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Microbiology LECTURE > Chapter 16 > Flashcards

Chapter 16 Flashcards

Innate immunity

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1
Q

First line of defense

A

Physical and chemical factors that include:
•Normal microbiota
•Intact skin
•Mucous membranes and their secretions

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2
Q

Second line of defense

A
  • Phagocytes: neutrophils, eosinophils, dendritic cells, macrophages
  • Natural killers
  • Inflammation
  • Fever
  • Antimicrobial substances
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3
Q

What defenses are involved in Innate immunity and what does it do?

A

▪︎First and second line of defense
▪︎ Early warning system
▪︎ Prevents microbes from gaining access in body
▪︎ Eliminates those that do gain access

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4
Q

What is involved in Adaptive immunity

A

▪︎Specialized lymphocytes: T cell, B cells
▪︎ Antibody production
▪︎ Responds once innate system is breached
▪︎ Slower to respond than innate system
▪︎ Memory component

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5
Q

Third line of defense is also

A

Adaptive immunity

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6
Q

Susceptibility

A

Lack of resistance to a disease

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7
Q

Immunity

A

Ability to ward off disease

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8
Q

Innate immunity (basic definition)

A

Defense against any pathogen

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9
Q

Adaptive immunity (basic definition)

A

Immunity and resistance to a specific pathogen

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10
Q

Host Toll like receptors (TLRs)

A
  1. Protein receptor that recognize pathogens
  2. Attach to PAMPs
  3. Induce cytokines that regulate the intensity and duration of immune response
  4. Located in plasma membrane of defensive cells
  5. Activate innate system
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11
Q

Host defensives that produce resistance against infection can be both

A

Adaptive or innate

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12
Q

What type of immunity are adaptive defenses and what in particular do they respond to

A
  1. Specific immunity

2. Antigens

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13
Q

What type of immunity are Innate defenses and what do they respond to

A
  1. Nonspecific immunity

2. Act against any type of invading agent

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14
Q

How do adaptive defenses respond to antigens

A

By producing antibodies and activating lymphocytes

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15
Q

Lymphocytes

A

Specific cells of the body’s immune system

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16
Q

Antibody and cellular responses of the adaptive defenses are more effective against

A

Invasions by same pathogen than against initial infection

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17
Q

Physical barriers

A

Skin, mucous membranes, chemicals they secrete

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18
Q

Chemical barriers

A

Antimicrobial substances in body fluids such as saliva, mucus, gastric juices, and iron limitation mechanism

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19
Q

What are innate defenses

A
  1. Physical barriers
  2. Chemical barriers
  3. Cellular defenses
  4. Inflammation
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20
Q

Cellular defenses

A

Certain cells that engulf invading microorganisms

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21
Q

Inflammation

A

Reddening, swelling, temperature increases,

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22
Q

What are the 2 types of immunity

A
  1. Adaptive immunity

2. Innate immunity

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23
Q

Does innate immunity have a memory response

A

No

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24
Q

PAMPs

A

▪︎Pathogen associated molecular patterns
▪︎ Commonly found on pathogens such as Ex.
1. LPS of g(-) bacteria
2. Flagella
3. Peptidoglycan if g(+) bacteria
4. DNA of bacteria
5. DNA and RNA of viruses

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25
Q

Cytokines

A

▪︎ Released from defense cells
▪︎It’s a chemical protein that regulates the intensity and duration of immune response.
▪︎ Recruits other macrophages, dendritic and defensive cells (isolate and destroy during inflammatory response )
▪︎ Activate T cells and B cells

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26
Q

Keratin

A

Top layer of epidermal cells are dead and contain this as a protective protein. This periodic shedding of this layer helps remove microbes on surface

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27
Q

Why is it important for skin to be dry rather than moist

A

Normal microbiota and other microbes are most numerous on moist areas of the skin. During hot and humid conditions, skin infections are common. Fungi hydrolyze keratin when water is available.

