Chapter 16 Flashcards

Innate immunity

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
Cytokines
▪︎ 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
26
Keratin
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
27
Why is it important for skin to be dry rather than moist
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.
28
What does epithelial layer of mucous membrane secrete
Mucus: slightly viscous glycoprotein produced by goblet cells
29
How is mucus part of the first line of defense
Prevents tract from drying out and traps microbes
30
What are the physical forms of defense of the respiratory tracts
1. Mucus 2. Mucus coated hairs in nose 3. Cilia, cilia escalator of lower respiratory tract 4. Epiglottis
31
Physical factor protecting eye
Lacrimal apparatus, makes tears, dilutes and washes microorganisms out of eye,
32
What in mouth helps prevent colonization
Saliva produced by salivary glands, help dilute the number of microorganisms on teeth and mucous membranes of mouth and washes them from their surface
33
Gastrointestinal tract physical defense
1. Mucus produced by goblet cells of mucous membranes
34
Ear physical and chemical barriers
Earwax Px--> prevents microbes, dust, water from entering C--> mixture of secretions from glands producing earwax and from sebaceous glands, which produce sebum
35
How do earwax and sebum inhibit pathogenic microbial growth
Fatty acids decrease pH between 3 and 5, preventing their growth (fungistatic)
36
Genitourinary physical barriers
1. Flow of urine prevents microbial colonization | 2. Vaginal secretions move microorganisms out of female body
37
GI physical barriers
Peristalsis, defecation, vomiting, diarrhea; Expel microbes from body (Microbial toxins cause GI tract muscles to contract)
38
Chemical factors of innate immunity
Sebum, perspiration, lysozyme, low pH if skin, saliva, gastric juices, vaginal secretions, urine
39
Where is Lysozyme found
In sweat,tears, saliva, nasal secretions, tissue fluids, urine
40
Skins pH and how doe this help in innate response
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
41
Saliva chemical barriers
* Lysozyme, urea, uric acid--> pH 5.55-6.85; inhibits microbial growth * Antibody immunoglobulin A--> prevents attachment of microbes
42
Gastric juices chemical barriers
1. Hydrochloric acid, enzymes, mucus | 2. Acidity: pH 1.2-3 destroys bacteria and most of their toxins
43
Vaginal secretions chemical barriers
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
44
Urines chemical barriers
1. Lysozyme | 2. pH average 6 inhibits microbes
45
How does microbial antagonism help innate immunity
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
46
Commenalism ? Where are most of these organisms found? Can they cause infection?
1. One organism benefits while the other is not affected 2. Skin and gastrointestinal tract 3. Yes, they may be opportunistic pathogens
47
What is another name for microbial antagonism
Comparative exclusion
48
Granulocytes
1. Presence of large granules in their cytoplasm | 2. Include Neutrophils, basophils, eosinophils
49
Neutrophils
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
50
Basophils
1. Release histamine | 2. Important in inflammation and allergic responses
51
Eosinophils
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
52
Agranulocytes
1. Absence of granules in cytoplasm | 2. Three different types: Monocytes, macrophages, dendritic cells, lymphocytes, T cells, B cells
53
Monocytes
1. Do not actively phagocyte until leave circulating blood, enter tissues, and mature into macrophages
54
What is responsible for swelling of lymph nodes during infection
Proliferation of lymphocytes
55
Macrophages
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.
