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Immunology - DVM year 1 > Exam 1: Dr. Kaplan Inflammation: Mechanisms 1 > Flashcards

Exam 1: Dr. Kaplan Inflammation: Mechanisms 1 Flashcards

1
Q

What are the roles of inflammation?

A

Deliver additional effector molecules and cells to infection site
Augment the killing of microorganisms
Induce local blood clotting to provide a physical barrier to spread of infection
Promote repair of injured tissue

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2
Q

What are the signs of inflammation?

A 
Rubor (redness)
Tumor (swelling)
Calor (heat)
Dolor (pain)
Functio Laesa (loss of function)
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3
Q

What is acute inflammation often like?

A

Self-limiting

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4
Q

What is the onset of actue inflammation like?

A

Quick

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5
Q

What is the resolution of inflammation like?

A

Often quick

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6
Q

What does acute inflammation predominantly involve?

A

The innate immune system

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7
Q

What is tissue injury like with acute inflammation?

A

Mild

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8
Q

How apparent are local and systemic signs of acute inflammation?

A

Obvious

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9
Q

When can chronic inflammation occur?

A

If the pathogen is adapted to resist antimicrobial mechanisms

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10
Q

What are the processes of chronic inflammation like?

A

Diverse, dependent on the pathogen

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11
Q

What is the onset of chronic inflammation like?

A

Can be days to years

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12
Q

What does chronic inflammation often involve?

A

Adaptive immune response

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13
Q

What are signs of chronic inflammation like?

A

Subtle or absent, but tissue injury can be severe

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14
Q

When does adaptive immunity begin?

A

When T cells come into play

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15
Q

What is the most common initiator of acute inflammation?

A

Sentinel cell detection of PAMPs

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16
Q

What are the typical sentinel cells in tissues?

A

Macrophages

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17
Q

Once activated, what do macrophages synthesize and release?

A

Cytokines and chemokines

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18
Q

What are some examples of cytokines?

A

IL-1β
IL-6
TNF-α

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19
Q

What do cytokines do?

A

Signal other inflammatory cells or blood vessels in the area

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20
Q

What is an example of chemokines?

A

CXCL8

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21
Q

What do chemokines do?

A

Recruit other inflammatory cells to the area

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22
Q

What is the most common trigger of inflammation?

A

Microbial infections

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23
Q

What other tissue insults can initiate inflammation?

A

Trauma
Physical or chemical injury
Foreign bodies
Inappropriate products of adaptive immunity

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24
Q

What does sterile inflammation often result in?

A

Release of endogenously produced DAMPs, which activate macrophages

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25
Q

What are examples of sterile inflammation?

A

Liver ischemia/reperfusion following surgery or acute myocardial infarction

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26
Q

What is an inflammasome?

A

Multi-subunit complex of proteins that cleave IL-1β and IL-18

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27
Q

What does an inflammasome typically conatin?

A

Sensor protein
Adaptor protein
Enzyme that cleaves IL-1β and IL-18 from their pro form to their active form

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28
Q

In addition to cytokines and chemokines, what are inflammatory processes regulated by?

A

Eicosonoids

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29
Q

What are eicosonoids?

A

Fatty acid derivatives

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30
Q

What are 2 kinds of eicosonoids?

A

Leukotrienes

Prostaglandins

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31
Q

What are eicosonoids synthesized from?

A

Membranes following liberation of arachidonic acid from diacylglycerols or phospholipids

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32
Q

What are prostaglandins synthesized from?

A

Arachidonic acid by cyclooxygenase enzymes

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33
Q

What are the different cyclooxygenase enzymes?

A

COX-1 and COX-2

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34
Q

How is COX-2 induced? COX-1?

A

Induced in inflammation

It is constitutive

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35
Q

What does PGE2 do?

A

Vascular permeability and vasodilation

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36
Q

What are leukotrienes synthesized from?

A

Arachidonic acid by lipoxygenase

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37
Q

What does LTB4 do?

A

Chemoattractant for neutrophils

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38
Q

What do LTB4 and LTD4 do?

A

Vascular permeability

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39
Q

What are examples anti-inflammatories and anti-pyretics?

