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

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

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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
Neutrophil (class, action)
most abundant WBC, first responder, granulocyte, phagocytic (polymorphonuclear cell)
26
what are PRR?
pattern recognition receptors (special proteins) that can feel abnormal proteins on non-self cells
27
PAMPs?
pathogen associated molecular patterns (abnormal proteins on invading cells)
28
TLRs?
toll-like receptors, whcih are special PRRs (pattern recognition receptors) that are on phagocytes (neutrophils, macrophages)
29
lysosome?
destructive body
30
phagolysosome?
an eating and destructive body
31
7 steps of phagocytosis?
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
32
phagocytosis results in...
intracellular killing of microbes
33
what is the oxygen-dependent mechanism of intracellular killing of microbes?
toxins are called reactive oxygen species (either OH radicals or hypochlorite)
34
what is the oxygen-independent mechanism of intracellular killing of microbes?
electrically charged proteins damage membrane, lysozymes damage cell wall, lactoferrins compete for Fe binding, proteases digest and degrade proteins
35
what is a platelet?
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
chemokine
chemical signal released by neutrophils to attract monocytes and macrophages by chemotaxis. coordinates 2 effects of inflammation: vasoactive or chemotactic effects
37
chemotaxis
process where neutrophils send chemokines to attract monocytes and macrophages
38
monocyte
have granules, but NOT granulocytes, are the largest WBCs, are phagocytic, and produce cytokines, leading to inflammation. (premature form of macrophages)
39
eosinophil
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
4 parts of 2nd line defense of inflammation?
1) rubur (redness) 2) calor (warmth) 3) tumor (swelling) 4) dolor (pain)
41
vasoactive actions
vasodilation, vasoconstriction
42
chemotactic actiosn
cells migrate to site of damage, mediators released, phagocytes
43
substances with chemotactic effects
endotoxins, platelet activating factor, leukotriene, mast cell chemotactic factors, bacterial peptides, PAMPs, endotoxin
44
substances with vasoactive effects
histamine, serotonin, bradykinin, prostaglandins
45
substances with both vasoactive and chemotactic effects
complement components, cytokines such as interferon and interleukin, arachidonic acid metabolism products, platelet activators
46
histamine
formed by basophils and mast cells, released from granules and act quickly
47
prostaglandin
from basophils and mast cells; made when needed and act slowly
48
serotonin
invovled in intestinal movements and happy feelings after feeding. secreted by platelets to induce blood clotting
49
bradykinin
increases sensation of pain, and vasodilation
50
steps of 2nd line inflammation
1) margination 2) diapedisis 3) chemotaxis
51
margination
endothelial cells of blood vessels express ICAMs (intercellular adhesion molecules) and stick to WBCs in teh damaged area
52
ICAMs
intercellular adhesion molecules
53
diapedesis
endothelial cells shrink and there's an opening
54
chemotaxis
WBCs are pulled through the opening, and attracted to the site of infection
55
name 3 chemical mediators of immunity
1) TNF- tumor necrosis factor 2) IFN- interferon 3) IL- interleukins (IL-1, IL-6, IL-8, IL-12)
56
TNF
tumor necrosis factor made by macrophages, T and B cells to increase chemotaxis, phagocytosis, temperature. also involved in weight loss
57
IFN
interferon: made by leukocytes, fibroblasts, and is an anti-viral/anti-tumor
58
IL
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
which interleukins are pyrogenic?
IL-1, IL-6
60
which interleukins activate B/T-cells
IL-1, IL-6
61
which interleukins are non-pyrogenic
IL-8, IL-12
62
cytokine storm?
a systemic induction of cytokines, leads to shock
63
what is the complement system?
a complex of proteins that pokes a hole in the surface of the cell; it is vasoactive and chemotactic, increasing inflammatory response
64
where are complement proteins produced?
in teh liver
65
what is an APP
acute phase protein- a protein that increases many-fold during early stage inflammation
66
3 complement pathways?
1) classical pathway 2) MB-Lectin Pathway 3) Alternate Pathway
67
classical pathway
complement-fixing antibodies (C3--> C3b)
68
MB-Lectin pathway
sugars on teh surface of pathogens is binded by mannose-binding lectin (nonspecific for bacteria and viruses)
69
Alternate pathway
C3 binds pathogens directly, molecules on surfaces of bacteria, fungi, viruses and parasites (nonspecific)
70
what do all the pathways end up at?
C3--> C3b
71
C5b does what to the membrane?
starting point for polymerization of a pore through membrane: MAC
72
MAC
membrane attack complex (pore through the membrane)
73
what does C3b do?
coverts C5--> C5b
74
C3a and C5a?
involved in inflammation, chemokine
75
C3b and C5b?
phagocytosis, opsonization
76
what does C5b also lead to?
induces binding of C6, C7, C8
77
what is an opsonin?
any protein that opsonizes the cell
78
which complement proteins induces opsonization?
C3b, C5b
79
what does C9 do?
complete the pore complex (MAC)
80
Complement Fixation Test for H1N1 antigen
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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