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Pathology > 2.5 Chemotaxis > Flashcards

2.5 Chemotaxis Flashcards

1
Q

Chemotaxis

A

movement of a cell up a concentration gradient of a signal. When receptors bind their ligand they lock and aggregate so binding on on side leads the cells in that direction

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2
Q

mediators of chemotaxis

A

bacterial wall product - n-formyl-methionine terminal amino acid which is specifically in bacteria, endogenous inflammatory mediators - C5a, leukotrienes (LTB4), chemokines (IL8)

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3
Q

leukocyte receptors

A

7TM Gprotein coupled receptors, TLRs (10)

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4
Q

7 transmembrane g - protein coupled receptors bind

A

n-formylmethinyl residues, and a number of cytokines and other inflammatory mediators such as C5a and LTB4. (chemotaxis)

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5
Q

TLRs are linked to CD14 bind

A

bacterial products like: LPS, unmethylated CpG sequences and double stranded RNAs (leukocyte activation and function changes)

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6
Q

cytokine receptor binds

A

cytokines

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7
Q

phagocitic receptor binds

A

probably opsonins

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8
Q

7tm receptor initiates

A

cytoskeletal changes

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9
Q

7tm downstream signal transduction

A

increased integrin avidity –> adhesion to endothelium, chemotaxis –>migration into tissues

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10
Q

TLRs and cytokine receptsr lead to

A

production of mediators like arachidonic acid metabolites and cytokines, production of ROS and lysosomal enzymes

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11
Q

TLR–>mediators like AA metabolites and cytokines lead to

A

amplification of the inflammatory reaction

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12
Q

TLR–>production of ROS and lysosomal enzymes leads to

A

leukocyte activation –> killing of microbes

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13
Q

phagocytic receptor binding leads to

A

production of ROS and lysosomal enzymes, phagocytosis of mocrobe into phagosome

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14
Q

phagocytic receptor –> ROS production and phagocytosis of micorbe leads to –>

A

leukocyte activation –> killing of microbes

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15
Q

mechanisms of chemoattractants

A

receptor-ligand interaction, cytoskeletal modulation, intra-cellular ca2+ concentration - a major factor in actin and myosin assemble and disassembly

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16
Q

ex of gprotein signal

A

binding to rec –> PLC –> PIP2 –> DAG + IP3 –> inc intracellular Ca++

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17
Q

in alveolar space bacteria cause

A

acute inflammation and recruitment of neutrophils. The bacteria can survive in the spaces themselves so you’ll see a flood of neutorphils

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18
Q

in alveolar space viruses cause

A

chronic inflammation and recrutiment of lymphocytes. Viruses need host cells so you see lypmphocyte accumulation in interstitium, not in acutaly spaces

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19
Q

next step after chemotaxis

A

leukocyte activation and phagocytosis

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20
Q

leukocyte activation

A

aquiring additional functions induced by chemical mediators such as: production of arachidonic acid products, degranulation and secretion of enzymes, activation of oxidative burst, secretion of cytokines, modulation of adhesion molecules, mediated mostly by TLRs and cytokine receptors

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21
Q

how can you die due to leukocyte activation

A

if enough LPS leaks out all the macs will get activated releasing inflammatory mediators sending you into septic shock

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22
Q

phagocytosis

A

recognition/attachment, engulfment - energy dependant, degredation/killing

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23
Q

recognition of what to eat by

A

complement and Ig opsonins

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24
Q

leukocytes + bacteria

A

nothing happens

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25
Q

leukocytes + bacteria + plasma

A

only some eating of bacteria bc the ca has been chelated and no clotting can occur and no complement. Some eating only bc some samples may have Ig

26
Q

leukocytes + bacteria + serum

A

they eat all the bacteria bc the serum has clotted and is pathogenic and has activated complement (C3b) and Ig to opsonize bacteria and activate leukocytes

27
Q

C3b receptor on leukocyte is also called

A

Mac-1

28
Q

what else is Mac-1 involved in

A

Mac -1 along with LFA1 are integrins that bind Icam and play a role in rolling adhesion