A

Meloxicam
Phenylbutazone
Carprofen

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40
Q

What is meloxicam selective for?

A

Slight selectivity for COX-2

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41
Q

What is phenylbutazone used in?

A

Horses

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42
Q

What is carprofen selective for?

A

COX-2

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43
Q

What do anti-pyretics do?

A

Help with fever

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44
Q

What kind of vascular changes can cause inflammation?

A

Vasodilation
Increased blood flow
Increased vascular permeability
Expression of cell-adhesion molecules on vascular endothelium

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45
Q

What does vasodilation occur through?

A

The action of inflammatory mediators on arteriole and postcapillary venule smooth muscle

46
Q

In vasodilation, what does the decreased tone to smooth muscle do?

A

Widens the lumen of the vessels

47
Q

What does the widening of the vessels in vasodilation do?

A

Slows blood flow in the area

48
Q

What is vasodilation mediated by?

A

Histamine and 5-HT (serotonin; mast cells), PGE2 (macrophages and mast cells), and nitric oxide (endothelium)

49
Q

What does vasodilation contribute to? How?

A

Both rubor and calor by increasing blood volume

50
Q

What do PAMPs, DAMPs, macrophages, mast cells, inflammatory mediators, and inflammatory molecules act on? What does it do?

A

Acts on blood vessel to make it bigger

51
Q

What does increased vascular permeability occur through?

A

The action of inflammatory mediators on endothelial cells

52
Q

What does increased vascular permeability form?

A

An exudate that moves from vasculature to affected interstitial tissue

53
Q

What does increased vascular permeability contribute to?

A

Blood flow stasis

54
Q

What does endothelial cell contraction during increased vascular permeability cause?

A

Gaps in the tight junctions between endothelial cells

55
Q

What are other mechanisms for increased permeability?

A

Transcytosis

Direct damage to enothelial cell layer

56
Q

What is transcytosis?

A

Active transport of fluid and macromolecules across the endothelial cell cytoplasm through vesicles
Another way to form pores for cells and mediators to get through

57
Q

What is the first cell to respond when there is an infection?

A

Neutrophils; however, macrophages are the resident cell so they are there initially and then release something to attract the neutrophils

58
Q

What are the 4 stages of leukocyte extravasation?

A

Tethering and rolling
Firm adhesion and crawling
Transmigration
Chemotaxis through tissue

59
Q

What is tethering?

A

IL-1 and TNF-α activate endothelial cells to express adhesion molecules to which neutrophils can bind

60
Q

What does E-selectin bind to?

A

Sialylated Lewis-X modified glycoprotein

61
Q

What does P-selectin bind to?

A

Platelet selectin glycoprotein ligand 1

62
Q

What are the interactions like during tethering?

A

Low affinity but many interactions increases the strength of binding neutrophils and endothelial cells

63
Q

What are integrin interactions like?

A

Initially low affinity, but switch to high affinity

64
Q

What does ICAM-1 bind to?

A

LFA-1

65
Q

What will the high affinity interaction during firm adhesion do?

A

It will stop the neutrophil from rolling

66
Q

What is transmigration?

A

Movement of leukocytes from lumen of blood vessel through the vessel wall and into interstitium

67
Q

Where does transmigration usually occur?

A

In thin-walled postcapillary venules, but neutrophils still have to penetrate the endothelial barrier and underlying basement membrane

68
Q

Where do neutrophils typically transmigrate?

A

Through small gaps between endothelial cells and digest basement membrane with collagenase

69
Q

Once out of the vasculature, what do neutrophils do?

A

Respond to chemical gradients to move to the site of infection

70
Q

What are endogenous products produced by?

A

Innate cells

71
Q

Where do exogenous microbial products diffused from?

A

The site of infection

72
Q

What do neutrophils do once in the tissue?

A

Adopt an amoeboid-like morphology with a leading pseudopod

73
Q

What do receptors for chemoattractants on the pseudopod bind? What does it do?

A

The liagand and moves the rest of the cell toward the stimulus

74
Q

What happens as the neutrophil moves toward infection?

