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Immunology > Week 2: Acute Inflammation > Flashcards

Week 2: Acute Inflammation Flashcards

1
Q

Describe the characteristics of the inflammatory response?

A
  1. Nonspecific, innate defense mechanism that is initiated by injury of infection in vascularized tissue
  2. Develops quickly after an injury
  3. Important process for developing acquired immune response
  4. Tightly regulated
    5.Mostly protective, but can cause injury
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2
Q

What is acute inflammation?

A

A rapid response to an injurious agent that serves to deliver mediators of host defense—leukocytes and plasma proteins—to the site of injury

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3
Q

What is itis?

A

Nomenclature to describe inflammation

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4
Q

What are the 3 components of acute inflammation?

A
  1. Altered vascular caliber (increased or restriction of blood flow)
  2. Structural changes in the microvasculature that permit plasma proteins and leukocytes to leave the circulation
  3. Emigration of the leukocytes from the microcirculation, their accumulation in the focus of the injury, and their activation to eliminate the agent
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5
Q

What are the functions of inflammation?

A
  1. Deliver defensive materials to the site that are needed to destroy and remove pathogens and their toxins
  2. If destruction is not possible, then to limit effects by confining the pathogen and its products
  3. Repair and replace tissue damaged by the pathogen and its products
  4. Inflammatory responses consist of both vascular and cellular reactions
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6
Q

What are the cardinal signs of inflammation?

A
  1. Redness “RUBOR”
  2. Swelling “TUMOR”
    3, Heat “CALOR”
  3. Pain “DOLOR”
  4. Loss of Function
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7
Q

What are the steps in acute inflammation?

A
  1. Inflammatory stimulus
  2. Inflammatory mediators
  3. Vascular response (effect of capillaries)
  4. Leukocyte migration/ phagocyte function
  5. Increased leukocyte/phagocytic function
  6. Inflammatory repair
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8
Q

What are examples of inflammatory stimuli?

A
  1. Biological (infectious agent)
  2. Ischemia (necrotic cells due to lack of blood supply)
  3. Immunological: Hypersensitivity reaction and immune complexes
  4. Thermal (burn)
  5. Chemical (silica, pollutants)
  6. Mechanical (blunt or penetrating trauma)
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9
Q

What are the outcomes of having different inflammatory stimuli?

A

Provokes a characteristic pattern of response that represents a minor variation on a similar theme

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10
Q

What are sentinel cells?

A

Macrophages and dendritic cells

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11
Q

Describe the release of inflammatory mediators?

A
  1. PAMPs and/or DAMPs from the inflammatory stimulus are recognized by PRRs on sentinel cells residing in the tissues
  2. Activated macrophages release inflammatory mediators to trigger the acute inflammatory response.
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12
Q

What are the responses of sentinel macrophages?

A
  1. Activated and secrete cytokines and chemokines
  2. Secrete TNF and IL-1 to increase vascular permeability
  3. IL-6 triggers the acute phase response
  4. Chemokine are released to draw neutrophils to the site of infected or damaged area
  5. Digest foreign antigen and damaged/necrotic cells
  6. Necrosis is a less ordered form of cell death that leads to the release of cellular contents
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13
Q

What are the chemical mediators that induce an inflammatory response?

A
  1. Complement proteins
  2. Histamine
  3. Serotonin
  4. Kinins/Bradykinin
  5. Prostaglandins
  6. Leukotrienes
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14
Q

What cells release histamine?

A

Mast cells, basophils, platelets

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15
Q

What is the function of histamine?

A
  1. Increased capillary permeability
  2. Causes vascular smooth muscle contraction
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16
Q

What produces serotonin?

A

Platelets

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17
Q

What is the function of serotonin?

A

Vasoconstriction

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18
Q

What produces kinins?

A

Platelets

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19
Q

What is function of kinins?

A
  1. Plasma protein
  2. Vasodilator
  3. Increases vascular permeability
  4. Leukocyte chemotaxis
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20
Q

What produces prostaglandins?

A

Mast cells, neutrophils, basophils, and other immune cells

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21
Q

What is the function of prostaglandins?

A
  1. Platelet aggregation
  2. Vasodilation
  3. Neutrophil chemotaxis
  4. Induces pain
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22
Q

What produces leukotrienes?

A

Produced in same pathway as prostaglandins

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23
Q

What is the function of leukotrienes?

A
  1. Chemotactic effect on neutrophils
  2. Increased vascular permeability
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24
Q

How does the vascular respond to inflammation?