56
Dendritic cells
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
57
Lymphocytes
1. Include NT killers, T cells, B cells | 2. Found in spleen, lymph nodes, red bones marrow
58
NK cells
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
59
What does the binding of NK cells to a target cell release
NK cells release vesicles containing toxic substances
60
Perforin
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
61
Cytolysis
Bursting of cell as a result of extracellular fluid flowing into cell
62
Granzymes
1. Protein digesting enzyme 2. Induces apoptosis of target cell 3. released by some granules of NK cells
63
Do granzymes kill microbes inside targeted cells
NO. It kills infected cells, released microbes can be destroyed by phagocytosis
64
Where are T cells and B cells located
Lymphoid tissues of lymphatic system and circulate in blood
65
What is included in lymphatic system
fluid called lymph, lymphatic vessels, organs that contain lymphoid tissue, re bone marrow
66
What does lymphoid tissue contain
Large number of lymphocytes: T calls and B calls, and phagocytic cells
67
Where are T cells and B cells activated
lymph nodes
68
What is the function of the lymphatic system
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
List WBCs in order from most abundantly seen in the blood to least
``` Neutrophils Lymphocytes Monocytes Eosinophils Basophils ```
70
Phagocytosis
The ingestion of microorganisms or other substances by a cell
71
What are phagocytes
1. WBCs that are part of second line of defense
72
What cells are involved in phagocytosis
1. Neutrophils 2. Fixed macrophages 3. Wandering macrophages 4. Dendritic cells
73
What cells migrate to infection site
granulocytes, monocytes, dendritic cells
74
What happens to monocytes during migration to infected area
They leave blood and migrate into tissues where they enlarge and develop into phagocytic macrophages
75
Fixed macrophages
resident in certain tissues and organs
76
Free (wandering) macrophages
motile, will roam tissues and gather at infection or inflammation sites
77
Name the main steps involved in the mechanism of phagocytosis
1. Chemotaxis and Adherence 2. Ingestion 3. Digestion 4. Waste is discharged from cell
78
Chemotaxis
Chemical attraction of phagocytes to microorganisms
79
How are microorganisms attracted to phagocytes
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
Adherence to phagocyte
This is facilitated by attachment of PAMPs on microbes, to Toll receptors on the surface of phagocytes
81
What does adherence to phagocyte induce
release of specific cytokines by phagocyte and initiates phagocyte
82
What protein facilitates adherence
If microorganism is coated with a serum protein called opsonization
83
Ingestion of microbe
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
Digestion microbe
Phagosome pinches off from plasma membrane and enters cytoplasm, lysosomes are contacted, form a phagolysosome, products are digested
85
What do lysosomal enzymes contain
lysozyme, other enzymes, and toxic oxygen products
86
What happens after enzymes are digested in phagocytes
Residual body within phagolysosome is moved towards cell boundary and discharged as waste products
87
Microbial evasion of phagocytosis
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
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?
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
What triggers inflammation in the body
it's a defense mechanism to damage of body's tissues
90
What are the four signs and symptoms of inflammation
1. Rubor: redness 2. Dolor: pain 3. Color: heat 4. Tumor: swelling (edema) 5. Sometimes a loss of function
91
What is the function of inflammation
1. Destroy agent causing injury 2. Confining or walling of injurious agent and its products 3. Repair and replace damaged tissue
92
Acute phase proteins
1. A group of proteins activated indirectly by inflammation | 2. Induce local and systemic responses
93
What occurs immediately following tissue damage
Vasodilation to damaged area causing increasing vessel permeability, and increased blood flow, redness, heat, and inflammation
94
What is vasodilation
dilation of blood vessels
95
What function does increased permeability of vessels have on damaged tissue
It permits defensive substances normally retained in the blood to pass through walls of blood vessels and enter injured area
96
What causes edema
Increased permeability of blood vessels allows fluid to move from blood into tissues
97
What causes pain of inflammation
This is caused by nerve damage, irritation of toxins, pressure of edema
98
What causes vasodilation and increased permeability of blood vessels
A number of chemicals released by damaged cells at injury site, including histamine**
99
Histamine
A chemical released in direct response to stimulation by certain components of the complement system
100
Can phagocytic granulocytes cause the release of histamine
Yes, they produce chemicals that cause their release
101
Kinins
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
Prostaglandins
Chemical substance released by damaged cells, intensify the effects of histamine and kinins and help phagocytes move through capillary walls
103
Leukotrienes
1. Chemical substances produced by mast cells and basophils 2. Increase permeability of blood vessels 3. Help attach phagocytes to pathogens
104
What do activated fixed macrophages secrete during inflammation process
cytokines which bring about vasodilation and increased permeability
105
How are clotting elements delivered into injured site
By increased permeability and vasodilation of blood vessels
106
How do the formation of clots help the site of injury
They form sound the site of activity and prevent microbes or toxins from spreading to the parts of the body
107
Pus
A localized collection and mixture of dead cells and body fluids in a cavity formed by breakdown of body tissues
108
Abscess
A focus of infection filled with pus; pustules, boils
109
What chemical mediator is is associated with pain related to inflammation
prostagladins
110
What occurs after inflammation and as the flow of blood gradually decreases to injured site
margination of phagocytes to inner surface of endothelium of blood vessels
111
What is margination
The sticking process in response local cytokines
112
How do cytokines cause margination
They alter cellular adhesion molecules (CAMs) on cells lining blood vessels causing phagocytes to stick to site of inflammation
113
How do phagocytes reach injured area
(diapedesis): squeeze between the endothelial cells of blood vessels to reach the area
114
List the stages of inflammation
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
When does repair of tissues begin? when does it end?
