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chapter 6 innate immunity Flashcards

1
Q

physical barriers–epithelial cells

A 
skin sloughs off microorganisms.  
	Upper resp tract traps them by producing mucous , cough, sneeze.
	 GI—vomiting/defacation.  
	Urinary tract—urination.  
	Low temp on skin, low pH in stomach.
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2
Q

physical barriers: cell derived chemical

A

produced by epithelial cells
 Mucous, perspiration, saliva, tears, earwax. Trap and contain.
 Lysozymes (in swat, tears and saliva) attach cell walls of gram + bacteria
 Fatty acids and lactic acids secreted from sebaceous glands on skin kill bacteria and fungi and create a acidic environment on skin
 Epithelial cells contain antimicrobial peptids
• Defensins—from neutrophils and epithelial cells disrupt bacterial membrane
• Collectin—soluble glycoprotein that facilitate recognition by macrophages

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3
Q

physical barriers: normal microbiome

A

 Produces enzymes that facilitate digestion of large polysaccharids and fatty acids
 Synthesize vitamins (K and B)
 Release ammonia, phenol and indols (toxic to pathogens)
 Competes with pathogens for nutrients and blocks attachment
 Fosters adaptive immunity by inducing growth of gut-associated lymphoid tissue
 Contributes to bidirectional communication between brain and GI tractimplications for cognitive function, behavior, pain modulation, stress responses and disease

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4
Q

Inflammation is characterized by

A
  1. Occurs in vascularized tissue, 2. Rapid response (seconds) 3. Cellular and chemical 4. NONSPECIFIC. Same regardless of injury
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5
Q

acute signs of inflammation

A

rubor (red), calor (heat), tumor (swelling), dolor (pain), function laesa (loss of function)

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6
Q

what happens @ site of injury/inflammation

A

increased coagulation, vasodilation, WBC adhesion, increased vascular permeability, pain

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7
Q

what is lymphangitis and lymphadenitis and why do they occur with acute inflammation?

A

swelling of lymph vessels and lymph nodes due to increased work (draining extravascular fluid to lymph nodes)

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8
Q

benefits of inflammation

A
  • Prevents infection and further damage
  • Limit scope of inflammatory process (clotting, plasma enzymes and blood tissue cells prevent spreading of inflammation to healthy tissue)
  • Preparation of injury for healing and repair (removal of bacterial organisms, dead cells and debris)
  • Facilitates adaptive immunity—antigens+macrophages and lymphocytes concentrated in nodesinitiates adaptive immunity to protect from future exposures.
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9
Q

3 key system of plasma protein systems in innate immunity

A

complement, clotting and kinen

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10
Q

Complement

A

plasma system of innate immunity
complements the capacity of antibodies and phagocytes to clear pathogens and dead cells and activate inflammation
• Consists of complement factors (proteins).

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11
Q

Activation of C3 and C5 results in 3 potent molecules being released, what are they and what do they do?

A
  • C3b—opsonins—coat bacteria
  • C5a—chemotactic—like a magnet attracts leukocytes
  • C3a and C5a together are called anaphylatoxins—degranulates mast cells to release histamine which increases vasodilation and capillary permeability
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12
Q

What is a membrane attack complex (MAC)?

A

• Complements c6-c9. Leads to bacterial destruction and tissue injury by creating pores in outer membranes of cells or bacteria. These cause the infusion of water into the cellscell death

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13
Q

What are the 3 pathways for complement activation?

A

classical, alternative and lectin

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14
Q

describe the classical complement activation system

A

activated by antibody/antigen complexes, or CRP—activate C1 and leads to cascade

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15
Q

describe the alternative complement activation system

A

doesn’t need antibodies. activated directly by substances on the surfaces of infectious microorganisms (lipopolysaccharides/endotoxins on bacteria or zymosan (carbohydrate on yeast cells). Uses factor B, D and properdin to form complex that activates C3 and C5, then converges with classical pathway.

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16
Q

describe the lectin pathway (3rd complement pathway)

A

independent of antibodies. Activated by plasma proteins like mannose-binding lectin (MBL). Binds to bacterial polysacc. That contain mannose (a carm) and activates the complement cascade
(mannose binding lectin)

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17
Q

describe the clotting system in innate immunity

A

plasma proteins form a blood clot. Can be activated by collagen, enzymes and toxins released during tissue injury or infection
• Blood clot consists of mesh of fibrin strands and platelets (primary initiator of clotting).
• Function to plug the vessel and stop bleeding, trap the microorganism and prevent spread.