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28
Q

What does epithelial layer of mucous membrane secrete

A

Mucus: slightly viscous glycoprotein produced by goblet cells

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29
Q

How is mucus part of the first line of defense

A

Prevents tract from drying out and traps microbes

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30
Q

What are the physical forms of defense of the respiratory tracts

A
  1. Mucus
  2. Mucus coated hairs in nose
  3. Cilia, cilia escalator of lower respiratory tract
  4. Epiglottis
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31
Q

Physical factor protecting eye

A

Lacrimal apparatus, makes tears, dilutes and washes microorganisms out of eye,

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32
Q

What in mouth helps prevent colonization

A

Saliva produced by salivary glands, help dilute the number of microorganisms on teeth and mucous membranes of mouth and washes them from their surface

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33
Q

Gastrointestinal tract physical defense

A
  1. Mucus produced by goblet cells of mucous membranes
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34
Q

Ear physical and chemical barriers

A

Earwax
Px–> prevents microbes, dust, water from entering
C–> mixture of secretions from glands producing earwax and from sebaceous glands, which produce sebum

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35
Q

How do earwax and sebum inhibit pathogenic microbial growth

A

Fatty acids decrease pH between 3 and 5, preventing their growth (fungistatic)

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36
Q

Genitourinary physical barriers

A
  1. Flow of urine prevents microbial colonization

2. Vaginal secretions move microorganisms out of female body

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37
Q

GI physical barriers

A

Peristalsis, defecation, vomiting, diarrhea;
Expel microbes from body
(Microbial toxins cause GI tract muscles to contract)

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38
Q

Chemical factors of innate immunity

A

Sebum, perspiration, lysozyme, low pH if skin, saliva, gastric juices, vaginal secretions, urine

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39
Q

Where is Lysozyme found

A

In sweat,tears, saliva, nasal secretions, tissue fluids, urine

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40
Q

Skins pH and how doe this help in innate response

A

The secretion of of fatty acids and lactic acid causes the pH of skin to be between 3-5, acidicity prevents growth of other microorganisms

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41
Q

Saliva chemical barriers

A
  • Lysozyme, urea, uric acid–> pH 5.55-6.85; inhibits microbial growth
  • Antibody immunoglobulin A–> prevents attachment of microbes
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42
Q

Gastric juices chemical barriers

A
  1. Hydrochloric acid, enzymes, mucus

2. Acidity: pH 1.2-3 destroys bacteria and most of their toxins

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43
Q

Vaginal secretions chemical barriers

A
  1. Glycogen produced by vaginal epithelial cells broken down into lactic acid by L. Acidophilus and creates acid pH 3-5
  2. Cervical mucushas antimicrobial activity
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44
Q

Urines chemical barriers

A
  1. Lysozyme

2. pH average 6 inhibits microbes

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45
Q

How does microbial antagonism help innate immunity

A

Normal microbiota prevents colonization of pathogens by competing with for nutrients, producing harmful substances to them, altering conditions that affect their survival such as pH and oxygen availability

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46
Q

Commenalism ? Where are most of these organisms found? Can they cause infection?

A
  1. One organism benefits while the other is not affected
  2. Skin and gastrointestinal tract
  3. Yes, they may be opportunistic pathogens
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47
Q

What is another name for microbial antagonism

A

Comparative exclusion

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48
Q

Granulocytes

A
  1. Presence of large granules in their cytoplasm

2. Include Neutrophils, basophils, eosinophils

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49
Q

Neutrophils

A
  1. Highly phagocytic and motile,
  2. active in the intial stages of infection
  3. Ability to leave blood and enter infected tissue and destroy microbes and foriegn particles
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50
Q

Basophils

A
  1. Release histamine

2. Important in inflammation and allergic responses

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51
Q

Eosinophils

A
  1. Somewhat phagocytic
  2. Have ability to leave blood
  3. Major function is to produce toxic proteins again certain parasites
  4. They attach to outer surface of helminths and discharge peroxide ions that destroy them
  5. Their numbers increase a lot during certain parasitic worm infections and hypersensitivity reactions
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52
Q

Agranulocytes

A
  1. Absence of granules in cytoplasm

2. Three different types: Monocytes, macrophages, dendritic cells, lymphocytes, T cells, B cells

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53
Q

Monocytes

A
  1. Do not actively phagocyte until leave circulating blood, enter tissues, and mature into macrophages
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54
Q