A
  1. Blood vessels dilate increasing blood flow and tissue perfusion
  2. Capillary permeability increases
  3. Adhesion molecules become expressed on endothelial cells
  4. Increases infection-fighting weapons
  5. Triggered by chemicals released by damaged cells
  6. Causes the redness, swelling, and heat
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25
Q

What causes an edema?

A

Inflammatory mediator release causes vascular changes and fluid leakage during acute inflammation

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26
Q

What is transudate?

A
  1. Caused by hydrostatic or osmotic imbalance
  2. Ultrafiltrate of plasma
  3. Low protein content
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27
Q

What is exudate?

A
  1. Caused by inflammation
  2. Increased leukocytes (neutrophils)
  3. Increased vascular permeability
  4. High protein content (complement, antibodies, clotting factors)
  5. Leads to edema
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28
Q

What is the hallmark of acute inflammation?

A

Increased vascular permeability and edema

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29
Q

What allows edema leakage?

A

Restricted to venues of 20-60mm caused by endothelial gaps

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30
Q

How fast is leakage response?

A

Immediate and transient (30 minutes)

31
Q

What causes endothelial gaps?

A

Contract and shortening of the individual endothelial cell

32
Q

How does loss of protein from plasma lead to edemas?

A

Reduces osmotic pressure in the vasculature and increased osmotic pressure in the interstitium

33
Q

What is the critical function of vascular inflammatory response?

A

To deliver leukocytes to the site of injury in order to clear infectious/injurious agents

34
Q

What is first inflammatory cells recruited to the site?

A

Neutrophils (6-24hrs)

35
Q

What is extravasation of leukocytes?

A

A coordinated event of rolling adhesion, tight binding, diapedesis (transmigration), and migration

36
Q

What are the vascular inflammatory responses?

A

Stasis and vascular permeability

37
Q

What occurs during leukocyte migration?

A
  1. Blood flow slows (stasis), leukocytes marginate (stick to lining of vessels) and interact with the endothelium
  2. Cells are arrested and extravasation begins (movement between vessels)
  3. Macrophages release matrix metalloproteases (MMPs) to facilitate movement through the basement membrane
38
Q

What occurs during phagocyte mobilization?

A
  1. In order for leukocytes to leave the vessel lumen, endothelial cells need to be activated with up regulates adhesion molecules that can interact with complementary adhesion molecules on leukocytes
  2. Upregulation of adhesion molecules on endothelial cells is induced by inflammatory mediators such as TNF-a, IL-1, and histamine produced by resident macrophages and damaged tissues (endothelium and platelets)
39
Q

What are adhesion molecule for leukocyte migration?

A
  1. Weaker affinity interactions that are needed for rolling adhesion
  2. Higher affinity interactions that are needed for tight binding
40
Q

What are the 4 families of adhesion molecules?

A
  1. Selectincs
  2. Mucin-like glycoproteins
  3. Immunoglobulin-like molecules
  4. Integrins
41
Q

What are types of selectins?

A
  1. E-selectins (endothelium)
  2. P-selectins (platelets and endothelium)
  3. L-selectins (leukocytes)
42
Q

What are the types of mucin-like glycoproteins?

A
  1. Sialyated glycoproteins (sialyated Lewis X) bind to E and P-selectins
  2. Heparin sulfate (glycans on endothelium) binds to L-selectins
43
Q

What are the low affinity adhesion molecules?

A

Selectins and Mucin-like glycoproteins

44
Q

What are the high affinity adhesion molecules?

A

Immunoglobulin-like molecules and Integrins

45
Q

What are the types of immunoglobulin-like molecules?

A
  1. ICAM: intercellular adhesion molecule
  2. VCAM: vascular adhesion molecule
  3. Expressed on activated endothelium
  4. Ligands are integrins on leukocytes
46
Q

What are the types of integrins?

A
  1. LFA-1 (binds to ICAM)
  2. VLA-4 (binds to VCAM)
  3. Expressed on leukocytes
47
Q

What are the steps of leukocyte migration?

A
  1. Rolling adhesion
  2. Tight binding
  3. Diapedesis
  4. Migration
48
Q

What mediates rolling adhesion between leukocytes and endothelium?

A

Glycoproteins and selctins
Sialyated-Lewis XE/P selectins
L-selectinHeparin Sulfate

49
Q

What is the process of rolling adhesion?

A
  1. Brings the leukocyte closer to the endothelial lining (margination) which slows down leukocyte movement
  2. Allows for the binding of other cell surface receptors and their ligands.
50
Q

What occurs during tight adhesion?

