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BIO 325 - Medical Microbiology > Chapter 15 - Nonspecific Lines of Defence > Flashcards

Chapter 15 - Nonspecific Lines of Defence Flashcards

1
Q

What are the different types of nonspecific defence?

A

1st Line

2nd Line

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2
Q

What is the first line of defence composed of?

A

Skin, mucous membranes, lacrimal apparatus, chemicals (defensins/AMPs)

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3
Q

What is the first line of defence?

A

Structures, chemicals, and processes that work together to prevent pathogens ENTERING the body

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4
Q

What are the physical components of the skin that help it as a defence?

A

Epidermis - tightly packed + shedding + dendritic cells

Dermis - collagen

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5
Q

What are the chemical components of the skin to help it as a defence?

A

Salt
Lysozyme
AMPs
Sebum

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6
Q

What does lysozyme do?

A

It is an enzyme that breaks down the cell wall of bacteria

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7
Q

What are some skin diseases we looked at?

A

Impetigo

Scalded Skin Syndrome

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8
Q

How is epithelia related to mucous membranes?

A

The epithelium is the outer layer of the mucous membrane

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9
Q

What is the lacrimal apparatus?

A

It produces and drains tears

Located above and to the sides of eyes

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10
Q

How does the lacrimal apparatus protect us?

A

The tears either evaporate or drain into small lacrimal canals, where the tears connect to the nasal mucous and go into the pharynx
Also, lysozyme, lactoferrin, and salt defend too

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11
Q

Where can AMPs be found?

A

Secreted onto the skin
In mucous membranes
In neutrophils

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12
Q

What is the mechanism of AMPs?

A

Some punch holes in cytoplasmic membranes, some interrupt internal signaling or enzymatic action, some act as chemotactic factors

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13
Q

What are PAMPs?

What recognize them?

A

Pathogen-associated molecular patterns

Pattern recognition receptors in the innate immune system expressed on cells

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14
Q

What are TLRs?

A

Involved in early innate immune system by sensing microorganisms

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15
Q

What do TLRs do?

A

Binding can result in cytokine production, defensin secretion, phagocytosis and antigen presentation, interferon production, apoptosis

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16
Q

What are NODs?

A

Nucleotide Oligomerization Domain proteins

Intracellular receptors for microbial components (eg. PG, LPS, lipotechoic acids, nucleic acids)

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17
Q

What do NODs do?

A

Mediate inflammation (chemokine production), apoptosis, and possibly defensins

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18
Q

What is the second line composed of?

A

Cells (eg. phagocytes), Antimicrobial chemicals, and Processes (eg. inflammation)
NO barriers

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19
Q

When does the second line come into effect?

A

When the pathogen successfully “enters” the human body

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20
Q

What are the different components of blood?

A

Plasma, RBCs, WBCs (leukocytes)

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21
Q

What is plasma?

A

The water component of the blood that contains dissolved gases, electrolytes, nutrients, and proteins (most important)

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22
Q

What is serum?

A

The fluid left behind when clotting factors are removed from plasma

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23
Q

Why is iron so important for humans? How do we carry it and why?

A

Iron is important because it is a component of the cytochromes, serves as a cofactor, and is an important part of hemoglobin
It is carried by a protein carrier called Transferrin, because it is insoluble otherwise

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24
Q

How is iron stored in the liver?

