Unit 3 Innate Host Defenses Against Microbial Invasion Flashcards

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1
Q

Immunity can be split into two parts:

Do they work separately or together?

A

Innate and Adaptive

Together, each with different roles

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2
Q

The study of the components and processes of the immune esystem

A

Immunology

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3
Q

The immune system distinguishes foreign substances from _______

A

Self structures

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4
Q

Innate immune defenses are found in all ____ organisms

A

Multicellular (insects, tiny worms, etc count)

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5
Q

Which provides the first line of defense against microbes, the innate or adaptive immune system?

It provides what type of defense a lot of the time?

A

The innate

Barriers (doesn’t let microbe in cells)

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6
Q

How does the innate immune system recognize microbes vs. host cells

A

Biochemical differences

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7
Q

The innate immune defenses can recognize microbes as foreign, but it can’t do what?

So what is the response then?

A

Determine the precise identity of the microbe

It responds in the same manner for an entire group of similar microbes

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8
Q

This term is used to describe the innate immune defenses, in that they respond to entire groups of microbes in the same manner

A

Nonspecific Response

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9
Q

Does the innate immune response have memory?

A

No. It occurs at the same level every time (doesn’t get better over time towards same pathogen)

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10
Q

The innate immune system is always activated

A

!

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11
Q

This immune defense is only found in vertebrates

A

Adaptive Immune Defense

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12
Q

This immune defense works with innate responses to achieve a stronger level of defense to provide a much stronger protection than each individually

Is it specific?

A

Adaptive Immune Defense

Yes

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13
Q

The adaptive immune defense response is mediated by molecules that bind to specific ___

A

pathogens

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14
Q

After initial exposure, does the adaptive immune defense system retain memory of the response used towards a specific pathogen?

A

Yes. It can initiate more quickly! Hence, adaptive immunity

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15
Q

This is made by the human as part of the adaptive immune system

this is made by the microbe that is targeted by the adaptive immune system

A

Anitbody

Antigen

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16
Q

What is the drawback of the adaptive immune defenses?

A

It is slow to activate the first time.

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17
Q

Why is the skin a barrier to infection

A

It is inhospitable to foreign microbes

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18
Q

What about the skin makes it so inhospitable for so many microbes?

A
  1. Cool, dry, acidic (ph 5.0)
  2. Dead layer of cells
  3. provides armor
  4. A layer of oil on top of the armor
  5. Sweat provides antimicrobial barrier
  6. Normal flora can crowd out potential invaders (starve them)
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19
Q

What is the pH of the skin?

What is the oil on the skin called?

Why is sweat toxic?

A

5.0

Sebum

Salt (hypertonic environment)

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20
Q

Where might a microbe colonize in the skin?

A

Hair follice, sweat gland, sebaceous gland

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21
Q

This is an interior surface coated with wet mucous that is a barrier to infection

A

Mucosal Membrane

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22
Q

How does the mucosal membrane prevent microbe attachment?

A

Moving along the surface

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23
Q

What are the 3 antimicrobial molecules that are contained in the mucosal membrane?

What else contributes to the barrier?

A

Defensin Proteins
Lysozyme
Lactoferrin

Normal flora crowding out infection

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24
Q

What prevents microbes from moving to underlying tissue if they get passed the mucosal membrane?

A

Tight junctions between cells. Makes it leak proof

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25
Q

Can water slip in between the tight junctions of underlying tissues of mucous?

A

No.

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26
Q

What sweep back and forth on the mucosal membrane to cause movement?

A

Cilia

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27
Q

These antimicrobial substances are proteins that can form pores in bacteria found in mucous. They also have a developmental role by leading to differentiation of cell

A

Defensin proteins

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28
Q

These antimicrobial substances are found in the mucosal membrane targets cell walls

A

Lysozyme

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29
Q

This antimicrobial substance is found in mucosal membranes and binds to iron in bacteria

A

Lactoferrin

Ferrin is a key word

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30
Q

It’s safer to use saliva than tap water for bacteria because tap water sometimes has protozoans that can get in your eye

A

!

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31
Q

What 4 areas are associated with mucosal membranes

A

Eye
Digestive Tract
Respiratory Tract
Urogenital Tract

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32
Q

What are the 4 defenses of the eye?