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18
Q

name the 2 pathways for clotting and describe each

A

intrinsic and extrinsic
• Tissue factor (EXTRINSIC) pathway—activated by TF aka thromboplastin released by damaged endothelial cells of blood vessels. Reacts with activated factor VII
• Contact activation (INTRINSIC) pathway—activated when vessel wall damage causes negatively charged subendothelial subst. to come into contact with factor XII (Hageman factor) in plasma
• BOTH CONVERGE AT FACTOR X
 Activates fibrinfibrin clot activates clotting systemfibrinopeptides which attracts neutrophils (chemotaxis) and increase vascular permeability

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19
Q

What is the kinin system?

A

interacts with clotting system. Clotting AND kinin initiated through activation of Hageman factor (XII) which results in formation of factor XIIa activates prekalikreinkallikreinkininogenbradykinin (final product)
• Bradykinin causes dilation of blood vessels and induces pain, smooth muscle cell contraction and increases vascular permeability

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20
Q

name 6 inhibitors of inflammation

A 
protease inhibitor
carboxypeptidase
kininase
histaminase
fibrinolytic system
plasminogen
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21
Q

define protease inhibitor

A

inhibits activation of complement (inhibits inflammation)

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22
Q

how dose carboxypeptidase stop inflammation

A

inactivates C3a and C5a

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23
Q

kininase

A

degrenates kinins (inhibits inflammation)

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24
Q

histaminase

A

degrades histamin and kallikrein (inhibits inflammation)