What is responsible for swelling of lymph nodes during infection

A

Proliferation of lymphocytes

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55
Q

Macrophages

A
  1. As blood and lymph that contain microorganisms pass through organs with macrophages the microrganisms are removed by phagocytosis.
  2. They also dispose of worn out blood cells.
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56
Q

Dendritic cells

A
  1. Possibly derived from monocytes
  2. Have long extensions
  3. Abundant in epidermis of skin, mucous membranes, thymus, lymph nodes
  4. Function is to destroy microbes by phagocytosis and initiate adaptive immunity response
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57
Q

Lymphocytes

A
  1. Include NT killers, T cells, B cells

2. Found in spleen, lymph nodes, red bones marrow

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58
Q

NK cells

A
  1. Have ability to kill wide variety of infected body cells and certain tumor cells
  2. Attack those that display abnormal or unusual plasma membrane proteins
  3. Found in blood of spleen, lymph nodes, red bone marrow
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59
Q

What does the binding of NK cells to a target cell release

A

NK cells release vesicles containing toxic substances

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60
Q

Perforin

A
  1. Contained in some granules
  2. A protein that inserts into the plasma membrane of target cells and creates perforations in membrane
  3. Causing cytolysis
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61
Q

Cytolysis

A

Bursting of cell as a result of extracellular fluid flowing into cell

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62
Q

Granzymes

A
  1. Protein digesting enzyme
  2. Induces apoptosis of target cell
  3. released by some granules of NK cells
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63
Q

Do granzymes kill microbes inside targeted cells

A

NO. It kills infected cells, released microbes can be destroyed by phagocytosis

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64
Q

Where are T cells and B cells located

A

Lymphoid tissues of lymphatic system and circulate in blood

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65
Q

What is included in lymphatic system

A

fluid called lymph, lymphatic vessels, organs that contain lymphoid tissue, re bone marrow

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66
Q

What does lymphoid tissue contain

A

Large number of lymphocytes: T calls and B calls, and phagocytic cells

67
Q

Where are T cells and B cells activated

A

lymph nodes

68
Q

What is the function of the lymphatic system

A
  1. Directly involved in adaptive immunity
  2. Serves as surveillance system that screens for foreign molecules
  3. Microbes are trapped and destroyed here; removes waste
  4. Has one way valves, flows in one direction
69
Q

List WBCs in order from most abundantly seen in the blood to least

A 
Neutrophils
Lymphocytes
Monocytes
Eosinophils
Basophils
70
Q

Phagocytosis

A

The ingestion of microorganisms or other substances by a cell

71
Q

What are phagocytes

A
  1. WBCs that are part of second line of defense
72
Q

What cells are involved in phagocytosis

A
  1. Neutrophils
  2. Fixed macrophages
  3. Wandering macrophages
  4. Dendritic cells
73
Q

What cells migrate to infection site

A

granulocytes, monocytes, dendritic cells

74
Q

What happens to monocytes during migration to infected area

A

They leave blood and migrate into tissues where they enlarge and develop into phagocytic macrophages

75
Q

Fixed macrophages

A

resident in certain tissues and organs

76
Q

Free (wandering) macrophages

A

motile, will roam tissues and gather at infection or inflammation sites

77
Q

Name the main steps involved in the mechanism of phagocytosis

A
  1. Chemotaxis and Adherence
  2. Ingestion
  3. Digestion
  4. Waste is discharged from cell
78
Q

Chemotaxis

A

Chemical attraction of phagocytes to microorganisms

79
Q

How are microorganisms attracted to phagocytes

A
  1. Release of microbial products: their receptors pick up chemical stimuli such as oxygen, ribose, and galactose and in response move towards it
  2. Components of WBCs and damaged tissues cells are released
  3. Cytokines released
  4. Peptides
80
Q

Adherence to phagocyte

A

This is facilitated by attachment of PAMPs on microbes, to Toll receptors on the surface of phagocytes

81
Q

What does adherence to phagocyte induce

A

release of specific cytokines by phagocyte and initiates phagocyte

82
Q

What protein facilitates adherence

A

If microorganism is coated with a serum protein called opsonization

83
Q

Ingestion of microbe

A

Phagocytes extend pseudopods from plasma membrane, surround microbe, meet and fuse, form phagosome, engulf microbe, pump it with protons and reduce pH, activating hydrolytic enzymes

