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MICROBIOLOGY!225-80 > Chap 16 > Flashcards

Chap 16 Flashcards

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1
Q

Nonspecific defenses of the host

A

Innate immunity

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2
Q

Mature cell that releases antibodies

A

Plasma cell

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3
Q

Cells that make up innate immunity

A

-Basophil
-Eosinophil
-Mast cell

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4
Q

Granulocytes

A

-Basophil
-Eosinophil
-Mast cell
-Neutrophil

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5
Q

Both innate and adaptive cells

A

-Neutrophil
-Monocyte
-Dendritic cell
- Natural Killer cell

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6
Q

Adaptive immunity cells

A

Plasma cell
B cell
T cells

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7
Q

Types of T cells

A

-T helper
-Cytotoxic T cells (lymphocytes)
-T regulatory cell

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8
Q

Agranulocyte with many surface projections

A

Dendritic cells

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9
Q

Releases histamines that cause inflammation

A

Basophil

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10
Q

Kills parasites with oxidative burst

A

Eosinophil

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11
Q

Antigen-presenting cells; produce antibacterial peptides

A

Mast cell

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12
Q

Phagocytizes bacteria and fungi

A

Neutrophil

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13
Q

Precursor to macrophages. Some macrophages can be fixed in certain organs while others wander tissues, causing inflammation. All perform phagocytosis.

A

Monocyte

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14
Q

In skin and respiratory and intestinal mucosa, phagocytizes bacteria and presents antigens to T cells

A

Dendritic cell

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15
Q

Kills cancer cells and virus-infected cells

A

NK cell

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16
Q

Recognizes antigens and produces antibodies

A

Plasma cell, B cell

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17
Q

TH (T helper cell)

A

secrete cytokines

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18
Q

They are CD4+ cells that bind MHC class II molecules on APCs.

A

Helper T cells

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19
Q

recognize and kill specific “non-self” cells. They are CD8+ cells that bind to MHC class I molecules. T

A

Cytotoxic T lymphocyte CTL

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20
Q

Cells are CD4+ cells that destroy cells that do not correctly recognize “self” cells.

A

T regulatory cells

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21
Q

measure leukocytes in the blood

A

White blood cell (WBC) counts

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22
Q

High WBC counts may indicate

A

bacterial infections, autoimmune diseases, or side effects of medications

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23
Q

Low WBC counts may indicate

A

viral infections, pneumonia, autoimmune diseases, or cancers

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24
Q

Normal WBC range

A

5,000-10,000 WBCs per cubic milimeter or 5.0-10.0 x 10^9 WBCs per liter

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25
Q

Normal neutrophils percentage

A

60-70%

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26
Q

Normal lymphocytes percentage

A

20% to 25%

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27
Q

Normal monocytes percentage

A

3% to 8%

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28
Q

Normal Eosinophils percentage

A

2% to 4%

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29
Q

Normal basophils percentage

A

0.5% to 1%

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30
Q

Immunity

A

ability to ward off disease

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31
Q

Susceptibility

A

lack of resistance to a disease

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32
Q

Innate immunity

A

defenses against any pathogen; rapid, present at birth

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33
Q

Adaptive immunity:

A

immunity or resistance to a specific pathogen; slower to respond, has memory component

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34
Q

Toll-like receptors (TLRs)

A

on host cells attach to pathogen-associated molecular patterns (PAMPs)

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35
Q

TLRs bound to PAMPs induce

A

the release of cytokines from the host cell that regulate the intensity and duration of immune responses

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36
Q

First line defenses

A

Skin
Mucous membranes

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37
Q

Innate (Non-specific) Defenses

A
  1. First-line defenses
  2. Phagocytosis
  3. inflammation
  4. Complement system
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38
Q

Two main divisions of adaptive defense

A
  1. humoral immunity
  2. Cell-mediated immunity
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39
Q

Antigen presenting/processing cells aid in

A

activation of adaptive defenses

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40
Q

humoral immune response

A

consists of the activity of B cells and the antibodies they produce

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41
Q

Cell-mediated immunity

A

host defense used to fight intracellular pathogens and abnormal body cells such as cancer cells.

