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Biology 2401 > unit 8 micro > Flashcards

unit 8 micro Flashcards

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1
Q

innate immunity is:

A

initial defenses to prevent infection

non-specific: defenses act in response to all pathogens

built in mechanisms: structures/chemicals are present at birth

no memory: same response regardless of prior exposure

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2
Q

adaptive immunity is:

A

response to pathogens

specific: defenses act in response to one type of bacterial strain or virus

builds up over time: requires exposure to antigens

has a memory: strong response with a second exposure to the same antigen

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3
Q

first line of defense consists of

A

initial barriers to pathogens to prevent entry and colonization

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4
Q

second line of defense is

A

a response to infection once the first line has been bypassed

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5
Q

physical factors in first line

A

barriers that prevent entry OR processes that remove microbes from the body surface

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6
Q

barriers include

A

skin: tightly packed epithelial cells that contain keratin

mucus membranes: contain epithelial cells bound by tight junctions; line nose, mouth, lungs, urinary and digestive tracts

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7
Q

mucus is produced to

A

cover and protect the cell layers, and to trap debris and microbes

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8
Q

endothelia is

A

tightly packed cells lining the urogenital

one well known example is blood brain barrier, which contains very tight cell junctions preventing pathogens from entering the CNS

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9
Q

mechanical action is then used to

A

flush mucus-trapped microbes out of the body

mucociliary escalator in the lungs use cilia to propel mucus out of the lungs, which is then swallowed or coughed/sneezed out

shedding of skin cells

flushing action of urine, tears

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10
Q

normal flora

A

through competitive inhibition, our microbiome prevents the growth of other microbes by out-competing pathogens for nutrients and by taking up spaces that can be colonized

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11
Q

chemical factors (1st)

A

substances or enzymes continuously produced by body cells.

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12
Q

sebum

A

produced by sebaceous glands in the dermis to seal off pores of hair follicles

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13
Q

production of oleic acid by

A

normal flora to create a mildly acidic environment on the skin to inhibit pathogen colonization

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14
Q

what in saliva, sweat and tears can break down bacterial cell walls

A

lysozyme

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15
Q

what antibodies that protect the respiratory tract

A

IgA

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16
Q

what in saliva (salivary amylase), lower digestive tract (pancreatic enzymes)

A

digestive enzymes

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17
Q

name chemical defenses involved in the second line of defense

A

antimicrobial peptides (AMPs), plasma protein mediators: acute phase proteins & complement proteins & cytokines & inflammation-eliciting mediators

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18
Q

AMPs are (antimicrobial peptides)

A

group of chemicals with broad-spectrum anti-microbial activity

some are produced continuously and some are produced in response to pathogen infection

some are produced by body cells and some are produced by normal flora

examples: cathelicidin, dermicidin, histatin

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19
Q

plasma protein mediators are

A

proteins found in the blood that play a role in the nonspecific innate immune response

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20
Q

acute phase proteins are

A

produced in the liver and secreted into the blood in response to inflammatory molecules

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21
Q

examples of acute proteins

A

different examples with different methods of inhibiting or destroying microbes, such as ferritin, fibrinogen, mannose-binding lectin

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22
Q

complement proteins are

A

group of proteins that circulate in inactive forms in the blood

activated in a cascade allowing for a rapid response to infection

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23
Q

method 1 of complement proteins

A

classical complement activation:

  1. antibody binds to bacterium
  2. C1 protein is recruited and activated & C3 protein is recruited and activated
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24
Q

method 2 of complement proteins

A

mannose-binding lectin:

  1. mannose-binding lectin binds to. carbohydrates on microbial surface
  2. C3 protein is recruited and activated
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25
Q

method 3 of complement proteins

A

alternative activation:

  1. C3 protein is directly recruited and activated
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26
Q

upon activation, C3

A

splits into 2 separate proteins C3a & C3b

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27
Q

outcome 1: opsonization

A

C3b protein coats the microbe, which makes the microbe more easily identified by macrophages