84
Q

Digestion microbe

A

Phagosome pinches off from plasma membrane and enters cytoplasm, lysosomes are contacted, form a phagolysosome, products are digested

85
Q

What do lysosomal enzymes contain

A

lysozyme, other enzymes, and toxic oxygen products

86
Q

What happens after enzymes are digested in phagocytes

A

Residual body within phagolysosome is moved towards cell boundary and discharged as waste products

87
Q

Microbial evasion of phagocytosis

A
  1. Avoid adherence, Ex. M protein and capsules
  2. Kill phagocytes by releasing leukocidins
  3. Lyse phagocytes
  4. Escape phagosome
  5. Prevent phagosome-lysosome fusion
  6. Survive in phagolysosome
88
Q

What does the M protein on a bacterial cell resemble that’s in the body and how can this cause harm to someone that has produced antibodies against this protein?

A

The M protein resembles an antigen on the heart. If someone produces antibodies for the M protein, their body can mistake antigens in the heart for that and attack it. This can lead to the destruction of heart valves. It can happen as a result of untreated strep throat or rheumatic fever.

89
Q

What triggers inflammation in the body

A

it’s a defense mechanism to damage of body’s tissues

90
Q

What are the four signs and symptoms of inflammation

A
  1. Rubor: redness
  2. Dolor: pain
  3. Color: heat
  4. Tumor: swelling (edema)
  5. Sometimes a loss of function
91
Q

What is the function of inflammation

A
  1. Destroy agent causing injury
  2. Confining or walling of injurious agent and its products
  3. Repair and replace damaged tissue
92
Q

Acute phase proteins

A
  1. A group of proteins activated indirectly by inflammation

2. Induce local and systemic responses

93
Q

What occurs immediately following tissue damage

A

Vasodilation to damaged area causing increasing vessel permeability, and increased blood flow, redness, heat, and inflammation

94
Q

What is vasodilation

A

dilation of blood vessels

95
Q

What function does increased permeability of vessels have on damaged tissue

A

It permits defensive substances normally retained in the blood to pass through walls of blood vessels and enter injured area

96
Q

What causes edema

A

Increased permeability of blood vessels allows fluid to move from blood into tissues

97
Q

What causes pain of inflammation

A

This is caused by nerve damage, irritation of toxins, pressure of edema

98
Q

What causes vasodilation and increased permeability of blood vessels

A

A number of chemicals released by damaged cells at injury site, including histamine**

99
Q

Histamine

A

A chemical released in direct response to stimulation by certain components of the complement system

100
Q

Can phagocytic granulocytes cause the release of histamine

A

Yes, they produce chemicals that cause their release

101
Q

Kinins

A

Chemicals present in blood plasma and once activated cause vasodilation and increased permeability of blood vessels, act as chemotaxis by attracting phagocytic granulocytes, especially neutrophils to injured area

102
Q

Prostaglandins

A

Chemical substance released by damaged cells, intensify the effects of histamine and kinins and help phagocytes move through capillary walls

103
Q

Leukotrienes

A
  1. Chemical substances produced by mast cells and basophils
  2. Increase permeability of blood vessels
  3. Help attach phagocytes to pathogens
104
Q

What do activated fixed macrophages secrete during inflammation process

A

cytokines which bring about vasodilation and increased permeability

105
Q

How are clotting elements delivered into injured site

A

By increased permeability and vasodilation of blood vessels

106
Q

How do the formation of clots help the site of injury

A

They form sound the site of activity and prevent microbes or toxins from spreading to the parts of the body

107
Q

Pus

A

A localized collection and mixture of dead cells and body fluids in a cavity formed by breakdown of body tissues

108
Q

Abscess

A

A focus of infection filled with pus; pustules, boils

109
Q

What chemical mediator is is associated with pain related to inflammation

A

prostagladins

110
Q

What occurs after inflammation and as the flow of blood gradually decreases to injured site

A

margination of phagocytes to inner surface of endothelium of blood vessels

111
Q

What is margination

A

The sticking process in response local cytokines

112
Q

How do cytokines cause margination

A

They alter cellular adhesion molecules (CAMs) on cells lining blood vessels causing phagocytes to stick to site of inflammation

113
Q

How do phagocytes reach injured area

A

(diapedesis): squeeze between the endothelial cells of blood vessels to reach the area

114
Q

List the stages of inflammation

A
  1. Tissue damage
  2. Vasodilation and Increased permeability, release of chemicals by damaged cells
  3. Blood clot forms
  4. Abscess Starts to form
  5. Margination of phagocytes
  6. Diapedesis
  7. Phagocytosis of invading bacteria
  8. Tissue repair
115
Q

When does repair of tissues begin? when does it end?