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42
Q

Protagonists of cell-mediated immunity are

A

T lymphocytes

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43
Q

Helper T cells

A

secrete cytokines to activate other cells of the immune system

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44
Q

Cytotoxic T cells

A

attack infected cells directly

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45
Q

Dermis

A

inner portion made of connective tissue

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46
Q

Epidermis

A

outer portion made of tightly packed epithelial cells containing keratin, a protective protein

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47
Q

Shedding and dryness of skin inhibits

A

microbial growth

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48
Q

Mucous membranes

A

Epithelial layer that lines the gastrointestinal, respiratory, and genitourinary tracts

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49
Q

Mucus

A

viscous glycoproteins that trap microbes and prevent tracts from drying out

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50
Q

Lacrimal apparatus

A

drains tears; washes eye

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51
Q

Ciliary escalator

A

transports microbes trapped in mucus away from the lungs

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52
Q

Earwax

A

prevents microbes from entering the ear

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53
Q

Urine

A

cleans the urethra via flow

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54
Q

Vaginal secretions

A

move microorganisms out of the vaginal tract

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55
Q

Other physical factors

A

Peristalsis, defecation, vomiting, diarrhea

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56
Q

Sebum

A

forms a protective film and lowers the pH (3–5) of skin

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57
Q

To what level does sebum lower pH?

A

3-5

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58
Q

Lysozyme

A

in perspiration, tears, saliva, and urine destroys bacterial cell walls

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59
Q
A
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60
Q

gastric juice

A

destroys most bacteria and toxins

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61
Q

pH of gastric juice

A

1.2-3.0

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62
Q

Low pH (3–5) of vaginal secretions inhibits

A

microbes

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63
Q

pH of Vaginal secretions

A

3-5

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64
Q

Normal microbiota

A

compete with pathogens via microbial antagonism (competitive exclusion)

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65
Q

microbial antagonism

A

(competitive exclusion)

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66
Q

Competitive advantage for space and nutrients

A

normal microbiota

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67
Q

Produce substances harmful to pathogens

A

normal microbiota

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68
Q

Alter conditions that affect pathogen survival

A

normal microbiota

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69
Q

Commensalism:

A

one organism benefits while the other (host) is unharmed

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70
Q

Probiotics

A

live microbial cultures administered to exert a beneficial effect

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71
Q

Formed Elements in Blood

A

Cells and cell fragments suspended in plasma

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72
Q

Types of formed elements in blood

A

Erythrocytes (red blood cells)
Leukocytes (white blood cells)
Platelets

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73
Q

How are formed elements created?

A

Created in red bone marrow stem cells via hematopoiesis

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74
Q

Granulocytes

A

leukocytes with granules in their cytoplasm that are visible with a light microscope

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75
Q

Neutrophils

A

phagocytic; work in early stages of infection

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76
Q

Basophils

A

release histamine; work in allergic responses

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77
Q

Eosinophils:

A

phagocytic; toxic against parasites and helminths

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78
Q

60-70% of leukocytes
function: Phagocytosis

A

Neutrophils

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79
Q
A
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80
Q

Basophils percentage

A

(0.5-1%)

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81
Q

Basophils function

A

Production of histamine

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82
Q

Eosinophils percentage

A

2-4%

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83
Q

Eosinophils function:

A

Production of toxic proteins against certain parasites; some phagocytosis

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84
Q

Agranulocytes

A

leukocytes with granules in their cytoplasm that are not visible with a light microscope