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28
Q

outcome 2: cytolysis

A
  1. C3b recruits and activates C5 protein
  2. C5 splits into 2 separate proteins, named C5a & C5b
  3. C5b recruits and combines with C6, C7, C8 & C9 proteins to form a membrane attack complex, which inserts into the cell membrane causing extracellular fluid to rush in, leading to microbial cell lysis
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29
Q

outcome 3: enhanced inflammation

A

C3a & C5a combine together and binds to mast cells, leading to increased production of histamine by mast cells

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30
Q

how do microbes avoid the complement system

A

presence of a capsule inhibits opsonisation and prevents insertion of the MAC, gram-negative cells can alter the structure of the outer membrane to prevent insertion of the MAC, gram-positive cocci can release an enzyme that breaks down C5 protein

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31
Q

cytokines are

A

soluble proteins that act as communication signals between cells

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32
Q

in the immune response, cytokines are

A

important to stimulate production of other chemical mediators or to promote cell functions

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33
Q

3 main types of cytokines

A

interleukins - modulate many parts of immune system

chemokines - recruit white blood cells to sites of infections, tissue damage and inflammation

interferons - important for our defenses against viral replication (can be produced in the lab and used as treatment for viral infection but have significant side effects)

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34
Q

inflammation-eliciting mediators

A

contributes to the inflammation response

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35
Q

examples of inflammation-eliciting mediators

A

histamine - produced by mast cells
leukotrienes - longer lasting effects than histamine
prostaglandins - also plays role in fever
bradykinin - increases vascular permeability leading to edema

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36
Q

cellular defenses involved in the second line of defense

A

granulocytes & agranulocytes

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37
Q

granulocytes are

A

white blood cells with lobed nuclei and granules in the cytoplasm

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38
Q

mast cells

A

reside in tissues to produce histamine

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39
Q

basophils

A

produces histamine in response to allergic reactions

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40
Q

neutrophils

A

elimination and destruction of bacteria through direct phagocytosis or through the production of extracellular traps (NETs)

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41
Q

eosinophils

A

protect against protozoan and helminthic infections by releasing degradative enzymes

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42
Q

agranulocytes are

A

white blood cells with no granules in cytoplasm

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43
Q

agranulocytes use

A

nonspecific mechanisms to recognize abnormal body cells. upon recognition, NK cells will induce apoptosis in these abnormal body cells

44
Q

apoptosis

A

programmed cell death

45
Q

after movement into body tissue

A

monocytes will differentiate into dendritic cells and macrophages

46
Q

phagocytosis:

1. extravasation (diapedesis) of leukocytes to site of infection

A
  • site of injury leads to release of inflammation-elicitors and cytokines
  • through positive chemotaxis, phagocytes leave the blood stream through capillaries and enter tissues through process called extravasation
  • neutrophils usually arrive first, followed by monocytes (which differentiate into macrophages)
47
Q

phagocytosis:

2. pathogen recognition

A

-attachment of the phagocyte’s plasma membrane to the surface of the microorganism through the interaction of PAMPs on the pathogen with receptors on the phagocytes

48
Q

PAMPs are

A

pathogen-associated molecular patterns

49
Q

PRRs are

A

pathogen recognition receptors

50
Q

examples of PAMPs

A

peptidoglycan, flagellin, lipopolysaccharides, lipopeptides

51
Q

pathogen recognition can be enhanced by

A

opsonization

52
Q

phagocytosis:

pathogen degradation

A
  • pseudopods form around the microbe and a phagosome is made (phagocytic vesicle)
  • a lysosome containing hydrogen peroxide and several enzymes, fuse with the phagosome to form a phagolysosome
  • microbe is then digested
  • indigestible material (waste) are excreted by exocytosis
53
Q

how do microbes avoid phagocytosis

A
  • presence of capsule inhibits adherence of the phagocyte to the pathogen
  • some pathogens can release molecules that leads to phagocyte death
  • some pathogens use phagocytosis as a mechanism for entry into the cells, and then replication inside the phagocytes
  • formation of biofilms - phagocytes are unable to detach pathogens from a biofilm
54
Q

acute inflammation in 2nd line

A
  • immediate response to injury is vasoconstriction, which leads to the narrowing of blood vessels to minimize blood loss
  • this is followed by vasodilation and increased vascular permeability
  • phagocytes are then recruited due to tissue damage and release of chemicals such as histamine
  • pus is formed as damage tissue and pathogens are cleared
  • eventually tissue repair begins
55
Q

