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Immunology > Inflammation and The Acute Phase Response > Flashcards

Inflammation and The Acute Phase Response Flashcards

1
Q

Inflammation can be induced by many types of injuries, including:

A

infections, allergies, tumors, necrosis, bone fractures, cuts, burns, ischemia

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2
Q

What are the five classic local signs of inflammation? hint: PRISH

A

pain, redness, immobility, swelling, heat

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3
Q

What are the systemic signs of inflammation?

A

fever, the release of pro-inflammatory cytokines from leukocytes, the release of acute phase proteins from the liver

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4
Q

True or false? Acute inflammation most often leads to complete elimination of a pathogen followed by resolution of the damage, disappearance of leukocytes from the tissue, and full regeneration of tissue function in a short period of time.

A

true

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5
Q

What are the three principal tissue changes seen during acute inflammation?

A

increased blood supply, increased capillary permeability to serum proteins, and increased leukocyte migration into the tissue

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6
Q

Within the first ____-____ min of acute inflammation, the major leukocytes entering the area are neutrophils, which may eliminate the intruder almost immediately and halt any further response

A

30-60

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7
Q

If the cause of inflammation persists beyond the influx of neutrophils, then ____ and ____ enter the area within 4-6 hours

A

macrophages; lymphocytes

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8
Q

The macrophages destroy the intruders by phagocytosis and process and present antigens to T cells. The T cells induce what?

A

B cells to make antibodies specific for the intruder

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9
Q

How long does it take for antibodies secreted by B cells to be detectable in the serum?

A

5-7 days

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10
Q

Chronic inflammation results when the body tries to contain an infection or other insult that it cannot completely eliminate. What are some of the immune cells that help with chronic inflammation?

A

granulomas with macrophages, epithelia giant cells, and lymphocytes

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11
Q

Bacteria produce ____ molecules that will attract local macrophages. The macrophage will physically bind to the surface of the bacterium through many types of ____-____ interactions

A

cemotactic; receptor-ligand

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12
Q

The receptor-ligand interactions that occur between macrophages and microbial pathogens are called PRR-PAMP interactions. PRRs are pattern recognition receptors on leukocytes. PAMPS are pathogen associated molecular patterns, which are molecules shared by groups of related microbes essential for microbe survival. What are some important PAMPS?

A

formylated amino acids, inlcuding fMet-Leu-Phe, produced by bacteria (chemotactic for macrophages and neutrophils)

LPS, endotoxin from the outer cell membrane of Gram-negative cells

Lipoteichoic acids from Gram-positive bacterial cell wall

The sugar mannose made by many bacteria and fungi

Microbial nucleic acids including dsRNA

bacterial flaggelin

gluons from fungal cell walls

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13
Q

The PRRs that recognize these PAMPS include Toll-like Receptors (TLRs). TLR-4 binds to what? TLR-2 binds to what?

A

TLR-4: LPS in Gram-negative bacteria

TLR-2: lipoteichoic acid in Gram-positive bacteria

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14
Q

Both TLR-2 and TLR-4 use CD14 as a ____, and the MyD88 adaptor protein to mediate ____ ____

A

co-receptor; signal transduction

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15
Q

Additional PRRs include carbohydrate receptors for ___ and ___

A

mannose and glucan

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16
Q

NOD-like receptors, located in the leukocyte cytosol recognize the ____ ____ and toxins produced by intracellular bacteria, ____ produced by intracellular pathogens

A

structural components (peptidoglycan); RNA

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17
Q

Some NLRs can assemble into a multi-protein complex called the inflammasome, which in turn activates the enzyme _____

A

caspase-1

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18
Q

What does capsize-1 activate?

A

IL-1beta, a major contributor to inflammation, stimulating fever and movement of leukocytes out of the blood vessels and into the tissues

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19
Q

PRR-PAMP interactions stimulate the macrophage to perform two major functions simultaneously. These functions are?

A
  1. phagocytosis of the pathogen

2. synthesis of pro-inflammatory cytokines, especially IL-1, IL-6 and TNF alpha

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20
Q

What do the pro-inflammatory cytokines (IL-1, IL-6, and TNF alpha) induce?