A
  1. Filtering by eyelashes
  2. Lysozyme
  3. NaCl
  4. Flushing by tears
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33
Q

What else, not mentioned before. about the respiratory tract prevent microbes from going further into respiratory tract

A

Nostil Hairs

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34
Q

Loss of upper layers of tissue, occurs in the mouth and small intestine

A

Desquamanation

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35
Q

What does the urinary tract do to wash off pathogens and lower the count?? Explains why it’s important to be well hydrated

A

Flushing by urine

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36
Q

Microbes need ____ to grow, we need it for our own cells’ function, and several types of cells make molecules to keep it away from microbes

A

Iron

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37
Q

These two cells bind oxygen and have an iron component to keep it away from bacteria

A

Hemoglobin and myoglobin

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38
Q

These iron binding molecule transports iron around the body in plasma

A higher than normal level of it indicates

A

Transferrin

Infection

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39
Q

This iron bonding molecule is in milk tears and saliva, found in secretions and binds iron

A

Lactoferrin

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40
Q

This iron binding molecule of the body is in cells and has small amounts present in plasma. It stores iron

A

Ferritin

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41
Q

This is an important, early physiological response to microbial invasion and damage

A

Inflammation

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42
Q

Inflammation is triggered by release of proinflammatory molecules such ____ and ___ from local cells

A

Histamine and cytokines

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43
Q

What are the 4 signs of inflammation

Why is inflammation good?

A

Redness, heat, swelling, pain

It contains and eliminates pathogens

44
Q

In the inflammatory response, the first step is

Damaged tissues release this molecule, which communicates to mast cell and basophil (both types of white blood cells)

Bacteria then enter the tissue through it. ___ molecules are released such as histamine, prostaglandins, and serotonin

A

Tissue damage

bradykinin

Vasodilator Molecules

45
Q

Bradykinins cause which cells to migrate towards damaged tissue

This causes the release of what molecule via degranulation of these two cell types?

A

basophil and mast cells

Histamine

46
Q

What occurs after the release of histadine?

A

Vasodilation

47
Q

This term means making blood vessels bigger

This is associated with what symptoms of inflammation

What else occurs? This leads to…

A

Vasodilation

Redness and heat

Permeability of blood vessels (fluids, clotting factors, opsonization factors) , swelling aka pain

48
Q

There are two types of phagocytic white blood cells present in inflammation, these occur first

The second wave of white blood cells are these,

A

Neutrophils

Macrophages

49
Q

Macrophages are a differentiated phase of

A

Monocytes

50
Q

When neutrophils dominate, what phase of inflammation is occurring?

More macrophages is the ___ phase

A

Acute Phase

Chronic Phase

51
Q

The three consequences of local inflammation are…

A

Vasodilation
Extravasation
Increase in vessel permeability

52
Q

When white blood cells squeeze out of blood cells into surrounding tissues, it is called

These bring in immune cells, like phagocytes, to fight the infection. What are often used to communicate the status of the infection?

A

Extravasation

Cytokines

53
Q

What is the goal of inflammation?

A

Containing the infection

54
Q

What are the three responses that cytokines can induce?

A

Fever
Inflammation (attracting more white blood cells.
Further Immune Responses (like the adaptive response)

55
Q

If inflammation gets out of hand, it can be damaging. Especially when the microbes or their products get into the ____

What two things can they cause

A

Bloodstream

Septic Shock and Toxic Shock

56
Q

This response of systemic inflammation is widespread presence of bacteria in the body that induces system wide inflammation

This response is overstimulation of immune responses by bacterial exotoxins (superantigens) in the bloodstream

A

Septic Shock

Toxic Shock

57
Q

Death rates of 30-50% are not uncommon when septic or toxic shock set in!

____ and _____ cytokines are potent mediators of systemic inflammation induced by microbes or their products

A

IL-1 and TNF-α

58
Q

These are defined as structures found on foreign microbes but NOT on self cells

A

Pathogen associated molecular patterns (PAMPs)

59
Q

These are receptors on our cells that can bind PAMPs to begin the responses against them (like lipopolysaccharides or peptidoglycan)

A

Pattern Recognition receptors (PRRs)

60
Q

Are PRRs new or old? Why?

A

They are evolutionarily ancient, found in invertebrates, vertebrates, and plants

61
Q

Are PRRs specific to individual pathogens or do they associate with groups of pathogens?

A

They are non specific, recognize common molecules found on entire groups of pathogens

62
Q

These receptors are a form of PRR found in vertebrates and invertebrates. They recognize PAMP ligands and trigger internal signaling reactions (a cascade) in self cells

They were originally described in what organism’s embryo?

