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INNATE IMMUNITY:ACUTE INFLAMMATION
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Injurious stimuli cause a protective vascularconnective tissue reaction called inflammation.
Dilute
Destroy
Isolate
Initiate repair
Acute and chronic forms
Inflammation
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Inflammation.Response of tissues to the presence of microorganisms or to
injury. Protective mechanisms are focused on a localized region of tissue.
Blood vessel
Ouch!!
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Invading organisms
or trauma
injury
OpsonizationPhagocytosis
Destruction
Vasoactivefactors
Antibodies
andcomplement
IncreasedIncreased
vascularvascularpermeabilitypermeability
Chemotacticfactors
PhagocytesPhagocytesNeutrophilsNeutrophilsmacrophagesmacrophages
migration
The essential features of acute inflammation
Bloodvessel
Edema
Swelling
Pain
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ESSENTIAL FEATURES OF ACUTE INFLAMMATION
M, DC and mast cells.
pathogen-associatedmolecular patterns
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The major structural features of the cell walls of Gram-negative, Gram-positive, and acid-fast bacteria. These conserved structural moleculesserve as PAMPs and can bind to pattern-recognition receptors such asthe toll-like receptors.
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A C U T E
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ACUTE INFLAMMATION
The cardinal signs of acute inflammation
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rednessredness
heatheatpainpain
swellingswelling
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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.
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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.
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The principal cellular and vascular responses during the inflammatory response. The majority of leukocyte
transmigration and hemorrhage occurs in the capillaries and postcapillary venules.
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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.
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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) leukocyteemigration and accumulation in the
site of injury.
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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, CHOs, etc.).
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MAST CELL
scrolls
Metachromatic
granules
nucleus
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Mast Cells
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Mast Cells
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Some of the stimuli that make mast cell degranulate.
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Degranulating mast cellNormal mast cell
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Vascular leakage Four mechanisms known to cause vascular leakiness
1. Histamines, bradykinins, leukotrienes cause an early, brief (15 30min.) immediate transient response in the form of endothelial cell
contraction that widens intercellular gaps of venules (not arterioles,
capillaries).
Gingival edema. Dog.
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2. Cytokine mediators (TNF, IL-1) induce endothelialcell junction retraction through cytoskeleton
reorganization (4 6 hrs post injury, lasting 24 hrsor more).
Vascular leakage
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3. Severe injuries may cause immediate direct endothelial
cell damage (necrosis, detachment) making them leaky until
they are repaired (immediate sustained response), or maycause delayed damage as in thermal or UV injury, or some
bacterial toxins (delayed prolonged leakage).
Vascular leakage
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thrombus
necrosisnecrosis
necrosisnecrosis
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PMN
plasma celllymphocyte M
M
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4. Marginating and endothelial cell-adherent leukocytes maypile-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.
Vascular leakage
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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.
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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.
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Cell-membrane phospholipids
Arachidonic
acid
Lipooxigenase
Leucotrienes
Proinflammatory
ProagglutinationThrombotic
phospolipases
The production of leucotrienes and prostaglandins by the action oflipooxigenase and cyclooxygenase of arachidonic acid.
Prostaglandins
Thromboxans
Protacyclins
Ciclooxigenase
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