Inflamacion inata

8/14/2019 Inflamacion inata

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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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Inflamacion inata

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