A

septic shock, fever, acute phase protein release from liver, ROS production by phagocytes, migration of leukocytes out of blood and into tissue

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21
Q

Which pro-inflammatory cytokine is the most potent in inducing septic shock?

A

TNF alpha

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22
Q

Shaking chills, hyperthermia, hypothermia, weakness, tachypnea, tachycardia, and a drop in bp are all signs/symptoms of what?

A

septic shock

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23
Q

Which pro-inflammatory cytokine is the most potent in inducing fever?

A

IL-1

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24
Q

Pyrogens act on the ____ center within the ____, resulting in sympathetic nerve stimulation, vasoconstriction of skin vessels, and decreased heat dissipation.

A

vasomotor; hypothalamus

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25
Q

LPS and lipoteichoic acid, both of which induce IL-1 are potent ____ ____

A

exogenous pyrogens

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26
Q

Which pro-inflammatory cytokine is the most potent in inducing acute phase protein release from the liver?

A

IL-6

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27
Q

Acute phase proteins (APPs) aid as host defense by acting as ____, and participate in tissue repair. ____ APPs increase in serum concentration, while ____ APPs decrease in serum concentration during inflammatory events

A

opsonins; positive; negative

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28
Q

bacterial cell lysis, opsonization of bacteria for phagocytosis, chemotactic for neutrophils, and induction of mast cell degranulation are all caused by what system?

A

complement

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29
Q

In regards to complement, ___-____ protein binds to strep pneumoniae and other microbes, opsonizes bacteria for phagocytosis, induces the classical complement pathway, and is a clinically useful marker for inflammation/infection

A

c-reactive

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30
Q

Involved in tissue repair, remodels extracellular matrix, prevents oxidative tissue damage by neutrophils, and inhibits platelet activation

A

Serum amyloid A

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31
Q

This is the inactive precursor of the serine protease plasmin and functions to dissolve clots

A

plasminogen

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32
Q

This is the precursor of the serine protease thrombin

A

prothrombin

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33
Q

What does thrombin do?

A

converts soluble fibrinogen into insoluble fibrin strands

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34
Q

Fibrin strands are cross-linked by factor ___ form a ___ ___

A

XIII; blood clot

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35
Q

This is a serum protease inhibitor of serpin family. It protects tissues from enzymes of inflammatory cells (breaks down neutrophil elastase)

A

Alpa-1-antitrypsin

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36
Q

Alpha-1-antitrypsin deficiency leads to what?

A

COPD when lung elastin is broken down unabated

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37
Q

Migration of leukocytes out of bloodstream and into the tissues is called _____

A

extravasation (or diapedesis)

38
Q

Extravasation is controlled by expression of complementary adhesion molecules on the ___ and _____ _____ cells

A

leukocytes; vascular endothelial

39
Q

Adhesion molecule expression is up-regulated primarily by what two cytokines

A

IL-1 and TNF alpha

40
Q

What is margination?

A

when leukocytes move to the endothelial lining of small blood vessels

41
Q

In regards to margination, IL-1 and TNF alpha up-regulate expression of the adhesion molecules ___-____ and ___

A

E-selectin; ICAM-1

42
Q

The leukocytes become tethered to the endothelial cells when ___ ____ ___ on the neutrophil binds to _-___ on the endothelial cell. The cells then roll along the endothelial surface

A

sialyl Lewis X; E-selectin

43
Q

The chemokine ___ up-regulates expression of the adhesion molecule LFA-1 on the neutrophil surface. Rolling ceases when LFA-1 binds tightly to ____ on the endothelial cell. The neutrophil crawls to a junction between two endothelial cells

A

IL-8; ICAM-1

44
Q

Transendothelial migration is penetration of the what?

A

basement membrane

45
Q

In regards to chemotaxis, leukocytes migrate toward the site of infection by following the concentration gradient of what chemotactic molecules

A

f-met-leu-phe, IL-8, complement component C5a, or other chemotactic molecules

46
Q

Once a neutrophil arrives at the site of infection, it will recognize the pathogen using many of the same PRR-PAMP interactions used by macrophages. The pathogen will be ____ and killed by degradative enzymes in the ____, or by the respiratory burst

A

phagocytosed, phagolysosome

47
Q

Additional cellular changes that occur in blood vessels during inflammation include: adhesion of platelets to collagen exposed on damaged endothelium. This leads to ___ deposition and eventually a blood clot forms

A

fibrin

48
Q

Additional cellular changes that occur in blood vessels during inflammation include: roleaux formation of red blood cells due to fibrinogen deposition on their surfaces. This increases the ____ _____ rate

A

erythrocyte sedimentation

49
Q

In persons with leukocyte adhesion deficiency (LAD), certain adhesion molecules are missing, leading to an inability of leukocytes to extravasate from the vasculature and into the tissues. This results in what?