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85
Q

Monocytes

A

mature into macrophages in tissues where they are phagocytic

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86
Q

Dendritic cells found in

A

found in the skin, mucous membranes, and thymus; phagocytic

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87
Q

Lymphocytes

A

T cells, B cells, and NK cells; play a role in adaptive immunity

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88
Q

Monocytes percentage

A

3-8%

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89
Q

Function of monocytes

A

Phagocytosis (when they mature into macrophages)

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90
Q

Dendritic cells function

A

phagocytosis and initiation of adaptive immune responses

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91
Q
A
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92
Q

Lymphocytes percentage

A

20-25%

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93
Q

NK cells function

A

Destroy target cells by cytolysis and apoptosis

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94
Q

T cells function

A

Cell-mediated immunity

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95
Q

B cells function

A

Produce antibodies

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96
Q

Lymphatic system components

A

Lymph, lymphatic vessels, lymphoid tissue, and red bone marrow

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97
Q

Lymphatic system contains which cells?

A

lymphocytes and phagocytic cells

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98
Q

Lymph carries microbes to

A

lymph nodes

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99
Q

What happens at lymph nodes

A

lymphocytes and macrophages destroy the pathogen

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100
Q

Act against all pathogens; not specific to a given pathogen

A

Innate defenses

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101
Q

recognize a specific pathogen

A

Adaptive defenses

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102
Q

must be activated by APCs before they can work

A

adaptive, specific defenses

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103
Q

Examples of adaptive defenses

A

antibodies, cytotoxic cells

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104
Q

Innate and adaptive defenses make it very difficult for pathogens to

A

penetrate, colonize and cause disease

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105
Q

Phago:

A

from the Greek, meaning eat

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106
Q

Cyte

A

from the Greek, meaning cell

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107
Q

Fixed macrophages

A

are residents in tissues and organs

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108
Q

Free (wandering) macrophages

A

roam tissues and gather at sites of infection

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109
Q

Chemotaxis

A

Chemical signals attract phagocytes to microorganisms

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110
Q

Adherence

A

Attachment of a phagocyte to the surface of the microorganism

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111
Q

Ingestion

A

Opsonization: microorganism is coated with serum proteins, making ingestion easier

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112
Q

Digestion

A

Microorganism is digested inside a phagolysosome

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113
Q

The Mechanism of Phagocytosis steps

A
  1. Chemotaxis
  2. Adherence
  3. Ingestion
  4. Digestion
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114
Q

Ingestion of a solid - such as a microorganism or cellular debris by a eukaryotic cell

A

Phagocytosis

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115
Q

Used by some protozoans for obtaining nutrients

A

Phagocytosis

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116
Q

Used by certain cells of the immune system to fight infection

A

Phagocytosis

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117
Q

Examples of phagocytes

A

Macrophages, neutrophils

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118
Q

Movement of a cell towards or away from a chemical stimulus

A

Chemotaxis

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119
Q

Phagocytes use pseudopods to

A

move towards microorganisms or damaged cells at the site of infection. Arrive only minutes after infection

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120
Q

Chemotactic chemicals that attract phagocytes include:

A
  1. microbial products
  2. Components of damaged cells
  3. Chemicals released by other white blood cells
  4. Peptides derived from the complement system
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121
Q

The plasma membrane of phagocytes usually attaches to glycoproteins on the microorganism’s surface. This process is called ____________.

A

adherence

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122
Q

Adherence is made easier through

A

opsonization

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123
Q

opsonization

A

antibodies or complement proteins from the host coat the microbe’s surface, serve as handles so phagocyte can more easily attach to the microorganism.

