINE

SEROTONINE
VASOACTIVE POLYPEPTIDES

KININS

EICOSANOIDS
PROSTAGLANDIN
LEUCOTRIENS VASOACTIVE LIPIDS
(B4, C4, D4, E4)

PLATELET-
ACTIVATING
NEUTROPHIL-DERIVED MOLECULES
FACTOR
(PAF)

FIBRINOGEN
COAGULATION SYSTEM
BREAKDOWN
PRODUCTS

COMPLEMENT
C3a, C5a
Vascular leakage

2. Cytokine mediators (TNF, IL-1) induce endothelial


cell junction retraction through cytoskeleton
reorganization (4 – 6 hrs post injury, lasting 24 hrs
or more).
Vascular leakage

3. Severe injuries may cause immediate direct endothelial


cell damage (necrosis, detachment) making them leaky until
they are repaired (immediate sustained response), or may
cause delayed damage as in thermal or UV injury, or some
bacterial toxins (delayed prolonged leakage).
necrosis

necrosis

thrombus
lymphocyte Mφ plasma cell

PMN


Vascular leakage

4. Marginating and endothelial cell-adherent leukocytes may


pile-up and damage the endothelium through activation and
release of toxic oxygen radicals and proteolytic enzymes
(leukocyte-dependent endothelial cell injury) making the
vessel leaky.
Vasodilation: leads to greater blood flow to the area of inflammation, resulting in redness and heat.
Vascular permeability: endothelial cells become "leaky" from either direct endothelial cell injury or via chemical
mediators.
Exudation: fluid, proteins, red blood cells, and white blood cells escape from the intravascular space as a result of
increased osmotic pressure extravascularly and increased hydrostatic pressure intravascularly
Vascular stasis: slowing of the blood in the bloodstream with vasodilation and fluid exudation to allow chemical
mediators and inflammatory cells to collect and respond to the stimulus.
Chemical mediators producing endothelial contraction include:
histamine, leukotrienes, bradykinin, platelet activating factor, and the
C3a and C5a components from complement activation. Mediators of
this process over a longer term include tumor necrosis factor and
interleukin-1. Chemical mediators that promote vasodilation include:
histamine, prostaglandins, and nitric oxide.
Cell-membrane phospholipids

phospolipases

Arachidonic
acid
Lipooxigenase Ciclooxigenase

Leucotrienes Prostaglandins
Thromboxans
Protacyclins

Proinflammatory
Proagglutination
Thrombotic

The production of leucotrienes and prostaglandins by the action of


lipooxigenase and cyclooxygenase of arachidonic acid.

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