A

leukocytosis, inability to form pus, and impaired wound healing

50
Q

Patients with LAD present with what?

A

soft tissue bacterial infections, especially of the mouth and GI tract

51
Q

In LAD1, there is a deficiency in the CD __ molecule comprising part of LFA-1. In LAD2, defective fucose metabolism prevents expression of ___-___ __

A

18; sialyl-Lewis X

52
Q

In addition to enzymatic degradation by lysosomal enzymes, microbes can be killed through the _____ ___ of the phagocyte

A

respiratory burst

53
Q

The respiratory burst is stimulated by many cytokines, including?

A

TNF alpha, IFN gamma, and GM-CSF

54
Q

The enzyme ___ oxidase initiates the respiratory burst. Ig generates superoxide anions from oxygen.

A

NADPH

55
Q

In regards to the respiratory burst, superoxide dismutase (SOD) catalyzes the formation of ____ ____

A

hydrogen peroxide

56
Q

In regards to the respiratory burst, _______ generates hypochlorite from hydrogen peroxide

A

myeloxperoxidase

57
Q

In regards to the respiratory burst, ____ splits hydrogen peroxide to water and oxygen, which protects the host cell from the damaging effects of hydrogen peroxide

A

catalase

58
Q

Deficiency of NADPH oxidase enzyme leads to the immunodeficiency disease ____ ____ disease

A

chronic granulomatous (CGD)

59
Q

CGD is marked by repeated infections by catalase-producing bacteria and fungi, especially ___ ___ and ____

A

staph aureus; aspergillus

60
Q

CGD is marked by ____ that form due to intracellular survival of certain microorganisms

A

granulomas

61
Q

CGD is marked by pneumonia, lymphadenitis, and accesses in the ____, ___, and ____ organs

A

skin, liver, visceral

62
Q

The short-lived respiratory burst is followed by sustained production of ___ ____ by the enzyme iNOS. NO and its metabolites are especially important in killing certain ____ bacteria such as listeria monocytogenes

A

nitric oxide (NO); intracellular

63
Q

Complement is a series of serum proteins that work in a cascade to mediate what?

A

bacterial lysis, opsonization, and leukocyte chemotaxis, activation, and degranulation

64
Q

The classical pathway is induced by what?

A

CRP, IgG, or IgM bound to the surface of target cell

65
Q

The alternative pathway is induced when?

A

C3b binds to endotoxin/LPS on gram-negative bacteria or zymosan on yeast

66
Q

The lectin pathway is induced by ___ residues on bacteria and other microbes

A

mannose

67
Q

Although each pathway is initiated differently, all three pathways end with the formation of what?

A

membrane attack complex (MAC)

68
Q

The MAC can directly lyse Gram-____ bacteria. Gram-____ bacteria have cell walls that are too thick to be lysed by complement but can still be opsonized for phagocytosis

A

negative; positve

69
Q

For each of the split products of the complement cascade, give its activity:

C3b > C4b
C5a >> C3a > C4a
C5a
C3a
C5b6789n
A

C3b > C4b: opsonization

C5a&raquo_space; C3a > C4a: anaphylatoxins

C5a: activator and chemotaxis for all myeloid cells, induces PMN degranulation, induces IL-1 and IL-6 production in monocytes

C3a: chemotactic for eosinophils

C5b6789n: MAC

70
Q

C3b > C4b is recognized by which complement receptors?

A

CR1, CR2, CR3, and CR4 on macrophages

71
Q

C5a&raquo_space; C3a > C4a cuase degranulation of mast cells, basophils and eosinophils. ____ release by mast cells and basophils induces smooth muscle contraction and increases capillary permeability leading to local edema

A

histamine

72
Q

What is the most potent anaphylatoxin

A

C5a

73
Q

The classical pathway is initiated when globular domains of ___ bind to the Fc fragment of IgG, IgM, or CRP coating the microbial surface.