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124
Q

Opsonins

A

proteins that coat the microbe are called

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125
Q

pseudopods fuse, forming a sac called a

A

phagosome

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126
Q

The phagosome enters the cytoplasm where it fuses with

A

lysosomes

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127
Q

Digestion of most bacteria within lysosome is complete within

A

10-30 mins

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128
Q

elimination (exocytosis)

A

after phagocytosis,
Phagolysosome fuses with the plasma membrane and expels the contents

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129
Q

Some of the contents of the phagolysosome may also be presented on the cell membrane through a process called

A

antigen processing and presentation

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130
Q

Phagocytes are able to detect foreign cells by looking for molecules on

A

the surface of those invaders that are not found on the human body

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131
Q

look for a specific antigen on the surface of invaders

A

adaptive defenses

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132
Q

When immune surveillance cells such as macrophages are looking for invaders, they search for surface molecules that are not found on host surfaces, such as

A

peptidoglycan

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133
Q

capsules protect microbes because

A

they’re made of polysaccharides similar to molecules found on host cells.

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134
Q

When a macrophage encounters an encapsulated bacterium

A

It doesnt recognize it as foreign and ignores it

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135
Q

Examples of encapsulated bacterium

A

Streptococcus pneumoniae, common cause of bacterial pneumonia

136
Q

are all bacteria killed after being swallowed by a phagocyte

A

no

137
Q

how does the tuberculosis bacterium survive phagocytosis?

A

by preventing the fusion of lysosome and phagosome. This keeps digestive enzymes away from the bacterium

138
Q

These two bacteria can actually escape the phagosome and live within the cytoplasm of the phagocyte

A

shigella and listeria

139
Q

Some microbes are not affected by lysosomal activity

A

Leishmania, a protozoan, can resist lysosomal enzymes

140
Q

inhibit the pathway that leads to oxidative killing within a phagocyte

A

legionella and some staphylococci

141
Q

Some bacteria actually reproduce within the

A

phagocyte

142
Q

Capable of hiding from host defenses by changing surface antigens ___________.

A

frequently

143
Q

Changing surface antigens can result from

A

mutations, genetic recombinations

144
Q

Viruses that frequently exhibit genetic recombination

A

RNA viruses such as:
influenzavirus, HIV

145
Q

Trypanosoma causes

A

sleeping sickness

146
Q

has a surface glycoprotein that undergoes frequent changes

A

Trypanosoma

147
Q

Complement

A

group of proteins that when activated, undergoes a series of reactions leading to inflammation, opsonization and cell lysis.

148
Q

Some bacteria simply invade complement by

A

covering the binding sites with a capsule

149
Q

Other bacteria have peptidases that

A

destroy key complement proteins and block the cascade

150
Q

mimic a control molecule that the human body uses to keep complement inactive when it is not needed.

A

Neisseria and some viruses

151
Q

Produce molecules called leukocidins

A

1.Pseudomonas,
2.group A streptococci
3.bacterial pathogens.

152
Q

Leukocidins cause

A

destruction of phagocytes, such as neutrophils and macrophages.

153
Q

Species of Neisseria that cause meningitis and gonorrhea secrete an enzyme called

A

IgA protease

154
Q

IgA protease destroys

A

a class of antibodies called IgA that are located in mucous membranes

155
Q

meningitis and gonorrhea are less likely to be detected in which regions

A

mucous membranes

156
Q

Examples of pathogens that can cause generalized suppressions of the immune system

A

HIV, measles and several viruses

157
Q

How do viruses cause generalized suppression

A

suppress activity of cytokines, or reproduce within macrophages and T cells.

158
Q

Superantigens role in invasion

A

toxins that distract adaptive defenses, causing them to produce a non-specific exaggerated response, and fail to respond to the actual invader

159
Q

Signs and symptoms of inflammation:

A

pain, redness, immobility, swelling (edema), heat

160
Q

Function of inflammation

A

Destroys injurious agent or limits its effects on the body

161
Q

inflammation repairs

A

and replaces tissue damaged by the injurious agent

162
Q

Inflammation activates

A

acute-phase proteins by the liver

163
Q

Acute phase proteins by the liver cause

A

vasodilation and increased permeability of blood vessels

164
Q

acute-phase proteins

A

Serum proteins whose concentration changes by at least 25% during inflammation.

165
Q

Histamine

A
  1. Vasodilation
  2. Permeability
  3. Smooth muscle contraction
166
Q

Kinin

A

A substance released from tissue cells that causes vasodilation.