A

It is stored by binding to a protein called Ferritin

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25
How do bacteria try to steal our iron? How do we counteract this?
They release siderophores, which have a higher iron-binding affinity than Transferrin. We respond by producing Lactoferrin, which is even better than siderphores
26
What is hemolysin? Why is it used?
Hemolysin is a protein released by pathogens to bypass the iron "tug of war" Hemolysin punches holes in the membranes of RBCs, releasing hemoglobin. Other proteins then get involved and strip the hemoglobin of its iron
27
What proteins can be found in plasma?
Antibodies (immunoglobins), transferrin, complement
28
What are formed elements? What do they consist of?
All the cells and cell fragments suspended in plasma | Erythrocytes, leukocytes, and platelets
29
What are the roles of each of the formed elements?
Erythrocytes - carry oxygen and CO2 Platelets - involved in blood clotting Leukocytes - protect body from invaders
30
What are leukocytes divided into?
Granulocytes and Agranulocytes
31
What are the different types of granulocytes?
Basophils, Eosinophils, Neutrophils
32
What do basophils have?
Contains heparin and histamine, binds IgE
33
What do eosinophils have?
Contain cationic proteins, ROS
34
What do neutrophils have?
Lactoferrin and defensins
35
What are some special features of some of the granulocytes?
Eosinophils and neutrophils are capable of diapedesis and phagocytosing pathogens
36
What are the different types of Agranulocytes?
Lymphocytes and monocytes
37
What are lymphocytes?
Small cells (large nucleus) involved with specific immunity
38
What are monocytes?
Leave the blood to mature and become macrophages
39
What are the functions of macrophages?
They are in the 2nd line. They devour foreign objects such as dust, dead cells, bacteria, etc.
40
What are dendritic cells?
Phagocytes (but NOT wbcs) that await microbes, phagocytose them, and then tell the adaptive immune response
41
What is hematopoiesis?
The formation of blood cellular components (from the bone marrow) Makes all of the formed elements
42
What are the different types of macrophages?
Wandering and fixed
43
What are the different fixed macrophages?
Langerhans cells (epidermis), alveolar macrophages (lungs), microglia (central nervous system), Küpffer cells (liver), cavities of spleen, in kidneys, in joints.
44
What is the mononuclear phagocyte system?
a part of the immune system that consists of the phagocytic cells located in reticular connective tissue
45
What is the WBC test called? What is it for?
Differential white blood cell count. | The proportions of WBCs can be a sign of a disease.
46
What does an increase in eosinophils indicate?
Allergies or parasitic worm infection
47
What does an increase in neutrophils indicate?
Bacterial disease
48
What does an increase in lymphocytes indicate?
Viral infection
49
What are the steps of phagocytosis?
chemotaxis, adherence, ingestion, maturation, killing, and elimination
50
What different PRRs are there? What do they recognize?
Molecules in the blood and lymph (opsonize and trigger complement) Surface receptors on phagocytes (eg. macrophages) TLRs NODs
51
What is Nonphagocytotic killing?
Killing without phagocytosis
52
How do eosinophils kill?
``` Can phagocytose (not main way) Attack parasitic helminths by binding to the surface of the worm and releasing protein toxins which weaken or kill it ```
53
How do NK lymphocytes kill?
Secrete toxins onto the surface of virally infected cells and tumours (neoplasms)
54
Why don't NK cells kill the rest of our body cells?
B/c they have membrane proteins similar to the NK cells
55
How do neutrophils kill?
Produce chemicals that kill nearby invaders (can generate H2O2 and NaClO (bleach) or can produce nitric oxide, an inflammatory) Generate extracellular fibers called neutrophil extracellular traps (NETs) that bind to and kill bacteria (form of suicide)
56
What are some nonspecific chemical defences?
Lysozyme, defensins, complement, and interferons
57
How were the complement proteins named?
The numbers were designated according to the order they were discovered
58
What are the three types of complement pathways?
Classical pathway Alternate pathway Lectin pathway
59
How is the classical pathway activated?
C1 becomes active as it binds to the antibody-antigen complex. C1 then cleaves C2 and C4...
60
How is the alternate pathway activated?
It is independent of antibodies Cleavage of C3 occurs naturally normally but they get degraded quick. When there is a microbe present, it can adhere long enough for proderpin factors to do their job and continue the cascade
61
Why is the alternate pathway even required?
Because we don't need antibodies for it. Antibodies can take 2 weeks to be generated it we havent seen the pathogen before
62
What is a lectin?
Lectins are chemicals that bind to specific polysaccharide subunits
63
How does the lectin pathway work?
Mannose sugars are rare in mammals, but are prevalent in bacteria, fungi, and viruses. Lectins bound to mannose trigger complement by cleaving C2 and C4. It then proceeds just like the classical pathway
64
What are interferons?
Protein molecules released by host cells to nonspecifically inhibit the spread of viral infections
65