A

Toll like receptors

Fruit fly embryos

63
Q

Do toll like receptors bind the same site on a pathogen?

A

No, lipotechoic acids, Flagella, Lipopeptides, etc can be bound to trigger the cascade which leads to phagocyctosis

64
Q

These are examples of opsonizing-secreted PRRs that are made by the body on white blood cells.

This one coats the mannose-rich surface of yeasts and bacteria (binds to mannose)

This one binds to phospholipids found in bacterial and fungal plasma membranes

A

Mannose binding lectin and C-reactive protein

Mannose binding lectin

C-reactive protein

65
Q

As review, this is defined as the coating of a microbe to enhance destruction or uptake by other cells

A

Opsonization

66
Q

What are the two things that can occur after MBL binds to mannose on a bacterial pathogen?

A

Shape change, receptor can be bind the bacteria and leads to phagocytosis

Activation of complements (cascade) that form pores in the bacterial membrane

67
Q

C-reactive protein levels can be monitored to tell if there if infection in the body (opsonization factor!)

A

!

68
Q

These are defined as a group of 30+ serum proteins that are involved in antimicrobial activities

How many particular complement proteins become activated in the presence of PAMPs?

Activation results in 3 things..

A

Complements

Nine

  1. Inflammation (attracting white blood cells)
  2. Opsonization (enhancing phagocytosis)
  3. Direct killing by MAC
69
Q

Three separate methods of activating the complement cascade exist…

A

Classical
Alternative (evolutionarily older)
Lectin (similar to classical, MBLs are an example)

70
Q

Antibodies bind what on the microbial cell to trigger the classical complement cascade?

Which two do this?

A

Antigens

IgG or p IgM

71
Q

What is the first step of the classical complement system? How many antibodies must it bind?

A

C1 binds antibody surface complex

It must bind two adjacent antibodies, there must be enough bound antibodies for this to occur.

72
Q

Once complement protein 1 binds two antibodies, it becomes a protease (cuts proteins), what interacts with it and is ultimately cleaved into two parts

This part is released and attracts white blood cells to the vicinity

This part is going to bind to the antigen

A

C4 (cleaved into C4a and b)

C4a

C4b

73
Q

This complement protein is cleaved after C4 by C1

This part flows away to recruit white blood cells

This one binds and attaches to the antibody

A

C2

C2b

C2a

(opposite to C4a and b)

74
Q

C4b and C2a work together to form _____ which cleaves C3

This part floats away to attract white blood cells

This part binds near C4b, and C2a

A

C3 convertase

C3a

C3b

75
Q

C4b, C2a, and C3b form this white cuts C5

This part is released to attract white blood cells

This part inserts into the membrane

What come in next?

What do these form?

A

C5 convertase

C5a

C5b

C6, C7, C8, and C9

The membrane attack complex (MAC)

76
Q

What do MACs do?

A

Form pores which disrupt osmotic regulation to lyse the bacteria

77
Q

What alternative can occur with C3b, etc in the complement cascade?

A

Opsonization

78
Q

This is another function of a complement, it coats the microbe with activated complement to increase chances for phagocytosis

What molecule in the classical cascade that is the opsonization factor?

If this doesn’t occur, what happens?

A

Opsonization

C3b

MAC forms

79
Q

C4a, C2b, C3a, C5a, can also trigger this event

A

Chemotaxis (white blood cells gobble up pathogens), leave a breadcrumb trail

80
Q

This can initiate a natural antiviral state, and can also increase activities of antiviral cells. More than 300 genes increase expresion when exposed to them. Even promotes antiviral responses in neighboring cells, or proliferation of natural killer cells.

A

Type I Interferons

Possible method of future treatment!

81
Q

Are interferons specific or nonspecific?

A

Specific

82
Q

These inteferons interfere with the ribosome binding, degrade RNA, and make changes in membrane components

A

IFN α/β

83
Q

What are the three methods that IFN α and β have antiviral effects

Which method leads to apoptosis of the infected cell?

Which affects neighboring cells of the infected cell?

A
Inhibit ribosome binding (cell protein production)
Degrade RNA (prevent viral protein production)
Changes membrane components (Block viral attachment and entry)

Ribosome binding

Membrane changes, they are induced in neighboring cells

84
Q

These are the immune system cells that engulf foreign invaders

What are the 4 types to know

What two ways are they activated?

