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Immunology > Test 3- L10 > Flashcards

Test 3- L10 Flashcards

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1
Q

What is the definition of acute inflammation

A

The rapid response (within minutes to hours) of tissues to injury and/or infection

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2
Q

What is the net result of inflammation

A

Release of vascular components into extravascular locations, increased blood and lymphatic flow

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3
Q

What do the released components of inflammation do

A

Destroy infectious agents, clear cell debris, and induce the release of cytokines that promote fibrin deposition and healing

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4
Q

What is the hallmark of inflammation

A

Influx of polymorphonuclear cells (neutrophils)

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5
Q

What does acute inflammation occur in response to

A

Host-produced factors, components of microorganisms (PRRs),
host tissue breakdown by-products

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6
Q

5 common signs of inflammation

A

Heat, redness, swelling, pain, loss of function

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7
Q

What causes the heat and redness from infection

A

Vasodilation (increased blood flow)

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8
Q

What causes the swelling associated with inflammation

A

Increased vascular permeability—> fluid release into tissues

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9
Q

What causes the pain associated with inflammation

A

Stimulation of nocireceptors

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10
Q

What causes the loss of function associated with inflammation

A

Pain, reflex muscle inhibition, disruption of tissue structure, fibroplasia/ metaplasia

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11
Q

What is the systemic response to inflammation

A

Fever & proliferation of leukocytes

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12
Q

What are the 4 main cytokines that contribute to inflammation

A

IL-1,IL-6,IL-8,TNF-α

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13
Q

When the cytokines are released in a controlled manner what do they lead to

A

Inflammation

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14
Q

If the stimulus that induces the release of the main cytokines isn’t easily removed what happens

A

Systemic release of these proteins lead to systemic changes

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15
Q

Example of when the cytokines would be released

A

Macrophage ingests gram negative bacteria containing LPS and is activated to secrete cytokines

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16
Q

What local and systemic effect does IL-8 have

A

Local: Chemotactic (chemoattractant), activates phagocytes
Systemic effects: none

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17
Q

What are the local and systemic effects of IL-1?

A

Local: Activates lymphocytes & macrophages, effects endothelium, local tissue destruction
Systemic effect: Fever, induction of IL-6

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18
Q

What local and systemic effect does TNFα have

A

Local: Effects endothelium, vascular permeability, activates macrophages
Systemic effect: Fever, shock

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19
Q

What local and systemic effects does IL-6 have

A

Local: Activates lymphocytes
Systemic effect: Fever, induction of acute phase proteins