What is the difference between type I and II interferons?
Type I interferons (alpha and beta) are present early in viral infections Type II interferons (gamma) appear later in the infection. Their actions are identical.
66
How do interferons work?
They are produced by the infected cell, which are released to nearby cells. This triggers the nearby cells to produce antiviral proteins, so they are ready if a virus attacks.
67
What is inflammation?
General, nonspecific response to tissue damage. Goal is for containment and tissue repair. Inflammation stimulates defensin production
68
What is the body's initial response to injury or invasion of pathogens?
First, localized dilation of blood vessels The process of blood clotting triggers the conversion of a plasma protein into bradykinin (9 A.A.), an inflammatory mediator Patrolling macrophages release prostaglandins and leukotrienes (inflammatory mediators) (identify invaders via TLRs and NODs) Basophils, platelets, mast cells also release inflammatory mediators (histamine) when exposed to C3a, C4a or C5a
69
What does bradykinin do? What else has same function? Why is this important?
Bradykinin and histamine cause vasodilation of the body's smallest arteries It brings oxygen, phagocytes, and nutrients to the site of infection
70
What do inflammatory mediators do?
Cause endothelia to produce adhesion molecules for leukocytes to recognize Also, cause gaps in veins for diapedesis
71
What specifically do prostaglandins and leukotrienes do?
They cause fluid to leak from the blood vessels and accumulate in the tissue, resulting in edema
72
Why do you get pain during inflammation?
Edema causes pressure on nerve endings = pain
73
What is fibrinogen? How does it get to the site?
It is a clotting protein | Vasodilation and increased permeability also deliver it to the site
74
Why is fibrinogen important?
Clotting allows for containment of the pathogen and its toxins
75
What is pus?
A fluid containing dead tissue cells, leukocytes (mostly wandering macrophages), and pathogens It may push up to the surface and erupt or get absorbed inside within days
76
How can inflammation be treated? Why?
Antihistamines block histamine receptors on the endothelium | Antiprostaglandins (ibuprofin and aspirin)
77
What is margination?
A process where leukocytes roll along the inside walls of blood vessels until they adhere to the receptors lining the vessels then they squeeze through
78
How are phagocytes attracted to the site of an infection?
By chemotatic (chemotaxis) factors such as C3a, C5a, leukotrienes, and microbial toxins and components
79
Which phagocytes arrive at the site of infection primarily?
First neutrophils, followed by monocytes. When monocytes leave the blood, they become wandering macrophages, which are super active cells that devour pathogens, damaged tissue, and dead neutrophils
80
What are the stages of inflammation?
Dilation and increased permeability of blood vessels Migration of phagocytes Tissue repair
81
Why can tissue repair sometimes not work correctly?
Because if it is somewhere that doesn't divide quickly or at all (unlike skin + mucous membranes), and it doesn't contain undifferentiated stem cells, then scar tissue is generated with fibroblasts.
82
Give an example of 2 organs that wouldn't be able to undergo proper tissue repair
Heart and brain
83
What is a fever?
When your body temperature is above 37 C
84
How is fever related to inflammation and interferons?
It enhances the effect of both of them
85
What causes fever?
Pyrogens trigger the hypothalamus to "reset" the body's thermostat to a higher temperature
86
What are pyrogens?
Chemicals (bacterial toxins, cytoplasmic bacterial components, antibody-antigen complexes, chemicals released by phagocytes after they have phagocytosed) Chemicals that reset the hypothalamus
87
How is a fever produced?
Pyrogens travel in the blood to the hypothalamus, where it releases prostaglandins which resets the thermostat The hypothalamus tells the other parts of the brain the new temperature setting, which they then release nerve impulses to do that
88
How does your body temperature rise after the thermostat is reset?
Repetitive muscle contractions (shivering), and increase in BMR, and constriction of blood vessels to the skin (explains paleness and coolness of skin, yet general hotness of body)
89
How does fever kind of ruin the effect of inflammation?
Fever constricts blood vessels which were dilated due to inflammation
90
How does fever come to an end?
Fever continues with the continuation of pyrogens. When there are less pathogens, there will be less pyrogens, so the fever will gradually be brought down to 37
91
Why do some doctors say you shouldn't take fever reducing medications?
Because fevers actually have lots of benefits: Enhances the effects of interferons Inhibits growth of some microorganisms May enhance the performance of phagocytes, cells of specific immunity, and the process of tissue repair
92
What are some downsides/risks of fever?
A too high of a fever can cause denaturation of important body proteins. Also, nerve impulses are inhibited, causing hallucinations, coma, even death Also, there are side effects such as tiredness and body aches

BIO 325 - Medical Microbiology (3 decks)

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