A
  1. Endothelial cells are activated by cytokines and inflammatory mediators
  2. Chemokines are secreted by activated endothelial cells (during inflammation)
  3. Chemokines bind to receptors on leukocytes to increase integrin expression
  4. Integrins (LFA-1, VLA-4) are cell adhesion molecules expressed on leukocytes that bind to ICAM or VCAM on endothelial cells.
51
Q

What integrins activate CAMS?

A

LFA-1-> ICAM
VLA-4 -> VCAM

52
Q

What occurs during diapedesis?

A
  1. ICAM becomes upregulated on endothelium by IL-1 and TNF-a
  2. Strengthens adhesion and arrests the leukocyte
  3. The leukocyte migrates through endothelial junctions (diapedesis)
53
Q

Where are complement proteins found?

A

Liver

54
Q

What occurs during leukocyte migration?

A

The leukocyte migrates through endothelial junctions (diapedesis)

55
Q

What is the function of IL-8 for leukocyte migration?

A

Serves as a chemoattractant for neutrophils

56
Q

What is the function of neutrophils for leukocyte migration?

A

Use a chemokine gradient to move toward the site of injury/infection

57
Q

What is the function of macrophages for leukocyte migration?

A

Release matrix metalloproteases (MMPs) break up basement membrane (collagen) for the neutrophil to move through the tissue

58
Q

What stimuli act as chemoattractants?

A
  1. Exogenous
  2. Endogenous
59
Q

What are examples of exogenous stimuli?

A

Bacterial products

60
Q

What are examples of endogenous stimuli?

A
  1. Anaphylatoxins (C3a, C4a, C5a)
  2. Leukotrienes
  3. Chemokines (IL-8)
61
Q

What is the function of anaphylatoxins?

A
  1. Trigger the release of histamines from mast cells
  2. Histamine causes smooth muscle contractions and increase of local vascular permeability
62
Q

How do monocyte help with leukocyte activation?

A

Differentiate into macrophages in the tissue

63
Q

How do tissue macrophages help with leukocyte activation?

A

Release cytokines and chemokines and increase their phagocytic activity

64
Q

How do neutrophils and macrophages help with leukocyte activation?

A

Release granules that contain antimicrobial oxygen radicals

65
Q

How do mast cells help with leukocyte activation?

A

Release histamine

66
Q

How do eosinophils help with leukocyte activation?

A

Release cytotoxic proteins

67
Q

Describe the timeline of leukocyte migration?

A

Innate comes first, adaptive comes after
1. Neutrophils (high number in <6hrs)
2. Monocytes (peak numbers around 12 hrs)
3. Lymphocytes are the last to arrive (days later)
4. Monocytes differentiate into macrophages
5. Neutrophils and macrophages work together to eliminate pathogens or damaged cells
Increase phagocytosis
Release cytotoxic molecules

68
Q

How does neutrophils kill pathogens?

A
  1. The use of oxygen radical (oxidative bursts)
  2. Form ROS and HOCl- that kills bacteria
  3. Phagosome-lysosome degradation leads to the complete destruction of the pathogen
  4. Form pus upon death
69
Q

How do macrophages increase phagocytic function?

A
  1. Coating of pathogen facilitates attachment to macrophage
  2. Opsonins include complement proteins (C3b, CRP) and antibodies
  3. Coating the pathogen helps with recognition and attachment of the pathogen to the macrophage
  4. Pathogen is phagocytized and degraded.
  5. Macrophages also remove dead neutrophils
70
Q

What is the general timeline of acute inflammation?

A
  1. BActeria and other pathogens enter wound
  2. Platelets from blood release blood-clotting proteins at site
  3. Mast cells secrete factors that mediate vasodilation and vascular constriction. Delivery of blood, plasma, and cells increase
  4. Neutrophils secrete factors that kill and degrade pathogen
  5. Neutrophils and macrophages remove pathogens by phagocytosis
  6. Macrophages secrete hormones (cytokines) that attract immune system cells to the site and activate cells involved the tissue repair
  7. Inflammatory response continue until foreign material is eliminated and wound is repaired
71
Q

Describe the termination of acute inflammation?

A
  1. Eradication of the offending agent
  2. Neutrophils have a short life span (1hr-1day)
  3. Most mediators are short lived and degrade quickly
  4. Anti-inflammatory cytokines (IL-10 and TGF-b) inhibit the production of pro-inflammatory cytokines (TNF-a, IL-1, IL-6)
72
Q

How is acute inflammation resolved?

A

Macrophages release growth factors

73
Q

What is the function of growth factors?

A
  1. Stimulate fibroblasts in tissue to regenrate
  2. Promotes angiogenesis
74
Q

What causes chronic inflammation?

A

If inflammation is not quickly resolved

Immunology (17 decks)

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