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BHSC 3329 > Unit 3- Non-Specific Resistance (Innate Immunity) > Flashcards

Unit 3- Non-Specific Resistance (Innate Immunity) Flashcards

1
Q

innate immunity

A

defense mechanisms present at birth

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2
Q

acquired immunity

A

defense mechanisms acquired by exposure to pathogens

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3
Q

first line of defense

A

surface protection, anatomical/physiolgoical, genetic barriers, non-specific chemical barriers

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4
Q

second line of defense

A

cellular and more specific chemical barriers

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5
Q

third line of defense

A

specific immune response developed against individual pathogens

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6
Q

physical barrier of respiratory tract?

A

epithelial tissue lining along the tract

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7
Q

chemical barrier of respiratory tract?

A

mucous secreted into tract

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8
Q

anatomical barrier of respiratory tract?

A

hair-like cilia sweeping mucous out of tract

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9
Q

what line of defense are T and B lymphocytes, and antibodies?

A

third line

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10
Q

what line of defense are phagocytosis, inflammation, fever and interferon?

A

second line

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11
Q

what are 3 behaviours that act as 1st line barrier?

A

hygine, contagion avoidance, healthy choices (avoid high-risk behaviours)

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12
Q

what are 2 physical first line barriers?

A

1) skin

2) mucous/wax (lines portals of entry)

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13
Q

what are 3 chemical barriers of 1st line defense?

A

1) acid (stomach, lactic)
2) salt (tears, sweat)
3) proteins (lysozymes and defensins in tears, digestive enzymes)

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14
Q

mechanism of lysozymes?

A

targets peptidoglycans of bacterial cell wall (non-specific defense)

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15
Q

Example of how some have a 1st line genetic barrier to HIV?

A

HIV-1 R5 requires CCR5 receptor to infect cells, but some Caucasian populations have a 32 bp deletion in the CCR5 gene, conferring to some resistance to infection

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16
Q

how does H.pylori overcome physical barriers of body?

A

uses flagellum to burrow into mucosal layer

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17
Q

how does H.pylori overcome chemical barriers of the body?

A

it produces basic NH4+ through urease to neutralize stomach acid

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18
Q

How does H. pylori overcome genetic barriers of the body?

A

It is well-adapted to survive in the human stomach

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19
Q

what are WBCs/leukocytes

A

cells of the immune system; they recognize non-self cells and molecules

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20
Q

which leukocytes are not active at birth?

A

B-cells and T-cells. all other leukocytes are part of the innate immune system and are active at birth

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21
Q

what is the common stem cell WBCs and RBCs share?

A

hematopoietic stem cell

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22
Q

what 4 locations can WBCs be found in?

A

1) bloodstream
2) lymphatic vessels
3) reticuloendothelial system (mesh-like network of connective tissue holding tissues together)
4) extracellular fluid

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23
Q

what are the components blood separates into after centrifugation?

A

plasma (blood minus cells), buffy coat (WBCs), red blood cells (unclotted)

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24
Q

what is serum?

A

plasma minus clotting proteins

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25
Q

Neutrophil (class, action)

A

most abundant WBC, first responder, granulocyte, phagocytic (polymorphonuclear cell)

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26
Q

what are PRR?

A

pattern recognition receptors (special proteins) that can feel abnormal proteins on non-self cells

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27
Q

PAMPs?

A

pathogen associated molecular patterns (abnormal proteins on invading cells)

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28
Q

TLRs?

A

toll-like receptors, whcih are special PRRs (pattern recognition receptors) that are on phagocytes (neutrophils, macrophages)

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29
Q

lysosome?

A

destructive body

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30
Q

phagolysosome?

A

an eating and destructive body

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31
Q

7 steps of phagocytosis?

A

1) PRRs recognize PAMPs
2) phagocytic cell engulfs pathogen
3) bubble forms inside the cell- phagosome
4) destructive chemicals/enzymes stored in lysosomes and granuals
5) phagolysosome forms (fused together)
6) digestion and nutrient absorption into the cell
7) waste is excreted from cell

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32
Q

phagocytosis results in…

A

intracellular killing of microbes

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33
Q

what is the oxygen-dependent mechanism of intracellular killing of microbes?

A

toxins are called reactive oxygen species (either OH radicals or hypochlorite)

34
Q

what is the oxygen-independent mechanism of intracellular killing of microbes?

A

electrically charged proteins damage membrane, lysozymes damage cell wall, lactoferrins compete for Fe binding, proteases digest and degrade proteins

35
Q

what is a platelet?

A

a thrombocyte, is anucleate, and a fragment of a larger cell, megakaryocyte. it aggregates to seal up fissures in the blood vessels and skin to form blood clots or scabs

36
Q

chemokine

A

chemical signal released by neutrophils to attract monocytes and macrophages by chemotaxis. coordinates 2 effects of inflammation: vasoactive or chemotactic effects

37
Q

chemotaxis

A

process where neutrophils send chemokines to attract monocytes and macrophages

38
Q

monocyte

A

have granules, but NOT granulocytes, are the largest WBCs, are phagocytic, and produce cytokines, leading to inflammation. (premature form of macrophages)

39
Q

eosinophil

A

granulocyte, non-phagocytic, releases peroxides, lysozymes and toxins into invader and targets fungi, worms that are too large to consume. involved in allergy/inflammation

40
Q

4 parts of 2nd line defense of inflammation?