A

C1q

74
Q

In regards to the classical pathway, two C1r molecules bind to C1q and become enzymatically active. The C1r molecules then activate two molecules of ___, which act as a serine protease to cleave C4 into C4a and C4b

A

C1s

75
Q

In regards to the classical pathway, C4b binds to the ____ surface, while C4a is released into the serum or tissue to act as a weak _____

A

microbial; anaphylatoxin

76
Q

In regards to the classical pathway, C1s next cleaves C2 into C2a and C2b. C2a binds to C4b, creating the classical pathway ___ convertase (C4b2a) on the microbial surface

A

C3

77
Q

In regards to the classical pathway, the C3 convertase initiates an amplification loop, in which it cleaves hundreds of molecules of C3 into C3a and C3b. C3a is released into the tissue space to act as an ____. C3b binds independently to the microbial surface to initiate the ____ pathway or act as a ____

A

anaphylatoxin; alternative; opsonin

78
Q

In regards to the classical pathway, some C3b molecules bind back to the C3 convertase to generate the classical pathway C5 convertase (C4b2a3b). The C5 convertase cleaves C5 into C5a and C5b. C5a is released into tissue to act as a _____, while C5b binds to the microbial surface to initiate the ___ pathway

A

anaphylatoxin; lytic

79
Q

In regards to the classical pathway, the lytic pathway proceeds with C6, C7, and C8 binding to C5b. Multiple molecules of C9 then polymerize in the microbial ___ ____, effectively creating a pore that causes osmotic disruption of the bacterial cell

A

cell membrane

80
Q

The lectin pathway is similar to the classical pathway except that it is initiated when mannan-binding lectin (MBL, an acute phase protein in the serum) binds to terminal mannose residues on the microorganism. Once MBL is bound, two mannose-associated serine proteases (MASP 1 and 2) join MBL. The MASP proteins cleave ___ into ___ and ____, and from that point onward, the lectin pathway is identical to the classical

A

C4; C4a; C4b

81
Q

The alternative pathway is triggered when C3b binds to endotoxin/LPS on the Gram-negative bacterial cell membrane. The C3b molecule can be generated from the classical or lectin pathway, or by spontaneous hydrolysis of C3 in the serum or tissue fluids. Surface-bound C3b binds to Factor __ to yield C3bB, which becomes a substrate for Factor ___

A

B; D

82
Q

In regards to the alternative pathway, Factor D is a serine esterase that please the Ba fragment, leaving _____ bound to the surface of the target cell.

A

C3bBb

83
Q

In regards to the alternative pathway, C3bBb is stabilized by ____

A

properdin (P)

note: forms the complex C3bBb(P) which acts as the alternative pathway C3 convertase

84
Q

C1 esterase inhibitor (C1INH) deficiency leads to hereditary ____

A

angioedema

note: C1INH disrupts the C1qrs complex, the MASP complex, and C3bBb

85
Q

Decay-accelerating factor (DAF) is a GPI-anchored protein; a deficiency in DAF leads to what?

A

paroxysmal nocturnal hemoglobinuria (PNH) with red cell lysis

note: DAF binds to C4b, disrupts C4b2a

86
Q

Factor H protects human cells from what?

A

Factor B

87
Q

Factor I inactivates ___ and ___

A

C4b; C3b

88
Q

Membrane protein CD59 interferes with the MAC. Its deficiency leads to what?

A

PNH

89
Q

C3 deficiency results in profound susceptibility to infections by ___ ___

A

encapsulated bacteria

ex: strep pneumoniae, H flu, and neisseria

90
Q

Deficiences in MAC (C5-C9) components increase susceptibility to ___

A

Neisseria

91
Q

Deficeincy in MBL increases susceptibility to many infections (viruses, bacteria, fungi, protozoa). The deficiency is especially problematic in which individuals?

A

infants after passively acquired maternal antibody has dissipated, and in cystic fibrosis patients

92
Q

Common symptoms of PNH include?

A

weakness, dyspnea, pallor, splenomegaly, iron deficiency, thromocytopenia leading to bleeding disorders, acute or chronic renal failure, sever headaches, eye pain, and chronic infections

Immunology (12 decks)

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