A

It becomes activated in response to cytokines or other pro-inflammatory mediators making it more efficient at its primary functions

75
Q

What are macrophages called in the liver?

A

Kupffer cells

76
Q

What are macrophages called in the lung?

A

Alveolar macrophages

77
Q

What are macrophages called in the CNS?

A

Microglial cells

78
Q

What are macrophages called in the spleen?

A

Splenic macrophages

79
Q

What does the type of cellular response depend on?

A

Pathogen

Types of adhesion molecules that are expressed

80
Q

What will neutrophils be recruited in response to?

A

CXCL8

81
Q

What will eosinophils be recruited in response to?

A

CCL11

82
Q

What will monocytes differentiate into once in the tissue?

A

Macrophages and further migrate toward the insult

83
Q

What are functions of macrophages?

A

Moderately proficient at killing
Phagocytose and break down debris
Clean up dead neutrophils, debris and dead microbes

84
Q

What are examples of systemic effects of inflammation? (9)

A 
Loss of appetite
Altered sleep patterns
Lethargy
Muscle wasting
Hemodynamic changes
Fever
Leukocytosis
Metabolic acidosis
Alterations in acute phase proteins
85
Q

What are examples of cytokines?

A

TNF-α
IL-1
IL-6

86
Q

What do cytokines do?

A

Rapidly disseminate throughout the body

Function to conserve energy and mobilize proteins

87
Q

What does TNF-α cause?

A

Loss of apepetite
Altered sleep patterns
Lethargy
Cachexia

88
Q

What can TNF-α and IL-1 stimulate?

A

Hypothalamus to produce PGE2

89
Q

What does the release of PGE2 in anterior hypothalamus do?

A

Acts on thermoregulatory neurons to cause fever

90
Q

What are the targets of inflammatory mediators that change the response from acute to systemic?

A

Bone marrow
Brain
Liver

91
Q

What is PGE2 a main player in?

A

Fever and vascular permeability

92
Q

Know the different proposed functions of fever

A

Know the different proposed functions of fever

93
Q

What is leukocytosis?

A

Increased number of leukocytes circulating in the blood

94
Q

What is leukocytosis known as in response to acute systemic inflammation?

A

Neutrophilia

95
Q

What does neutrophilia cause?

A

Increased release of neutrophils from bone marrow

96
Q

What does neutrophilia allow for?

A

More neutrophils to extravasate and contribute to immune defense at site of infection

97
Q

What will a prolonged release of neutrophils from bone marrow do?

A

Deplete its store of mature cells prompting increased neutrophil production, but less mature neutrophils
Causes a left shift

98
Q

What does a severe left shift in neutrophil maturation cause?

A

Acute inflammatory response

99
Q

What can acute systemic inflammation do?

A

Alter the serum acute phase proteins profile

100
Q

What does positive serum APP profile do?

A

Increase with inflammation

101
Q

What does negative serum APP profile do?

A

Decrease with inflammation

102
Q

Why are APPs used as diagnostic indicators of inflammation?

A

Because they can be induced so quickly and with high magnitude

103
Q

What does an opsonin do?

A

Helps macrophages phagocytose

104
Q

What are the positive APPs?

A 
C-reactive protein
Serum amyloid A
Haptoglobin
Alpha-1-acid glycoprotein
Ceruloplasmin
Hepcidin
Fibrinogen
105
Q

What are the negative APPs?

A

Albumin

Transferrin

106
Q

What do APPs do?

A

Act as opsonins and activate complement

107
Q

What is C-reactive protein a major APP in?

A

Dogs and pigs

108
Q

What is serum amyloid A and major APP in?

A

Dogs
Cats
Cattle
Pigs

109
Q

What is haptoglobin a major APP in? Moderate?

A

Pigs, cattle, sheep

Dogs, cats

110
Q

What is alpha-1-acid glycoprotein a major APP in? Moderate?

A

Cats

Dogs

111
Q

What is ceruloplasmin a moderate APP in? Minor?

A

Dogs

Cattle

112
Q

What is fibrinogen important in?

A

Horses and cattle

Immunology - DVM year 1 (35 decks)

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