167
Q

Prostaglandin

A

A hormonelike substance that is released by damaged cells, intensifies inflammation.

168
Q

Leukotrienes made by

A
  1. produced by mast cells and basophils
169
Q

Leukotrienes produced by

A

mast cells and basophils

170
Q

Leukotrienes cause

A

increased permeability of blood vessels

171
Q

Leukotrienes help

A

phagocytes attach to pathogens.

172
Q

cytokine

A

A small protein released from human cells that regulates the immune response; directly or indirectly may induce fever, pain, or T cell proliferation.

173
Q

Histamine comes from

A

Mast cells, basophils, platelets

174
Q

kinins come from

A

Blood plasma

175
Q

Prostaglandins come from

A

damaged cells

176
Q

Leukotrienes come from

A

Mast cells and basophils

177
Q

complement comes from

A

blood plasma

178
Q

cytokines come from

A

fixed macrophages

179
Q

Effects of histamine

A

Vasodilation & increased permeability of blood vessels

180
Q

effects of kinins

A

chemotaxis by attracting neutrophils

181
Q

effects of prostaglandins

A

intensify the effects of histamine and kinins, and help phagocytes move through capillary walls.

182
Q

Effects of leukotrienes

A

increase permeability of blood vessels and help attach phagocytes to pathogens

183
Q

effect of complement

A

stimulates release of histamine, attracts phagocytes and promotes phagocytosis

184
Q

effect of cytokines

A

vasodilation and increased permeability of blood vessels

185
Q

First step of inflammation

A

histamines, kinins, prostaglandins, leukotrienes and cytokines are released by damaged cells

186
Q

step 2 of inflammation

A

blood clot forms

187
Q

step 3 of inflammation

A

Abscess starts to form

188
Q

Step 4 of inflammation

A

margination- phagocytes stick to the endothelium

189
Q

step 5 of inflammation

A

phagocytosis of invading bacteria occurs

190
Q

Things that can trigger inflammation

A

sunburn, chemical burns, cuts, microbial infections

191
Q

Inflammation is a type of

A

general, nonspecific, defensive response

192
Q

Three main functions of inflammation

A
  1. Destroy agent causing injury
  2. Limit the effects of the agent on the rest of the body
  3. Repair or replace damaged tissue
193
Q

certain components of the complement system can also stimulate the release of ______

A

histamines

194
Q

histamines can result in

A

vasodilation

195
Q

Vasodilation results in

A

more blood (more phagocytes), more oxygen, and more nutrients being delivered to the site of injury.

196
Q

increased blood flow also results in

A

redness, heat and some of the pain associated with inflammation.

197
Q

What has a direct effect on the capillaries in the area of the injury?

A

histamines, prostaglandins and leukotrienes

198
Q

Cause the walls of the capillaries to become leakier

A

histamines, prostaglandins and leukotrienes

199
Q

Leaky capillaries cause

A

more fluid to leave the capillary and enter tissue spaces, causing swelling or edema

200
Q

Increased blood flow delivers

A

phagocytes such as monocytes and neutrophils to the scene.

201
Q

phagocytes stick to the walls of the blood vessels in a process called

A

margination

202
Q

After margination, the cells squeeze through the gaps in a process called

A

Diapedesis or emigration

203
Q

within about an hour of tissue damage, the phagocytes begin to

A

destroy the invading microorganisms by phagocytosis.

