Cells Sem 2 Test 1 Part 2

Front 1

what are the killing mechanisms used by phagocytes

Back 1

nitric oxide (used to kill bacteria in cystol, iNOS(induced nitric oxide synthase) used to inhibit growth)

defensins (exist in phagolysosomes)

proteases and hydrolases (in phagosomes, digestive enzyme specific for carbs (cell wall) and lipids (membrane) and can digest RNA/DNA)

Front 2

what is the classical compliment pathway

Back 2

a compliment is a fraction that can be added with an antibody to kill a bacteria

Front 3

what is the alternative pathway for compliments

Back 3

now a complement can be used w/o antibodies to kill the bacteria

Front 4

what kind of immunity is compliments part of

Back 4

innate

Front 5

what triggers the activation of complements

Back 5

bacterial surfaces or antibodies present in antibody-antigen complexes

Front 6

what is the most important complements

Back 6

C3

Front 7

what is the cascade of effects to form C3 convertase

Back 7

C3 (spontaneously breaks down to C3b and C3a)

C3a goes off into the serum

C3b must bind to a bacteria cell surface in order to become stable otherwise it will be unstable in the serum and will be broken down by factors H/I

once C3b is stable it binds to Factor B and forms CebB

Factor D cleaves C3bB forming C3 convertase

C3 convertase is self amplifying and causes C3 to break down faster liberating more C3b

Front 8

what controls the amount of C3 convertase

Back 8

C3b stability

if C3b doesnt become stable by binding the a bacteria cell surface it will be unstable in the serum and get broken down by Factos H/I

Front 9

what are the negative controls of C3 activation

Back 9

serum factors H/I because they destablize C3b

proteins on host cell surface, because they help C3b break down

Front 10

what is the positive control of C3 activation

Back 10

bacterial surfaces because they stabalize C3b

Front 11

how is C5 convertase made

Back 11

C5 convertase is made when C3 convertase binds with C3b

Front 12

what does C5 convertase do

Back 12

it cleaves C5 into C5a and C5b

Front 13

what occurs in the activation of complement by bacterial carbohydrates

Back 13

mannose binding lectin binds bacteria then recruits MASP-1 and MASP-2 to create a protease similar to C1qrs

Front 14

what does the activation of C1qrs do

Back 14

increases cleavage of C3

-protein activated by an antibody to initiate complement chain

Front 15

how can bacteria surfaces activate complement

Back 15

directly stabalizing C3b

forming structure similar to C1qrs


*both of these lead to the production of C3 convertase

Front 16

how is the membrane attack complex (MAC) formed

Back 16

C5 convertase is attached to bacteria surface and interacts with C5
-it cleaves C5 into C5a and C5b

C5a goes off into the fluid

C5b stays attached to the bacteria cell surface and recruits proteins C6-C8 and eventually C9 (forms the PORE)

Front 17

what is the purpose of the pore in the MAC

Back 17

it compromises the osmolarity of the bacteria allowing ions and fluid to pass through and the cytoplasm as well, leading to the eventual collapse of the bacteria

Front 18

what is C3b

Back 18

an opson that coats bacteria/microbes allowing phagocytes to bind

-since microbes are encoated w/ C3b phagocytes have a C3b receptor allowing them to bind

Front 19

what is CR1 and what does it do

Back 19

major complement receptor on phagocytes that binds to C3b

when C3b is bound to CR1 it no longer can make C3 convertase and the CR1 receptor blocks factor B from reacting w/ C3b

Front 20

what are the Anaphylatoxins

Back 20

C3a and C5a

Front 21

what do annaphylatoxins do

Back 21

mediate fast/acute inflammation that occurs right after an ijurey or immediately after an infection

Front 22

what do C3a and C5a do

Back 22

they bind to the surface of WBC mainly Neutrophils

induce neutrophile to make more C3b receptors

attract more neutrophils via CHEMOTAXIS

trigger mast cells to release histamine

Front 23

what is respiratory burst

Back 23

neutrophils in the presence of C3a and C5a have increased production of reactive oxygen

Front 24

why and how do mast cells release histamine

Back 24

mast cells are imbedded in tissue and they release histamine due to ANAPHYLATOXINS (C3a/C5a)

histamine will act on the endothelium of capillaries to create space between endothelial cells. Fluid carrying compliment components will be released and this is done in order to amplify the complement cascade.
-Neutrophils escape from the circulation in order to reach the damaged/infected tissue site.
*NEUTROPHILS ARE ATTRACTED BY CHEMOTACTIC FACTORS RELEASED BY MAST CELLS AND C5A/C3A this induces them to make C3b receptors which the use to see bacteria and phagocyte them

Front 25

how do macrophages mediate acute inflammation

Back 25

macrophages release factors that cause endothelial cells of capilarries to produce adhesion molecules to make them selves sticky for neutrophils to bind to them and squeeze through

Front 26

what is different about mast cells and macrophages

Back 26

macrophages can be stimulated by different kinds of stimulation but mast cells are only stimulated by anaphylatoxins

Front 27

what are the Humural Innate Mechanisms

Back 27

lysozymes - dissolve cell wall in saliva

interferons - produced by all cell types and have antiviral activity

Acute phase proteins
-macrophages produce CYTOKINS (cytokins get into circulation and have long half life, these cytokins act on the HYPOTHALAMUS and LIVER (they induce the liver to form acute phase proteins))

C reactive proteins (CRP) elevate themselves in serum allows Dr. to tell if disorder has an inflammatory component and can be used to evaluate severity of heart attack

Manose binding lectin - binds to surface of some microbes and helps to activate compliments