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25
fibrinolytic system
limits size of clot and degrades clot after bleeding stops
26
plasminogen
plasmin degrades the fibrin polymers in clots
27
what is the principal coordinator of clotting?
vascular endothelium
28
explain how cell receptros work
binding to these results in cell activation aka pattern recognition receptors (PRRs). they monitor for cell damage and infectious agents by recognizing inf. Micro org. and damaged cells in 2 ways PAMP (pathogen assoc. mol. patterns) and DAMPS (damage associated mol. patterns)
29
name the cellular components of inflammation
mast cells, macrophages and dendritic cells, RBCs, leukocytes (granulocyte, monocyte, lymphocyte)
30
what does a c-type lectin receptor recognize?
fungal antigens
31
intracellular receptors
NLR and NOD (nucleotide binding and nucleotide oligomerization) in lymphocytes, macrophages and dendritic cells.
32
cytokines
cell mediators: intercellular signaling molecules secreted by variety of cells to bind to specific cell membrane receptors. regulate innate/adaptive immunity. Can produce systemic effects like fever CAN BE Proinflammatory or antinflammatory lymphokines, monokines, , chomkines
33
Interleukins function to
alter behavior of cells  Regulate CAM (cell adhesion molecules)  Regulate Chemotaxis (attraction of leukocytes to inflammation)  Induction, proliferation and maturation of leukocytes in bone marrow  Enhance or suppress inflammation and adaptive immune response
34
interleukins are producted by
macrophages and lymphocytes
35
Proinflamatory cytokines
TNF Alpha and IL1 and IL6
36
TNF Alpha
proinflammatory cytokine interacts with IL1 and IL6 chemotaxis, phagocytosis, inflamm and adaptive immune prolif. • TNF contributes to damaging effects of chronic inflammation • Induces fever, increased liver synthesis of inflammation proteins, cachexia and intravascular thrombosis
37
IL1
proinflammatory cytokine produced by macrophagesactivates monocytes, lymphocytes and macrophages • Endogenous pyrogen (causes fever)
38
IL6
proinflammatory cytokine produced by macrophages, lymphocytes and fibroblasts. Induces hepatocytes in liver to produce proteins for inflammation.
39
Anti-inflammatory cytokine
IL-10, TGF-Beta | suppress lymphocytes
40
Interferon (IFN)
protect against viral infection type 1 produced/released by infected cell Type 2 produced by lymphocytes
41
Mast Cells are potent activators of
Inflammation
42
mast cells are activated by
tissue damage or complement cascade and IgE (allergies)
43
When a mast cell degranulates what is released?
release their contents within seconds of stimulus | What’s inside? Histaminesconstriction of smooth muscle and dilation of post capillary venulesincreased blood flow
44
H1
histamine binds to this and causes smooth muscle contraction and bronchoconstriction
45
H2
histamine binds to this and suppresses leukocyte function, | H2 blockers reduce gastric acidity
46
Mast cells synthesize:
mediators: leukotrienes, prostaglandins and platelet activating factor
47
Leukotrienes
induce smooth muscle contraction (bronchoconstriction) and increase vascular permeability, stimulate slow, prolonged inflammatory responses (as apposed to rapid acting histamine)
48
prostaglandins
increase vascular permeability, neutrophil chemotaxis and pain. Produced by COX COX-1 activates platelets and protects stomach lining Cox-02 associated with inflammation
49
platelet activating factor
produced by neutrophils, monocytes, endothelial cells, mast cells and platelets. Cause endothelial cell retractionincreased vascular permeability, adhesion of leukocytes and platelet activation (can also activate mast cells
50
How to endothelial cells help in healing/immune attack
when injured endothelial cells promote recruitment and invasion of leukocytes  Histamine and bradykinin stimulate endothelial cell contraction  Promote angiogenesis and facilitate wound healing
51
platelets
aneucleated. |  Can degranulate and release serotonins, similar to histamine.
52
Neutrophils in innate immunity
granulocyte with multilobed nucleus  PREDOMINANT phagocytes in early inflammation  Primary role to phagocytize microbes and cellular debris.  Short lived (incapable of division)  Component of pus
53
eosinophils
defend against parasites and in allergies
54
basophils
 Basophils—least prevelant granulocyte. Releases histamine, important in aX and asthma
55
dendritic cells
phagocytic cells in peripheral organs and skin. Eat them and bring to T lymphocytes (adaptive immunity)
56
lymphocytes and NK cells
lymphocytes are a type of WBC and activate macrophages and initiate immune response against pathogens and cancer.  B lymphocytes produce antibodies  T lymphocytes reulate immune cells, kill firuses and cancer  NK cells—type of lymphocyte eliminate virally infected and cancer cells. Have inhibitory and activating receptors bind to cells produce cytokines and kill target cells
57
Cells of phagocytosis
neutrophils and macrophages
58
opsonization
increases phagocyte adherence. coats the cell with opsonin. C3b and antibodies are good at this
59
describe endocytosis
microorganism drawn into phagocyte. Forms a phagocytic vacuole or phagosome. Lysosomes fuse with this and discharge their contents to destroy the organism
60
when phagocytes die what is released to inhibit inflammation associated with tissue damage from enzyme released from dead phagocyte?
• Alpha 1 antitrypsin (protease inhibitor) and catalase (breaks down h202) inhibit the destructive effects
61
systemic signs of acute inflammation
 Fever—d/t cytokines like TNF and IL1—endogenous pyrogens. Act on hypothalamous  Leukocytosis—increase in circulating WBCs >11,000  Left shift (increase in ratio of immature to mature neutrophils)  Plasma protein synthesis—produced by liver and inc. during inflammation  Maximal 10-40 hours after onset of inflammation • Increased fibrinogenincreased ESR )RBCs clumping with fibrinogen) • CRP increased—produced by liver, esp for autoimmune diseases and severity of inctious disease
62
Chronic inflammation
inflammation that lasts >2 weeks all chronic disease have a component of this. pus formations, purulent d/c and incomplete wound healing are signs.
63
granuloma
in chronic inflammation these can form to block off the area affected.  Causes caseous necrosis or liquefaction necrosis. Fluid eventually gets out and leaves a hollow walled structure (TB)
64
Wound healing with full regeneration (no scar tissue)
resolution. | epithelium in skin, liver and intestines
65
4 phases of wound healing
hemostasis (coagulation), inflammation, proliferation, remodeling/maturation  Phase 1: hemostasis (coagulation)
66
Phase 1 of wound healing
• Tissue damagebleedingvasoconstriction and vasodilationcoagulation cascade. Fibrin mesh + platelets. Platelets degranulateincreased capillary permeability initiatin proliferation of undamaged cells
67
phase 2 of wound healing
inflammation—begins within minutes—macrophages and mast cells release vasoactive cytokinesinc blood flow, neutrophils infiltrate, lymphocytes activate immune response
68
Phase 3 of wound healing
: proliferation and new tissue formation—days 3 to 4 lasting-up to 14. Fibrin clot replaced by normal tissue or scar tissue. • Invasion of macrophages which clear debris and promot collagen synthesis and angiogenesis • After clean up (debridement) vascular dilation and permeability is reversed preparing for regeneration or repair • Granulation tissue grows • Epithelialization occurs • Fibroblasts—deposit connective tissue. • Wound contraction occurs
69
phase 4 of wound healing
remodeling/maturation begins several weeks after injury and completed within 2 years. Continuation of cell differentiation, scar formation and remodeling.  Dysfunctional wound healing
70
Geriatric considerations of immunity
chronic disease, prone to overwhelming sepsis, skin loses regenerative ability, medications impair response, infection and inflammation more common
71
Pediatric considerations of immunity
decreased inflammatory immune function, neutrophils not as good @ chemotaxis, complement deficiency, decreased oxidation and bactreal response, prone to sepsis.
72
primary immune cells in the tissues
macrophages (were monocytes in the blood) and Mast cells
73
name two mediators that increase edema/vascular permeability in acute inflammation
histamine (d/t mast cell degranulation) and nitric oxide (produced from endothelium and macrophages) also eicosanoids (leukotrienes and prostaglandins
74
what happens with complement activation
after C1 is activated, C1-C4 are activated, result in mast cell degranulation, neutrophil chemotaxis, microbe opsonization, lysis, RBC mediated clearance and B-cell activation
75
What is complement?
system of molecules, regulators and receptors in host defence

advance pathophys (6 decks)

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