1. during active phase of inflammation | 2. when harmful substances have been neutralized or removed from area
116
When is a tissue repaired
when its storm or parenchyma produce new cells
117
stroma
supporting connective tissue, not involved in the functioning part of organ/tissue
118
parenchyma
the functioning part of the tissue
119
What is a local response of the body to injury? What is a systematic response?
1. inflammation | 2. fever
120
Fever
abnormal high body temperature, second line of defense, most frequent cause is infection from bacteria or virus
121
What is considered the body's thermostat and what is it normally set at
1. hypothalamus | 2. 37 ° C
122
What happens if a gram negative bacteria is ingested by a phagocyte
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
How does body try to readjust/increase the new thermostat setting
constricting blood vessels, increasing rate of metabolism, and shivering (all these will raise temperature)
124
What is the crisis phase of a fever
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
What are advantages to a fever
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
What disadvantages can a fever have
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
What are the proteins of the complement system
Interferons, iron-binding proteins, and antimicrobial peptides
128
The complement system
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
What is the main function of the complement system
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
In what manner do complement proteins act
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
What does the activation of C3 serum protein cause
It starts a cascade that results in cytolysis, inflammation, phagocytosis
132
What does inactive C3 split into when activated
C3a and C3b
133
What does C3a and C3b do
C3 binds to the surface of a microbe and receptors on phagocytes attach to C3b
134
How does C3 b enhance phagocytosis
by opsonization
135
What is opsonization
It is also known as immune adherence. It coats a microbe. By doing this it promises attachment of a phagocyte to a microbe
136
Other than phagocytosis, what does C3b initiate
A series of reactions that result in cytolysis
137
What do C5b, C6 through C8 and multiple C9 fragments form
Membrane attack complex (MAC)
138
What is MAC and where does it form
Transmembrane channels (holes) that are inserted into the plasma membrane of invading cell
139
What does MAC cause
the bursting of the microbial cells due to inflow of extracellular fluid through the channels
140
What do C3a and C5a cause after they bind to mast cells
They cause them to release histamine and other chemicals that increase blood vessel permeability during inflammation
141
What is another function of C5
A powerful chemotactic, attracting phagocytes to site of an infection
142
What is the cascade of complement proteins that occur during an infection called
Complement activation
143
What are the 3 pathways of complement cascade
1. Classical pathway 2. Alternative pathway 3. Lectin pathway
144
When is the classical pathway initiated
when antibodies bind to antigens on microbes
145
Classical pathway of complement activation
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
What activates alternative pathway
Contact between certain complement proteins and pathogen
147
Alternative pathway of complement activation
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
How is lectin pathway initiated
When macrophages ingest bacteria, viruses, foreign matter by phagocytosis, they release cytokines that stimulate liver to lectins
149
What are lectins
proteins that bind to carbohydrates
150
Lectin pathway of complement activation
1. Lectin binds to invading cell 2. Bound lectin splits C2 and C4 3. C2a and C4b combine and activate C3
151
What is an example of a lectin and how does it enhance phagocytosis
1. (MBL) mannose-binding-lectin | 2. functions as opsonin
152
What are the effects of complement activation
1. Opsonization or immune adherence 2. MAC: cytolysis 3. Attract phagocytes
153
Inflammation stimulated by complement
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
How do some bacteria evade complement
1. Capsules prevent C activation 2. Surface lipid-carbohydrates prevent MAC formation 3. Enzymatic digestion of C5a
155
Interferons
Cytokines and a class of similar antiviral (small) proteins produced by lymphocytes and macrophages, after viral stimulation.
156
What is the principle function an interferon
To interfere with viral multiplication
157
What is an interesting feature of interferons
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
What are the 3 principle types of interferons in humans
1. (IFN-a) alpha interferon 2. (IFN-B) beta interferon 3. (IFN-y) gamma interferon
159
Gamma interferons
1. Produced by lymphocytes | 2. Induces neutrophils and macrophages to kill bacteria
160
IFN-a and IFN-B
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
Antiviral proteins
Enzymes that disrupt various stages of viral multiplication
162
Antiviral actions of IFNs
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
What are the antimicrobial substances involved in innate immunity's second line of defense
1. Complement system 2. Interferons 3. Iron-binding proteins 4. Antimicrobial peptides