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20
Q

Local inflammation is accompanied by a systemic response called

A

Acute-phase response

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21
Q

What is the acute phase response characterized by

A

Production of lots of acute phase proteins by the LIVER

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22
Q

The acute phase proteins are produced in response to

A

Macrophage produced cytokines- IL-1, IL-6, TNFα

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23
Q

What induces acute phase protein- C-reactive protein

A

IL-6, IL-1, TNFα

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24
Q

What induces acute phase protein- Fibrinogen

A

ONLY IL-6

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25
C-reactive protein (CRP) is the most widely used indicator of what
An acute-phase response in humans for early detection of infections, inflammation, or other disease assoc. with tissue injury
26
CRP is synthesized where in response to what
Liver, IL-1, TNF, IL-6
27
Neutrophil enzymes cleave CRP into peptides that do what
Oposnize, enhance complement fixation, induce chemotaxis
28
Fibrinogen is an acute phase protein that does what
Reduces charge on RBCs (allows for better aggregation of RBCs), enhances their ability to sediment
29
Erythrocyte sedimentation rate (ESR) is a measure of what
The level of inflammation that is going on in a patient
30
If inflammation is occurring what is increased
Increased fibrinogen---> increased clumping---> increased ESR
31
What is an ESR useful for monitoring
TB, tissue necrosis, rheumatic fever, heart attack, malignant diseases
32
Chemical mediators mentioned impact what
Endothelial cells of local blood vessels, make it easier for immune cells to leave endothelium and extravasate to the site of injury/ infection
33
What is extravasation
The movement of white blood cells through an unruptured vessel wall into the surrounding tissue
34
What are the 4 steps of extravasation
Rolling, tight binding, diapedesis, chemotaxis
35
Step 1 (Rolling)- within minutes of exposure to an acute inflammatory signal (TNFα, leukotrienes, C5a, vasoactive peptides) induce what
Cell adhesion molecules on endothelium adjacent to the site of infection/injury
36
What is the main player on endothelial cells that increase its 'stickiness'
E-selectin
37
What is the main player on neutrophils that increase its 'stickiness'
Sialyl- Lewis (a carbohydrate on neutrophils)
38
What does rolling (step 1) allow
Signaling between the endothelial cell and the neutrophil to activate integrins on the neutrophil, which mediate Step 2, which is tight binding of the neutrophil to the vessel
39
Step 2- Tight binding is mediated by
Endothelial ICAM-1
40
What does ICAM-1 bind to
Neutrophil integrins – CD11a/CD18 (aka LFA-1: leukocyte functional antigen-1), CD11b/CD18 (aka Mac-1)
41
Step 3 Diapedesis is what
The passage of white blood cells through the intact wall of a blood vessel (transendothelial migration)
42
Diapedesis is mediated by what molecules binding
Endothelial CD31, Neutrophil integrins
43
What is step 4
Chemotaxis
44
What is chemotaxis
Directional movement of cells using a concentration gradient of a substance
45
What is chemotaxis regulated by
Receptors present on the neutrophil and a substance originating from the inflammatory stimulus
46
The substance originating from the inflammatory stimulus that induces chemotaxis is what
Chemokine such as IL-8, cytokine such as TNF α, complement components (C5a, C3a), fibrinolytic peptides, histamine, microbial products (LPS, fMLP)
47
What are the first leukocytes from the circulation entering the site of inflammation or infection
Neutrophils (a type of PMN)
48
Neutrophils are the hallmark of what
Acute inflammatory response
49
What is the first line of defense against inflammation
Neutrophils
50
What are the 3 enzymatic cascades initiated when fluid enters tissues during inflammation that contribute to inflammatory process during acute inflammation
The complement system, the coagulation system, the fibrinolytic system
51
What does the complement system do
Create opsonins (C3b) and anaphylatoxins (C5a) that act as chemokines to recruit cells to the site
52
What does the coagulation system do
Forms barrier to limit microbe movement beyond initial site of infection
53
What does the fibrinolytic system do
Fibrinopeptide is created and acts as a chemoattractant and activates alternative pathway
54
The 3 enzymatic cascades do what
Work together to recruit cells from the bloodstream and help their activation once they get there
55
At the site of inflammation, phagocytes receive signals that enhance their phagocytic ability, producing:
Superoxide, hydrogen peroxide, nitric oxide, other reactive oxygen and nitrogen radicals
56
Phagocytes release what
Proteolytic enzymes
57
What is the damage that the products of phagocytes produces
Damage cellular metabolism and membrane lipids, leading to more factors that increase capillary permeability
58
Phagocytes release what proteolytic enzymes and what do they do
Collagenases, elastases, other proteases (can convert cytokines to active or inactive forms), enhance movement of inflammatory cells through tissues
59
4 steps of acute inflammation
1: Cells are recruited from blood (chemotaxis due to C5a, fibrinopeptide B, IL-8), neutrophils are recruited first 2: Once there phagocytes release proteolytic enzymes to enhance movement of inflammatory cells at the site of infection (collagenases, elastases) 3: Phagocytes also produce and “listen to” signals that increase their activity (superoxide, hydrogen peroxide, NO) 4: Cells try and remove the stimulus
60
Hours after neutrophils arrive at the site of infection/injury, what cells arrive
Monocytes and lymphocytes (mononuclear cells)
61
What attracts the mononuclear cells
The same factors that attracted neutrophils, but in higher concentrations
62
Why are macrophages brought in
To clean up the mess created by neutrophils
63
What is the hallmark of chronic inflammation
Accumulation and activation of macrophages/ lymphocytes
64
What are the cells of chronic inflammation
Lymphocytes, eosinophils, plasma cells, giant cells, fibroblasts
65
What are chronic inflammatory lesions composed of
Can be purely Macrophages, lymphocytes, or plasma cells
66
What are 3 things activated macrophages do in chronic inflammation
1-Phagocytose bacteria, dead neutrophils, damaged tissue or cells, fibrin deposits, etc. 2-Secrete collagenases, elastases, gelatinases that directly destroy connective tissue 3- Release transforming growth factor-β(TGF-β) which attracts fibroblasts and stimulates them to secrete collagen to repair damaged tissue
67
If macrophages and neutrophils are incapable of removing the cause- what may form
A granuloma
68
What does prolonged chemotactic stimulation result in for chronic inflammation
Perpetual arrival of new macrophages, T cells, plasma cells, and fibroblasts * Fibroblasts contribute to excessive collagen deposition around the irritant * Macrophages contribute to excessive neovascularization which aids the inflammatory response to continue
69
What is a granuloma
Tumor-like mass or nodule that arises because of a chronic inflammatory response
70
What is a granuloma composed of
Many activated macrophages, epithelioid cells, T helper cells, multinucleated giant cells formed by the fusion of macrophages
71
Formation of a granuloma in an attempt to do what
“Wall-off” the organism, and release high concentrations of lytic enzymes which destroy surrounding tissue leading to damage of blood vessels with extensive tissue necrosis
72
The formation of granulomas can happen in response to what bacteria
Mycobacterium Tuberculosis
73
Macrophages with lots of cytoplasm form called what
Epithelioid cells
74
Multiple epithelioid cells joined together form a
Multinucleated giant cell
75
What are the cytokines important in granuloma formation that come from CD4+ cells
-IL-4 - causes aggregation and fusion of macrophages -IFN-γ - potent activator of macrophages and monocytes, causes cell fusion, inhibits migration (negative chemotactic signal) -IL-1- stimulates production of proteases which break down the extracellular matrix
76
What are the cytokines important in granuloma formation that come from macrophage cells
-TNF-α - potent macrophage activator and works synergistically with IFN-γ -TGF-β- stimulates fibrosis and scarring
77
3 hallmarks of granulomas
1- development of a necrotic center 2-Fibrosis & scar formation (healing) 3-Enlargement & replacement of normal tissue
78
If neutrophils dont stop the infection/ injury what is recruited
Monocytes
79
The proper order of steps in neutrophil extravasation (from left to right) is: A. diapedesis → rolling →tight binding → chemotaxis B. rolling → diapedesis → tight binding → chemotaxis C. chemotaxis → tight binding → diapedesis → rolling D. rolling → tight binding → diapedesis →chemotaxis E. None of the above
D
80
The “tight binding” step in the process of extravasation of neutrophils to sites of inflammation within a tissue is mediated by: A. EC E-selectin binding neutrophil sialyl-Lewisx B. EC integrins binding neutrophil ICAM-1 C. EC CD31 binding neutrophil integrins D. EC IL-8 binding neutrophil IL-8 receptor E. EC ICAM-1 binding neutrophil integrins
E
81
True or False? IL-8 is a macrophage-produced cytokine that induces fever
FALSE: IL-1, TNF-α, and IL-6 induce fever, but IL-8 is not known to induce a fever

Immunology (3 decks)

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