204
Q

After engulfing large numbers of microorganisms and damaged tissues,

A

the phagocytes die, forming pus

205
Q

other components of the blood lead to the formation of ______ _________ which seal off the site of injury

A

blood clots

206
Q

final stage of inflammation is

A

tissue repair

207
Q

The increased delivery of nutrients and oxygen aids in

A

tissue repair

208
Q

sticking of phagocytes to blood vessels in response to cytokines at the site of inflammation

A

margination

209
Q

Phagocytes squeeze between endothelial cells of blood vessels via

A

diapedesis

210
Q

tissue repair cannot be completed until

A

all harmful substances are removed or neutralized

211
Q

Stroma

A

is the supporting connective tissue that is repaired

212
Q

Parenchyma

A

is the functioning part of the tissue that is repaired

213
Q

regenerated epidermis

A

parenchyma

214
Q

Regenerated dermis is

A

Stroma

215
Q

Fever

A

Abnormally high body temperature

216
Q

Hypothalamus is normally set at

A

37 C

217
Q

cause the hypothalamus to release prostaglandins that reset the hypothalamus to a higher temperature

A

cytokines

218
Q

The body maintains the higher temperature until

A

the cytokines are eliminated

219
Q

crisis

A

The phase of a fever characterized by vasodilation and sweating.

220
Q

As body temperature falls (crisis),

A

vasodilation and sweating occurs

221
Q

How is fever beneficial?

A

Damaging pathogens
Fevers increase the temperature of infected tissues to a level that damages pathogens.
Impairing pathogen replication
The systemic temperature increase caused by a fever can make it harder for pathogens to replicate if they have spread.

222
Q

Complement system is made of

A

Serum proteins produced by the liver that enhances the immune system in destroying microbes

223
Q

The complement system acts in

A

a cascade in a process called complement activation

224
Q

Proteins are designated with

A

uppercase C and numbered in order of discovery

225
Q
A
226
Q

Activated fragments are indicated with

A

lowercase a and b

227
Q

set of proteins that circulate in the blood serum

A

complement system

228
Q

When the complement system is activated these proteins destroy foreign cells by

A

cytolysis

229
Q

the complement system also activates

A

the inflammatory response, and assists in phagocytosis

230
Q

The main components of the complement system are called

A

C1 through C9

231
Q

Complement can be activated through 3 different pathways

A
  1. Classical pathway
  2. Alternative pathway
  3. Lectin patway
232
Q

first activation pathway of complement system to be discovered

A

Classical pathway

233
Q

The classical pathway begins when

A

a pair of antibodies attaches to antigens on the surface of a bacterium

234
Q

Antigens can be

A

proteins or large polysaccharides on the surface of a bacterium

235
Q

The antibodies bind and activate

A

C1

236
Q

C1 then cleaves

A

several copies of C2 and C4

237
Q

Together, the C2a and C4b fragments form

A

an enzyme that cleaves C3, activating the complement system

238
Q

was named so because it was discovered after the classical pathway

A

Alternative pathway

239
Q

Classical pathway requires antibodies specific to the

A

invading microorganism

240
Q

The alternative pathway requires

A

three complement proteins called factor B, factor D and factor P

241
Q

Factor P stands for

A

properdin

242
Q
A
243
Q
A
243
Q
A
244
Q

Factors B, P, & D are attracted to

A

microbial cell-surface material such as the lipid-carbohydrate complexes of certain bacteria and fungi

245
Q

Together with C3, these proteins (B,P,D) result in the cleavage and activation of

A

C3 proteins

246
Q

C3 proteins in turn activate the

A

rest of the complement system

247
Q

Most recently discovered pathway of complement activatio is the

A

lectin pathway

248
Q

What stimulates the production of lectins?

A

Macrophages ingest materials through phagocytosis, they release chemicals that stimulate the production of lectins

249
Q

carbohydrate binding proteins

A

lectins

250
Q

The lectins bind to

A

distinctive patterns of carbohydrates on the surface of certain bacteria and viruses.