A
  1. during active phase of inflammation

2. when harmful substances have been neutralized or removed from area

116
Q

When is a tissue repaired

A

when its storm or parenchyma produce new cells

117
Q

stroma

A

supporting connective tissue, not involved in the functioning part of organ/tissue

118
Q

parenchyma

A

the functioning part of the tissue

119
Q

What is a local response of the body to injury? What is a systematic response?

A
  1. inflammation

2. fever

120
Q

Fever

A

abnormal high body temperature, second line of defense, most frequent cause is infection from bacteria or virus

121
Q

What is considered the body’s thermostat and what is it normally set at

A
  1. hypothalamus

2. 37 ° C

122
Q

What happens if a gram negative bacteria is ingested by a phagocyte

A

The lipopolysaccharides of the cell wall are released when it is ingested, releasing endotoxins. This causes phagocytes to release cytokines; interleukin-1, and TNF-a into the bloodstream. They travel to the hypothalalmus and cause it to release prostaglandins that reset the hypothalamic thermostat at a higher temperature, causing fever

123
Q

How does body try to readjust/increase the new thermostat setting

A

constricting blood vessels, increasing rate of metabolism, and shivering (all these will raise temperature)

124
Q

What is the crisis phase of a fever

A

This is when the body temperature is falling. Once the cytokines are eliminated from the body. The thermostat of the body is reset to 37° C, the body loses heat by vasodilation and sweating to bring the temperature back down.

125
Q

What are advantages to a fever

A
  1. Interleukin-1 helps step up production of T cells
  2. Intensifies the effect of of antiviral interferons
  3. Increases production of transferring that decrease available iron to microbes.
  4. It speeds up body’s reaction time which helps body tissues repair themselves more quickly
126
Q

What disadvantages can a fever have

A
  1. Tachycardia
  2. Increased metabolic rate causing acidosis
  3. Dehydration; electrolyte imbalance
  4. Death results with temperatures above 44-46°C
  5. Seizures in young children
  6. Delirium
  7. Coma
127
Q

What are the proteins of the complement system

A

Interferons, iron-binding proteins, and antimicrobial peptides

128
Q

The complement system

A

A defensive system consisting of over (*20 large regulatory) 30 proteins produced by the liver and found circulating in blood serum and within tissues throughout body

129
Q

What is the main function of the complement system

A

It complements immune cells in destroying microbes by

  1. Cytolysis of pathogens directly
  2. Generating peptide fragments that regulate inflammation and immune responses
  3. Enhancing phagocytosis and preventing excessive damage to host
130
Q

In what manner do complement proteins act

A

In a cascade, one reaction triggers another, more product is formed with each reaction, this set of reactions amplify some effect as many times as it continues

131
Q

What does the activation of C3 serum protein cause

A

It starts a cascade that results in cytolysis, inflammation, phagocytosis

132
Q

What does inactive C3 split into when activated

A

C3a and C3b

133
Q

What does C3a and C3b do

A

C3 binds to the surface of a microbe and receptors on phagocytes attach to C3b

134
Q

How does C3 b enhance phagocytosis

A

by opsonization

135
Q

What is opsonization

A

It is also known as immune adherence. It coats a microbe. By doing this it promises attachment of a phagocyte to a microbe

136
Q

Other than phagocytosis, what does C3b initiate

A

A series of reactions that result in cytolysis

137
Q

What do C5b, C6 through C8 and multiple C9 fragments form

A

Membrane attack complex (MAC)

138
Q

What is MAC and where does it form

A

Transmembrane channels (holes) that are inserted into the plasma membrane of invading cell