A

1) rubur (redness)
2) calor (warmth)
3) tumor (swelling)
4) dolor (pain)

41
Q

vasoactive actions

A

vasodilation, vasoconstriction

42
Q

chemotactic actiosn

A

cells migrate to site of damage, mediators released, phagocytes

43
Q

substances with chemotactic effects

A

endotoxins, platelet activating factor, leukotriene, mast cell chemotactic factors, bacterial peptides, PAMPs, endotoxin

44
Q

substances with vasoactive effects

A

histamine, serotonin, bradykinin, prostaglandins

45
Q

substances with both vasoactive and chemotactic effects

A

complement components, cytokines such as interferon and interleukin, arachidonic acid metabolism products, platelet activators

46
Q

histamine

A

formed by basophils and mast cells, released from granules and act quickly

47
Q

prostaglandin

A

from basophils and mast cells; made when needed and act slowly

48
Q

serotonin

A

invovled in intestinal movements and happy feelings after feeding. secreted by platelets to induce blood clotting

49
Q

bradykinin

A

increases sensation of pain, and vasodilation

50
Q

steps of 2nd line inflammation

A

1) margination
2) diapedisis
3) chemotaxis

51
Q

margination

A

endothelial cells of blood vessels express ICAMs (intercellular adhesion molecules) and stick to WBCs in teh damaged area

52
Q

ICAMs

A

intercellular adhesion molecules

53
Q

diapedesis

A

endothelial cells shrink and there’s an opening

54
Q

chemotaxis

A

WBCs are pulled through the opening, and attracted to the site of infection

55
Q

name 3 chemical mediators of immunity

A

1) TNF- tumor necrosis factor
2) IFN- interferon
3) IL- interleukins (IL-1, IL-6, IL-8, IL-12)

56
Q

TNF

A

tumor necrosis factor made by macrophages, T and B cells to increase chemotaxis, phagocytosis, temperature. also involved in weight loss

57
Q

IFN

A

interferon: made by leukocytes, fibroblasts, and is an anti-viral/anti-tumor

58
Q

IL

A

interleukins, made by leukocytes and others

1) IL-1: vasodilation, B/T cell activation, pyrogen
2) IL-6: B/T cell activation, pyrogen
3) IL-8, chemotactic, non-pyrogenic
4) IL-12, activates NK cells and T helper cells, non-pyrogenic

59
Q

which interleukins are pyrogenic?

A

IL-1, IL-6

60
Q

which interleukins activate B/T-cells

A

IL-1, IL-6

61
Q

which interleukins are non-pyrogenic

A

IL-8, IL-12

62
Q

cytokine storm?

A

a systemic induction of cytokines, leads to shock

63
Q

what is the complement system?

A

a complex of proteins that pokes a hole in the surface of the cell; it is vasoactive and chemotactic, increasing inflammatory response

64
Q

where are complement proteins produced?

A

in teh liver

65
Q

what is an APP

A

acute phase protein- a protein that increases many-fold during early stage inflammation

66
Q

3 complement pathways?

A

1) classical pathway
2) MB-Lectin Pathway
3) Alternate Pathway

67
Q

classical pathway

A

complement-fixing antibodies (C3–> C3b)

68
Q

MB-Lectin pathway

A

sugars on teh surface of pathogens is binded by mannose-binding lectin (nonspecific for bacteria and viruses)

69
Q

Alternate pathway

A

C3 binds pathogens directly, molecules on surfaces of bacteria, fungi, viruses and parasites (nonspecific)

70
Q

what do all the pathways end up at?

A

C3–> C3b

71
Q

C5b does what to the membrane?

A

starting point for polymerization of a pore through membrane: MAC

72
Q

MAC

A

membrane attack complex (pore through the membrane)

73
Q

what does C3b do?

A

coverts C5–> C5b

74
Q

C3a and C5a?

A

involved in inflammation, chemokine

75
Q

C3b and C5b?

A

phagocytosis, opsonization

76
Q

what does C5b also lead to?

A

induces binding of C6, C7, C8

77
Q

what is an opsonin?

A

any protein that opsonizes the cell

78
Q

which complement proteins induces opsonization?

A

C3b, C5b

79
Q

what does C9 do?

A

complete the pore complex (MAC)

80
Q

Complement Fixation Test for H1N1 antigen

A

add Abs to H1N1 to sheep rBCs, heat pt serum to destry complement, and add H1N1 antigen, add complement factors and sheep RBCs. if complement binds serum Abs, means pt has produced Abs to the H1N1 antigen (Abs are not denatured with heat). If lysis is observed, the complement had binded to the sRBC Abs because there are no serum Abs present–> pt does not have H1N1 strain

BHSC 3329 (3 decks)

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