5 signs/symptoms of inflammation

A

swelling, heat, redness, pain, altered function

56
Q

chronic inflammation in 2nd line

A

occurs when the immune system is unable to clear pathogen

when this occurs, tissue damage can occur, such as the formation of granulomas

57
Q

body temperature is regulated by

A

hypothalamus

58
Q

As a result of bacterial or viral infections

A

a series of chemicals are
released, eventually leading to the production of prostaglandins that
leads to elevated body temperature

59
Q

Fever can enhance the immune system by:

A

inhibiting the growth of many pathogens & stimulating the release of iron-sequestering compounds from the liver

60
Q

during fever:

A

vasoconstriction of the blood vessels occur, marking the skin appear pale & leads also to shivering and an increase in metabolism

61
Q

when fever breaks:

A

Vasodilation is stimulated, leading to release of heat from body

62
Q

Complications of fever in situations where the immune response is too strong:

A

Tissue and organ damage, tachycardia, metabolic acidosis, dehydration,
seizures, delirium, coma

63
Q

Antigens are found on pathogens and can stimulate the immune system. Examples
include:

A

bacteria: cell wall, flagella, fimbriae
viruses: spikes, fibres, envelope

64
Q

Specific regions on antigens where antibodies bind to

A

epitopes

65
Q

protein antigens

A

are generally more potent

66
Q

carbohydrate antigens

A

can only stimulate the humoral immune defense

67
Q

lipid and DNA antigens

A

least antigenic

68
Q

antibodies are also called

A

immunoglobulins and are produced by the immune system to target antigens

69
Q

5 classes of antibodies

A

IgG, IgM, IgA, IgD, IgE

70
Q

most abundant in the body

A

IgG

71
Q

found in respiratory secretions

A

IgA

72
Q

aids in allergic responses and defense against parasites

A

IgE

73
Q

cellular immunity involves

A

T cells & main target is to kill infected body cells and to boost the overall immune response

74
Q

humoral immunity involves

A

B cells & main target is to kill extracellular antigens

75
Q

describe how a T cell library is formed

A

hematopoietic (stem) cells are formed in bone marrow

half of these will migrate to the thymus and eventually become naive T cells

76
Q

naive helper T cells contain

A

T-cell receptor (TCR) capable of binding to a specific epitope & CD4 co-receptor

77
Q

naive cytotoxic T cells contain

A

T cell receptor capable of binding to a specific epitope & CD8 co-receptor

78
Q

activation of helper T cells

A
  1. pathogen/antigen is phagocytosed by a
    phagocyte (macrophage or dendritic cell)’
  2. Inside the macrophage, a protein complex called
    MHC-II combines with the antigens
  3. The MHC-II combined with the antigens are then
    presents on the plasma membrane

4.The macrophage is now called an antigen-presenting cell (APC)

  1. The corresponding TCR on a naïve helper
    T cell binds to the displayed antigen,
    partially activating the naïve helper T cell
  2. The CD4 co-receptor on the naïve helper T
    cell also binds to the displayed antigen to
    anchor the TCR-antigen complex
  3. The APC releases cytokines which further
    activates the naïve helper T cell
  4. Once activated, the naïve helper T cell will
    proliferate through mitosis and then differentiate into different types of cells (3)
79
Q

memory T cells

A 
function to remember the antigen. Should the antigen be
encountered again, these cells will rapidly switch to cytotoxic T cells
80
Q

T helper 1 (TH1)

A

stimulate other cells in the immune response

81
Q

T helper 2 (TH2)

A

function to stimulate the humoral immunity

82
Q

Cytotoxic T cells are activated

A

in the same way as helper T cells, with a few key
differences:

o Recognition of antigens are presented on MHC-I, not MHC-II

Anchoring is done by a CD8
co-receptor

Naïve cytotoxic T cells differentiate
into effector cytotoxic T cells

o Assistance from cytokines secreted
by TH1 cells leads to
longer-lasting effects

83
Q

Once activated, effector cytotoxic T cells will release:

A

o perforin to create pores in the target cell
o granzymes, which are proteases, which will enter the
pores and induce programmed cell death (apoptosis)