139
Q

What does MAC cause

A

the bursting of the microbial cells due to inflow of extracellular fluid through the channels

140
Q

What do C3a and C5a cause after they bind to mast cells

A

They cause them to release histamine and other chemicals that increase blood vessel permeability during inflammation

141
Q

What is another function of C5

A

A powerful chemotactic, attracting phagocytes to site of an infection

142
Q

What is the cascade of complement proteins that occur during an infection called

A

Complement activation

143
Q

What are the 3 pathways of complement cascade

A
  1. Classical pathway
  2. Alternative pathway
  3. Lectin pathway
144
Q

When is the classical pathway initiated

A

when antibodies bind to antigens on microbes

145
Q

Classical pathway of complement activation

A
  1. Antigen-antibody complex is formed and activate C1
  2. C1 activates C2 and C4==>C2a, C2b, C4a, Cb
  3. C2a and C4b combine and activate C3 (==> C3a and C3b)—-> initiate cytolysis, inflammation, opsonization
146
Q

What activates alternative pathway

A

Contact between certain complement proteins and pathogen

147
Q

Alternative pathway of complement activation

A
  1. C3 always present in blood, combines with complement proteins: factor B, factor D, factor P on the surface of pathogenic microbe
  2. After, C3 split, C3a–> inflammation, C3b–>cytolysis and opsonization
148
Q

How is lectin pathway initiated

A

When macrophages ingest bacteria, viruses, foreign matter by phagocytosis, they release cytokines that stimulate liver to lectins

149
Q

What are lectins

A

proteins that bind to carbohydrates

150
Q

Lectin pathway of complement activation

A
  1. Lectin binds to invading cell
  2. Bound lectin splits C2 and C4
  3. C2a and C4b combine and activate C3
151
Q

What is an example of a lectin and how does it enhance phagocytosis

A
  1. (MBL) mannose-binding-lectin

2. functions as opsonin

152
Q

What are the effects of complement activation

A
  1. Opsonization or immune adherence
  2. MAC: cytolysis
  3. Attract phagocytes
153
Q

Inflammation stimulated by complement

A
  1. C3a and C5a bound to mast cells, basophils, platelets trigger the release of histamine
  2. C5 functions as chemotactic factor that attracts phagocytes
154
Q

How do some bacteria evade complement

A
  1. Capsules prevent C activation
  2. Surface lipid-carbohydrates prevent MAC formation
  3. Enzymatic digestion of C5a
155
Q

Interferons

A

Cytokines and a class of similar antiviral (small) proteins produced by lymphocytes and macrophages, after viral stimulation.

156
Q

What is the principle function an interferon

A

To interfere with viral multiplication

157
Q

What is an interesting feature of interferons

A

They are host-cell specific, not virus-specific. Those produced by human cells protect human cells but produce little antiviral activity for cells of other species, such as mice or chickens

158
Q

What are the 3 principle types of interferons in humans

A
  1. (IFN-a) alpha interferon
  2. (IFN-B) beta interferon
  3. (IFN-y) gamma interferon
159
Q

Gamma interferons

A
  1. Produced by lymphocytes

2. Induces neutrophils and macrophages to kill bacteria

160
Q

IFN-a and IFN-B

A
  1. produced by virus-infected host cells only in very small quantities and diffuse to uninfected neighboring cells
  2. induce uninfected cells to produce antiviral proteins (AVPs)
161
Q

Antiviral proteins

A

Enzymes that disrupt various stages of viral multiplication

162
Q

Antiviral actions of IFNs

A
  1. Viral RNA from infecting virus enters cell
  2. It replicates into new viruses
  3. Infecting virus induces host cell to produce
    IFN-mRNA===> IFN-a, IFN-B
  4. IFNs are released from infected cell and bind to nuclear membrane receptors or plasma membrane on neighboring uninfected host cell, inducing AVP production
  5. New viruses released by infected cell infect neighboring host cells
  6. AVPS degrade viral mRNA and inhibit protein synthesis; interfering with viral replication
163
Q

What are the antimicrobial substances involved in innate immunity’s second line of defense

A
  1. Complement system
  2. Interferons
  3. Iron-binding proteins
  4. Antimicrobial peptides

Microbiology LECTURE (13 decks)

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