System
Chapter 21\
Innate Defenses
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Innate: structural defenses; responds to nonspecific foreign substances
" First
line: external surface epithelium & membranes
" Second line: inflammatory processes – antimicrobial proteins, phagocytes, etc.
First Line Defenses
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Skin
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Mucous Membrane
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physical barrier to microbes
Keratinized. Keratin is resistant to most bacterial enzymes & toxins physical barrier & produces a variety of protective chemicals
Protective chemicals produced
" Acid, enzymes, mucin, defensins, and other chemicals Second Line Defenses
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Phagocytes attack after pathogens get through first line defenses
" Macrophages:
derived from monocytes and do most
work
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Free Macrophages: roam through tissues
Fixed Macrophages: permanent residents in particular organs " Neutrophils:
most common WBC
Phagocytosis
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Phagocytic mechanisms:
" Phagocyte
engulfs pathogens by using opsonins
! Compliment proteins allowing phagocytes to bind to pathogens (opsonization)
" Ingestion: formation of phagolysosomes
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Respiratory Bursts: merge phagosome with lysosome & flood phagolysosome with free radicals (macrophage)
Defensins are used to pierce the pathogen's membrane
Phagocytosis occurs when phagocytes engulf pathogens
Phagocytosis
Figure 21.2
NK Cells – White Police
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Natural Killer Cells:
" Small
population of large granular lymphocytes that kill cancer and virus-infected body cells
" Non specific, attacking general abnormalities
" Not phagocytic: attack is directly contacting the target cell ! Apoptosis- programmed cell death
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Shortly after perforation the target nucleus disintegrates.
" Release
chemicals that enhance the inflammatory response Inflammation
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Inflammation- tissue response to injury
Inflammation response is triggered by injury – trauma, heat, chemical irritation, infection, etc.
Beneficial effects
" Prevents
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spread of damaging agents to nearby tissues
" Disposes of cellular debris & pathogens
" Promotes repair
" Alert the adaptive immune system
Cardinal signs: redness, heat, swelling, pain, and impaired function
" Impaired function forces rest to aid in healing
Inflammatory Chemical Response
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Starts with an alarm triggered by Toll-like receptors (TLRs) and flooding of chemicals from the mast cells occurs
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Histamines are released by the mast cells
! potent inflammatory chemical
Three other inflammatory chemicals are Kinins, Prostaglandins, and Complement
! Dilate local arterioles and make capillaries leakier
Vasodilation
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Redness and heat of inflamed region due to hyperemia
" Congestion
with blood occurs when arterioles
dilate
" Edema caused exudate leaking from blood into tissue spaces causing pain
" Pain also associated with bacterial toxins & some mediators (Kinins and Prostaglandins)
Innate, Internal Defenses:
Inflammatory Response
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Edema (swelling) is not only bad
" Sweeps harmful substances into lymphatic system " Enhances entry of clotting protein
! Enhances with complement and clotting factors Events in
Inflammation
Figure 21.3
Phagocyte Mobilization
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Phagocyte mobilization: infiltration of damaged area lead by neutrophils & followed by macrophages There are four steps to Phagocyte infiltration
" Leukocytosis
" Margination
" Diapedesis
" Chemotaxis
Phagocyte Mobilization
Leukocytosis: leukocytosis-inducing factors released by injured cells promote rapid release of WBCs from red bone marrow
"Neutrophils enter from red blood marrow and increase fourfold to five-fold
! Margination: increased vascular permeability causes decreased fluid in vessels; blood flow slows & neutrophils are able to move to vessel margins. Here endothelial markers (CAMs) allow neutrophils to cling to vessel walls
"Margination- phagocytes clinging