84
Q

describe how a B cell library is formed

A

• Hematopoietic (stem) cells are formed in the bone marrow

• Half of these cells remain in the bone marrow and eventually become B cells
o Each B cell is coated with IgM antibodies, capable of binding to a single epitope

85
Q

T-dependent B cell activation

A
  1. The IgM antibodies of an
    inactive B cell binds to a
    foreign antigen
  2. The IgM-antigen complex is
    then internalized into the
    inactive B cell
  3. Inside the B cell, the antigen is combined with MHC-II and the antigen is then presented onto the B cell plasma membrane
  4. The B cell becomes an antigen-presenting cell (APC)
  5. A corresponding TH2 cell
    (previously activated in cellular
    immunity) binds to the presented antigen
  6. After binding, the TH2 cell releases cytokines which activates the B cell
  7. Once activated, the B cell will proliferate through mitosis and then differentiate into
    different types of cells (2)
86
Q

plasma cells . . .

A

which secrete IgM antibodies initially, and later secrete

the longer-lasting IgG antibodies

87
Q

memory B cells

A

which remember the antigen. Should the antigen be

encountered again, these cells will rapidly switch to plasma cells to secrete antibodies

88
Q

T-dependent B cell activation is a

A

longer-lasting and leads to memory

89
Q

T-independent B cell activation

A
  1. This usually occurs with T-independent antigens (e.g.
    carbohydrate) which are sufficient to provide the first signal for activation
  2. The B cell is directly activated through binding of
    the IgM antibody to the foreign antigen
  3. Once activated, the B cell will proliferate through mitosis, and then differentiate into plasma cells, which secrete IgM antibodies; no memory cells are made

• This response is short -lived and requires boosting from
innate immunity pathways such as the complement pathway

90
Q

neutralization

A

the binding of antibodies to epitopes to prevent attachment to cells

91
Q

opsonization

A

the coating of a pathogen to enhance phagocytosis

92
Q

agglutination

A

the cross-linking of antigens to create large clumps

93
Q

complement

A

activation of the complement cascade

94
Q

antibody-dependent cell-mediated cytotoxicity

A

enhanced killing of pathogens that are too large to be phagocytosed

95
Q

active, natural immunity

A

immunity gained from illness and recovery

96
Q

active, artificial immunity

A

vaccination

97
Q

passive, natural immunity

A

antibodies passed through breast milk or placenta

98
Q

passive, artificial immunity

A

transfer of antibodies harvested from an individual or animal

99
Q

describe the function of vaccinations

A

The deliberate exposure of a person to an antigen to trigger a primary response without the person feeling the effects of the pathogen

• Therefore, when they actually encounter the pathogen, a secondary response occurs

100
Q

herd immunity is

A

when there are too few susceptible individuals for a disease to spread effectively

• This can be done by vaccination programs to reduce the number of susceptible individuals

• Susceptible individuals cannot be vaccinated for a variety of reasons, such as too young or allergic to a vaccine
ingredient

101
Q

live, but attenuated (weakened) organisms vaccine

A
  • Can still replicate, meaning boosters are not needed
  • Increased challenges for storage and transport
  • Example: chickenpox
102
Q

inactivated, dead organisms vaccine

A

• No risk of severe infections, but boosters are often needed

• Useful for vaccination programs for developing countries (easy to store and
administer)

• Example: influenza, hepatitis A vaccine

103
Q

subunit vaccines

A

contains only the key antigens of a pathogen

  • Produced through genetic engineering or isolation from a degraded pathogen
  • No protection against antigenic variation
  • Example: hepatitis B, HPV
104
Q

toxoid vaccines

A

contains inactivated toxins; pathogens themselves are not included

  • Least amount of side effects, but does not prevent infection by pathogen
  • Example: botulism, tetanus, pertussis
105
Q

conjugate vaccines

A

synthetic vaccines that combine carbohydrate antigens with larger
proteins to stimulate both cellular and humoral immunity

  • More expensive to produce
  • Example: meningitis
106
Q

nucleic acid vaccines

A

nucleic acid is injected; cells take up the nucleic acid and
use it as a template to make protein antigens

example: west nile vaccine (horses), covid-19 (pfizer, moderna)

Biology 2401 (30 decks)

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