251
Q

the lectins themselves can act as

A

opsonins for phagocytosis, but also activate C2 and C4

252
Q

the activation of C2 and C4 leads to the activation of C3 which

A

leads to the activation of the rest of the complement pathway

253
Q

Step 1 classical pathway

A

Antibodies bind to antigens, activating C1

254
Q

Step 2 classical pathway

A

C1 splits and activates C2 and C4

255
Q
A
256
Q

Step 3 classical pathway

A

C2a and C4b combine and activate C3

257
Q

C3a functions in

A

inflammation

258
Q

C3b functions in

A

cytolysis and opsonization

259
Q

Step 1 alternative pathway

A

C3 present in the blood combines with factors B, D, and P on microbe surface

260
Q

step 2 alternative pathway

A

C3 splits into C3a and C3b, functioning the same as in the classical pathway

261
Q

What happens in the lectin pathway ?

A

Macrophages ingest pathogens, releasing cytokines that stimulate lectin production in the liver

262
Q

Mannose-binding lectin (MBL) binds to

A

mannose, activating C2 and C4

263
Q

C2a and C4b activate

A

C3, which functions the same as in the classical and alternative pathways

264
Q

cytolysis

A

The destruction of cells, resulting from damage to their cell membrane, that causes cellular contents to leak out.

265
Q

Activated complement proteins create a membrane attack complex (MAC) leads to

A

cytolysis

266
Q

Promotes attachment of a phagocyte to a microbe

A

Opsonization

267
Q

Activated complement proteins bind to mast cells, releasing histamine

A

inflammation

268
Q

Outcomes of complement activation

A
  1. Cytolysis
  2. Opsonization
  3. Inflammation
269
Q

The complement system is another way the body

A

fights infection and destroys pathogens

270
Q

This component of innate immunity
“complements” other _______ _________.

A

immune reactions.

271
Q

The cascade can be activated by

A

a pathogen directly or by an antibody–antigen reaction

272
Q

Together these proteins destroy microbes by

A

cytolysis, (2) enhanced phagocytosis, and (3) inflammation

273
Q

C3a and C5a act as

A

chemotactic factors, attract phagocytes to the site of infection.

274
Q

C3a and c5a also bind to

A

mast cells , release histamine and cause inflammation. also relase other chemicals

275
Q

C3b acts as an

A

opsonin, coating the invading cell

276
Q

This coat makes it easier for the phagocyte to

A

adhere to the invading cell during phagocytosis

277
Q

C5b binds to C6 and C7 which attach to the

A

plasma membrane of the invading cell

278
Q

C8 and several C9 molecules bind to the C5b, C6, C7 complex and

A

forming a cylinder shaped membrane attack complex

279
Q

MACs make holes in membrane causing

A

water and ions to leave, cytolysis, killing the cell

280
Q

regulation of complement

A

Regulatory proteins readily break down complement proteins, minimizing host cell destruction

281
Q
A
282
Q

Complement and disease

A

Lack of complement proteins causes susceptibility to infections

283
Q

Evading the complement system

A

Capsules prevent complement activation

284
Q

Interferons

A

Cytokines produced by cells; have antiviral activity

285
Q

IFN-α and IFN-β

A

produced by cells in response to viral infections; cause neighboring cells to produce antiviral proteins (AVPs) that inhibit viral replication

286
Q

IFN-γ

A

causes neutrophils and macrophages to kill bacteria

287
Q

Antiviral Action of Alpha and Beta Interferons (IFNs) step 1

A

Viral RNA from
an infecting virus
enters the cell.

288
Q

Antiviral Action of Alpha and Beta Interferons (IFNs) step 2

A

The virus induces the host cell to
produce interferon mRNA
(IFN-mRNA), which is translated
into alpha and beta interferons.

289
Q

Antiviral Action of Alpha and Beta Interferons (IFNs) step 3

A

Interferons make contact with uninfected
neighboring host cells, where they bind either
to the plasma membrane or to nuclear
receptors. Interferons induce the cells to
synthesize antiviral proteins (AVPs).

290
Q

Antiviral Action of Alpha and Beta Interferons (IFNs) step 4

A

AVPs degrade viral mRNA and
inhibit protein synthesis—and
thus interfere with viral replication.