29
Q

what portion of IgG binds the leukocyte receptor

A

Fc fragment of the heavy chain

30
Q

other opsonins

A

mannan binding lectin (MBL), fibrinogen binds to integrins, c-reactive protein binds to specific receptors, fibronectin binds to specific receptors

31
Q

receptors for direct phagocytosis

A

mannose receptor, scavenger receptors

32
Q

mannose receptor

A

binds terminal mannose and fructose sugars on glycoproteins and glycolipids (mammalian has terminal sialic acid or n-acetylgalosamine)

33
Q

scavenger receptors

A

bind oxidized LDL but also bacterial wall products

34
Q

engulfment

A

opsonize and recognize something we want to eat and through cytoskeletal rearrangement that is energy dependent the particulate is taken in and it comes in as a membrane bound phagosome

35
Q

killing and degredation

A

phagosome merges with lysosome to form phagolysosome allwing for degredation and kill by O2-, H2O2, Ocl-, proteases, lysozyme, defensins, BPI, MBP

36
Q

NADPH oxidase system

A

make superoxide: NADPH + O2 ——>NADP + O2-

37
Q

2 superoxides join to form

A

H2O2 by super oxide dismutase

38
Q

H2O2 + Cl- joins to give

A

HOCl - hyperchlorus acid (bleach) by myeloperoxidase

39
Q

myeloperoxidase is only found in

A

neutrophils

40
Q

hyperchlorous acid (bleach) is bad bc

A

it is a potent oxidant/antimicrobial and if it gets into the extracellular space it can cause injury to the body

41
Q

NADPH oxidase is found on the

A

membrane and needs signals to activate its assembly

42
Q

bacterial permeability increasing protien (BPI)

A

Cationic protein that activates phospholipases

43
Q

Lysozyme

A

hydrolizes muramic acid-N-acetyly glucosamine bond found in all bacteria

44
Q

Defensins

A

highly cationic arginine rich peptides that re cytotoxic

45
Q

Lactoferrin

A

binds iron

46
Q

major basic protein

A

in eosinophils and kills parasites

47
Q

problem with killing parasites

A

it is eukaryotic and things that kill it can kill you like MBP

48
Q

inflammation/leukocyte fn hurting us

A

atherosclerosis, ARDS or DAD, Asthma, Transplant rejection, Glomerulonephritis, Septic shock, Vasculitis, Anaphylaxis

49
Q

atherosclerosis

A

proinflammation in vessels causing them to narrow, C reactive protein tells you that inflammation is at hand bc it is made by the liver to activate complement via C1Q complex

50
Q

ARDS or DAD

A

acute respiratory distress syndrom or diffuse alveolar damage in lungs of sick ppl_.high mortality

51
Q

Lukocyte adhesion deficiency 1 - LAD1

A

beta chain of CD11/CD18 (LFA1/Mac1) integrins defect

52
Q

Leukocyte adhesion deficiency 2

A

Sialylated oligosaccharide (receptor for selectin) defect

53
Q

Neutrophil-specific granule deficiency

A

absence of neutrophil-specific granules - defective chemotais

54
Q

chronic granulomatous disease

A

decreased oxidateve burst - 2 types, neutrophils cant kill the bugs so granulomas are the fall back but they are ineffective in clearing bacteria

55
Q

X linked CGH

A

NADPH oxidase (membrane component) defect

56
Q

Autosomal Recessive CGH

A

NADPH oxidase (cytoplasmic component) defet

57
Q

Myeloperoxidase deficiency

A

milder than CGH bc H2O2 can still form but not HOCl

58
Q

Chediak-Higashi syndrome

A

membrane associated protein involved in organelle membrane docking and fusion (no phagolysosome formation)

59
Q

aquired problems in chemotaxis

A

thermal injury, diabetes, malignancy, sepsis, immunodeficienceis

60
Q

acquired problems in adhesion

A

hemodialysis, diabetes mellitus

61
Q

acquired problems in phagocytosis and microbicidal activity

A

leukemia, anemia, sepsis, diabetes, neonates, malnutrition

62
Q

Steroids cause

A

immunosuppression and patients will suffer an increased rate of infection

Pathology (26 decks)

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