A

Phagocytes

Neutrophils
Monocytes
Macrophages
Dendritic

PRRs and cytokine signaling

85
Q

The monocyte can become two types of phagocytic cells

A

Macrophage and Dendritic Cell

86
Q

Monocytes work for innate, adaptive, or both?

What about macrophages and dendritic cells?

A

Innate only

Both

87
Q

What is the secondary role of macrophage and dendritic cells?

A

Antigen Present Cells

88
Q

___ prior to ingestion enhances uptake

____ granule contents released extracellularly attack invaders without having to phagocyte them

Once the invader is ingested, a complex process takes place to destroy it, often this process involves fusion with ___ and the use of a controlled respiratory burst

A

Opsonization (not necessary tho!)

Neutrophil

Lysosomes

89
Q

Once the opsonization factors of phagocytosis bind the receptors of the microbe, they change shape so the phagocyte receptor binds them

A

!

90
Q

In phagocytosis, the opsonized microbe binds to phagocyte surface receptors. Cytoplasmic extensions surround and engulf the bound microbe. What forms?

A

A Phagosome (like an endsosome, its a food vacuole)

91
Q

Once the phagosome has been formed in phagocytosis, what occurs next?

Next the phagosome fuses with ____ to form _____

_______ and lysosomal _____ kill the microbe

The debris are expelled by ____

A

Acidification

Lysosome to form phagolysosome

Oxidative Burst (toxic free radicals), lysosomal enzymes (breaks up microbe)

Exycytosis

92
Q

What cells can do phagocytosis?

A

Neutrophils
Macrophage
Dendritic cells (only in innate)

93
Q

Some cells are too big for phagocytosis, like extracellular parasitic worms and fungi. What cells help fight these pathogens by releasing toxic granule contents (degranulation process) near them?

A

Eosiniophils, basophils, mast cells

Note: basophils and mast cells increase inflammation by releasing histamines

94
Q

This cell, in contrast to basophils and mast cells turns down inflammatory responses (via degranulation as well)

A

Eosinophils

95
Q

This cell is useful for eliminating host cells infected with pathogens

Are they phagocytic?

A

Natural Killer Cells

No, but they make contact with target cells

96
Q

What type of cell are NK cells?

A

Lymphocytes, unique for innate defenses, usually lymphocytes are adaptive

97
Q

After contact is initiated with NK cells, what are released?

This granule produces a pore structure in target cell plasma membranes

These induce apoptosis

Also are useful for eliminating abnormal self cells aka

A

Granules

Perforin

Granzymes

Cancer

98
Q

What initiates necrosis?

What initiates apoptosis?

What does the first step of apoptosis result in

A

Physical or chemical trauma that damages the cell membrane

Cell signaling occurs

Decreased cell volume

99
Q

What does the damaged cell membrane in necrosis result in? Two things

A

Contents of the cell leak into the surrounding tissues

Nearby cells may be damaged by the released cell contents

100
Q

In apoptosis, what occurs when the cell decreases in volume?

What then occurs?

What digests the apoptitic bodies

A

Cytosplasmic blebbing and chromatin condensation

DNA fragmentation and the cell is parceled into apoptitic bodies

A phagocytic cell

101
Q

Which leads to inflammatory responses? Necrosis or Apoptosis?

Therefore which is safer? (used in destruction of webbed feet cell’s, or example)

A

Necrosis (damaged cell contents are released)

Apoptosis

102
Q

Normal nucleated cells have a surface molecule that NK cells recognize known as ______, virally infected cells often turn off its expression and cancer cells tend to shut down expression as well

A

Class I major histocompatibility complex (MHC 1)

It’s the self marker. Explains why twins don’t need to suppress the immune system in organ transplants but others do

103
Q

Does the NK cell have MCH 1?

A

Yes, all nucleated body cells have them (not red blood cells)

104
Q

MHC II must be on the surface of a cell in order for it to be…

A

Antigen presenting (like macrophages and dendritic cells)

105
Q

In the binding of a NK cell to a cell, it binds to the cell and it completes the activation signal

In healthy cells, there is a protein on NK cells that can bind to MHC 1 which has what type of effect?

A

Inhibitory Signaling effect

The cell is released.

106
Q

In an abnormal cell, there is no ______ so the activation signal is not inhibited

A

MHC 1

The NK cell kills it.