291
Q

Iron-Binding Proteins

A
  1. Transferrin
  2. Lactoferrin
  3. Ferritin
  4. Hemoglobin
292
Q

Transferrin found in

A

blood and tissue fluids

293
Q

Lactoferrin found in

A

milk, saliva, and mucus

294
Q

Ferritin found in

A

Liver, spleen, and red bone marrow

295
Q

Hemoglobin found in

A

located in red blood cells

296
Q

Bacteria produce

A

siderophores

297
Q

siderophores compete with

A

iron-binding proteins

298
Q

Antimicrobial Peptides

A

Short peptides produced in response to protein and sugar molecules on microbes

299
Q

What do antimicrobial peptides do?

A

Inhibit cell wall synthesis
Form pores in the plasma membrane

300
Q

have a Broad spectrum of activity

A

antimicrobial peptides

301
Q

Genetic resistance

A

Confers a selective survival advantage
E.g., sickle cell trait and Plasmodium falciparum

302
Q

Age

A

Confers a selective survival advantage
E.g., sickle cell trait and Plasmodium falciparum

303
Q

Observing healthy protocols

A

another factor that helps prevent infection

304
Q

20-25%

A

Lymphocytes

305
Q

3-8%

A

Monocytes

306
Q

2-4%

A

Eosinophils

307
Q

0.5-1%

A

Basophils

308
Q

60-70%

A

Neutrophils

309
Q

viral infections, pneumonia, autoimmune diseases, or cancers

A

Low WBC

310
Q

bacterial infections, autoimmune diseases, or side effects of medications

A

High WBC

311
Q

PAMPs stand for

A

pathogen-associated molecular patterns (PAMPs)

312
Q

Innate or adaptive: 1. First-line defenses

A

Innate

313
Q

Innate or adaptive: 2. Phagocytosis

A

Innate

314
Q

Innate or adaptive:
3. inflammation

A

Innate

315
Q

Innate or adaptive:
4. Complement system

A

Innate

316
Q

Innate or adaptive:
4. Complement system

A

Innate

317
Q

found in the skin, mucous membranes, and thymus; phagocytic

A

Dendritic cells

318
Q

T cells, B cells, and NK cells; play a role in adaptive immunity

A

Lymphocytes

319
Q

Destroy target cells by cytolysis and apoptosis

A

NK cells

320
Q

Opsonization:

A

microorganism is coated with serum proteins, making ingestion easier

321
Q

(IFN-mRNA), which is translated
into

A

alpha and beta interferons.

322
Q

(IFN-mRNA), which is translated
into

A

alpha and beta interferons.

323
Q

Arrive only minutes after infection

A

Phagocytes

324
Q

Complement activation leads to

A

inflammation, opsonization and cell lysis.

325
Q

A substance released by tissue cells that causes vasodilation, capillary permeability, and smooth muscle contraction.

A

Histamine

326
Q

Activates acute-phase proteins by the liver

A

Inflammation

327
Q

Serum proteins whose concentration changes by at least 25% during inflammation.

A

Acute phase proteins

328
Q

A substance released from tissue cells that causes vasodilation.

A

Kinin

329
Q

Leukotrienes cause

A

increased permeability of blood vessels

330
Q

Leukotrienes help

A

help phagocytes attach to pathogens.

331
Q

A small protein released from human cells that regulates the immune response;

A

Cytokine

332
Q

directly or indirectly may induce fever, pain, or T cell proliferation.

A

Cytokine

333
Q

Help phagocytes attach to pathogens

A

Leukotrienes

334
Q

increase permeability of blood vessels and help attach phagocytes to pathogens

A

Leukotrienes

335
Q

stimulates release of histamine, attracts phagocytes and promotes phagocytosis

A

Complement

336
Q

cause neighboring cells to produce antiviral proteins (AVPs) that inhibit viral replication

A

IFN a and IFN b

MICROBIOLOGY!225-80 (24 decks)

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