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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
Q

How do bacteria try to steal our iron? How do we counteract this?

A

They release siderophores, which have a higher iron-binding affinity than Transferrin.
We respond by producing Lactoferrin, which is even better than siderphores

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26
Q

What is hemolysin? Why is it used?

A

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

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27
Q

What proteins can be found in plasma?

A

Antibodies (immunoglobins), transferrin, complement

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28
Q

What are formed elements? What do they consist of?

A

All the cells and cell fragments suspended in plasma

Erythrocytes, leukocytes, and platelets

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29
Q

What are the roles of each of the formed elements?

A

Erythrocytes - carry oxygen and CO2
Platelets - involved in blood clotting
Leukocytes - protect body from invaders

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30
Q

What are leukocytes divided into?

A

Granulocytes and Agranulocytes

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31
Q

What are the different types of granulocytes?

A

Basophils, Eosinophils, Neutrophils

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32
Q

What do basophils have?

A

Contains heparin and histamine, binds IgE

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33
Q

What do eosinophils have?

A

Contain cationic proteins, ROS

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34
Q

What do neutrophils have?

A

Lactoferrin and defensins

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35
Q

What are some special features of some of the granulocytes?

A

Eosinophils and neutrophils are capable of diapedesis and phagocytosing pathogens

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36
Q

What are the different types of Agranulocytes?

A

Lymphocytes and monocytes

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37
Q

What are lymphocytes?

A

Small cells (large nucleus) involved with specific immunity

38
Q

What are monocytes?

A

Leave the blood to mature and become macrophages

39
Q

What are the functions of macrophages?

A

They are in the 2nd line. They devour foreign objects such as dust, dead cells, bacteria, etc.

40
Q

What are dendritic cells?

A

Phagocytes (but NOT wbcs) that await microbes, phagocytose them, and then tell the adaptive immune response

41
Q

What is hematopoiesis?

A

The formation of blood cellular components (from the bone marrow)
Makes all of the formed elements

42
Q

What are the different types of macrophages?

A

Wandering and fixed

43
Q

What are the different fixed macrophages?

A

Langerhans cells (epidermis), alveolar macrophages (lungs), microglia (central nervous system), Küpffer cells (liver), cavities of spleen, in kidneys, in joints.

44
Q

What is the mononuclear phagocyte system?

A

a part of the immune system that consists of the phagocytic cells located in reticular connective tissue

45
Q

What is the WBC test called? What is it for?

A

Differential white blood cell count.

The proportions of WBCs can be a sign of a disease.

46
Q

What does an increase in eosinophils indicate?

A

Allergies or parasitic worm infection

47
Q

What does an increase in neutrophils indicate?

A

Bacterial disease

48
Q

What does an increase in lymphocytes indicate?

A

Viral infection

49
Q

What are the steps of phagocytosis?

A

chemotaxis, adherence, ingestion, maturation, killing, and elimination

50
Q

What different PRRs are there? What do they recognize?

A

Molecules in the blood and lymph (opsonize and trigger complement)
Surface receptors on phagocytes (eg. macrophages)
TLRs
NODs

51
Q

What is Nonphagocytotic killing?

A

Killing without phagocytosis

52
Q

How do eosinophils kill?

A 
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
Q

How do NK lymphocytes kill?

A

Secrete toxins onto the surface of virally infected cells and tumours (neoplasms)

54
Q

Why don’t NK cells kill the rest of our body cells?

A

B/c they have membrane proteins similar to the NK cells

55
Q

How do neutrophils kill?

A

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
Q

What are some nonspecific chemical defences?

A

Lysozyme, defensins, complement, and interferons

57
Q

How were the complement proteins named?

A

The numbers were designated according to the order they were discovered

58
Q

What are the three types of complement pathways?

A

Classical pathway
Alternate pathway
Lectin pathway

59
Q

How is the classical pathway activated?

A

C1 becomes active as it binds to the antibody-antigen complex.
C1 then cleaves C2 and C4…

60
Q

How is the alternate pathway activated?

A

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
Q

Why is the alternate pathway even required?

A

Because we don’t need antibodies for it. Antibodies can take 2 weeks to be generated it we havent seen the pathogen before

62
Q

What is a lectin?

A

Lectins are chemicals that bind to specific polysaccharide subunits

63
Q

How does the lectin pathway work?

A

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
Q

What are interferons?

A

Protein molecules released by host cells to nonspecifically inhibit the spread of viral infections

65
Q

What is the difference between type I and II interferons?

A

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
Q

How do interferons work?

A

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
Q

What is inflammation?

A

General, nonspecific response to tissue damage. Goal is for containment and tissue repair. Inflammation stimulates defensin production

68
Q

What is the body’s initial response to injury or invasion of pathogens?

A

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
Q

What does bradykinin do? What else has same function? Why is this important?

A

Bradykinin and histamine cause vasodilation of the body’s smallest arteries

It brings oxygen, phagocytes, and nutrients to the site of infection

70
Q

What do inflammatory mediators do?

A

Cause endothelia to produce adhesion molecules for leukocytes to recognize
Also, cause gaps in veins for diapedesis

71
Q

What specifically do prostaglandins and leukotrienes do?

A

They cause fluid to leak from the blood vessels and accumulate in the tissue, resulting in edema

72
Q

Why do you get pain during inflammation?

A

Edema causes pressure on nerve endings = pain

73
Q

What is fibrinogen? How does it get to the site?

A

It is a clotting protein

Vasodilation and increased permeability also deliver it to the site

74
Q

Why is fibrinogen important?

A

Clotting allows for containment of the pathogen and its toxins

75
Q

What is pus?

A

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
Q

How can inflammation be treated? Why?

A

Antihistamines block histamine receptors on the endothelium

Antiprostaglandins (ibuprofin and aspirin)

77
Q

What is margination?

A

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
Q

How are phagocytes attracted to the site of an infection?

A

By chemotatic (chemotaxis) factors such as C3a, C5a, leukotrienes, and microbial toxins and components

79
Q

Which phagocytes arrive at the site of infection primarily?

A

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
Q

What are the stages of inflammation?

A

Dilation and increased permeability of blood vessels
Migration of phagocytes
Tissue repair

81
Q

Why can tissue repair sometimes not work correctly?

A

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
Q

Give an example of 2 organs that wouldn’t be able to undergo proper tissue repair

A

Heart and brain

83
Q

What is a fever?

A

When your body temperature is above 37 C

84
Q

How is fever related to inflammation and interferons?

A

It enhances the effect of both of them

85
Q

What causes fever?

A

Pyrogens trigger the hypothalamus to “reset” the body’s thermostat to a higher temperature

86
Q

What are pyrogens?

A

Chemicals (bacterial toxins, cytoplasmic bacterial components, antibody-antigen complexes, chemicals released by phagocytes after they have phagocytosed)

Chemicals that reset the hypothalamus

87
Q

How is a fever produced?

A

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
Q

How does your body temperature rise after the thermostat is reset?

A

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
Q

How does fever kind of ruin the effect of inflammation?

A

Fever constricts blood vessels which were dilated due to inflammation

90
Q

How does fever come to an end?

A

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
Q

Why do some doctors say you shouldn’t take fever reducing medications?

A

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
Q

What are some downsides/risks of fever?

A

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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