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YEAR 2 S2 IMMUNO > Theme 2- innate 2b > Flashcards

Theme 2- innate 2b Flashcards

1
Q

what happens in the ingestion part of phagocytosis
what forms
what is req

A
  • after direct or indirect recognition
  • PSEUDOPODIA form and surrounds particle
  • fuse particle in PHAGOSOME
  • req energy and cytoskeletal rearrangement
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2
Q

what has to happen for cytoskeletal rearrangement to occur

A
  • phagocyte receptors bind particle

- surface receptors are CLUSTERED

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3
Q

in pseudopodia formation, what helps

A

cytoskeletal rearrangement causes the FORCE OF FLUID to push pseudopodia out so it surrounds the particle

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4
Q

which organelle has a role in phagosome formation

A

ER

phagocytic and endocytic vesicle membranes are recycled

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5
Q

what are the 2 types of digestion in phagocytosis

A

oxygen dependent

oxygen independent

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6
Q

what can be involved in oxygen independent digestion

A 
Acidification
•Lysozyme
•Other enzymes
•Defensins 
•Lactoferrin
•Cathelicidins
•S100 proteins
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7
Q

what can be involved in oxygen dependent digestion

A
  • Reactive oxygen intermediates
  • Reactive nitrogen intermediates

in the RESPIRATORY BURST

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8
Q

how is acidification used in ox independent digestion

A

phagolysosome ACIDIFIES at the same time as lysosome FUSION, ENHANCING the activities of many enzymes and INHIBITING pathogen growth

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9
Q

how is lysozyme used in ox independent digestion

A
  • main enzyme in lysosomes
  • mediates digestion of G+ve bac cell walls
  • works best with other enzymes
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10
Q

how are other enzymes used in ox independent digestion

A

acid hydrolases:
phosphatases, sulphatases, glycosidases, deoxyribonucleases

lipases: phospholipase A2

neutral proteases: collagenases, elastase, cystein proteases

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11
Q

how is lactoferrin used in ox independent digestion

A

binds to essential nutrients, inhibiting bacterial and fungal growth

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12
Q

how are defensins used in ox independent digestion

A
  • +vely charged polypeptides that bind -ve PAMPs eg LPS, LTA
  • specific for microbial cells
  • aggregate to form pores in cytoplasmic membranes
  • activate complement- classical pathway
  • most abundant protein in neutrophils
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13
Q

how are cationic proteins used in ox independent digestion

A
  • found in Neu granules, some in Eo
  • high molecular weight and most active at alkaline pH
  • damage microbial membranes, proteins
  • eg elastase, cathepsin G, proteinase 3 (serine proteases)
  • mostly anti-bac (cap G= also anti-fungal)
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14
Q

how is TNF alpha used in ox independent digestion

A
  • secreted by macrophages

- cytotoxic to tumour cells

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15
Q

describe the ox dep of digestion in phagocytosis

A

phagocytes prod Reactive Oxygen and Reactive Nitrogen Intermediates

  • damage proteins, lipids, DNA and cell membs of microorganisms
  • superoxide and H2O2 released cause damage
  • RNI= chort lived but act with ROI
  • Catalase, superoxide dismutase and glutathione are free radical scavengers
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16
Q

describe ROI

A
  • RAPID inc in O2 consumption
  • involves cytoplasmic and memb associated enzymes
  • O2 converted to superoxide, peroxide or hydroxyl anion w/ unpaired e-
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17
Q

describe RNI

A
  • inducible Nitric oxide synthase activated by microbial prod and cytokines
  • Within phagocytes = large ‘burst’ and LOTS of NO produced with potent antimicrobial activity
  • Can combine with superoxide to be even more potent
18
Q

most microbial mediators are prod where

where do they produce microbial mediators

A

MC/MFs and Neu
(professional phagocytes)

lysosomes- mc and macrophages
primary and secondary granules- neus

19
Q

neutrophils are more likely to kill how

A

ingested microorganisms due to higher respiratory burst and higher levels of defensins

20
Q

what happens if pathogens are’nt killed by RO| or RNI

A

can be detected by cytoplasmic PRRs and undergo autophagy or succumb to pyroptosis

21
Q

what are the hallmarks of inflammation

A

5 hallmarks:rubor (redness) et tumor (swelling) cum calor (heat) et dolor (pain), & loss of function

22
Q

acute phase response in inflammation lasts how long

A

0-24hours

23
Q

what is the aim of inflammation

A

increasing blood flow, permeability of vasculature – allowing leukocyte migration to aid limiting the spread of infection, tissue damage and to promote healing

24
Q

whata re the systemic effects of mediators being released from activated tissue cells

A
  • stim release of granulocytes and monocytes from BONE MARROW
    (hypothalamus-> fever)
    (liver-> Acute Phase Protein production (CRP, SAA, MBL)
25
Q

what are the local effects of mediators being released from activated tissue cells

A

inc expression of ADHESION MOLECULES on endothelial cells lining blood vessels and on leukocytes allowing endothelium attachment
Other:
- affect vascular TONE of endothelial layer allowing attached cells to pass to tissues

26
Q

what are ways of destroying an organism

A

anti-microbial proteins/peptides (AMPS) enzymes or by respiratory burst in granules/phagolysosomes, Neutrophil Extracellular Traps (NETs)

27
Q

inflammatory mediators

A
  • produced by mast cells, basophils, macrophages
  • produce: prostaglandins, leukotrienes, thromboxanes, histamine, cytokines, chemokines

also: plasma has 4 intercoonnected mediator producing systems: kinin, clotting, fibrinolytic, complement

28
Q

what do cytokines do

eg

A
  • role in inflammation
  • include: Interleukin-1, 6, 8, 10, 12 (IL-1, IL-6 etc), Tumour necrosis factor a (TNF-a), Transforming growth factor β (TGF-β) and interferon γ (IFNg)
29
Q

what are the alarm cytokines

A

IL-1, IL-6 and TNFα for acute inflammation causing local and systemic activation of fever, increased vascular permeability, production of acute phase proteins and increased adhesion molecule expression

30
Q

what do anti-inflammatory cytokines do

A
  • down reg responses inc IL-10 and transforming growth factor bets (TGF-β)
31
Q

what do IL-12 and IL-18 do

A

induce DIFFERENTIATION of PRO INFLAMMATORY T cells

IL-8 is a potent chemokine for neutrophils

32
Q

what does IFNγ do

A

acts in the acute phase contributing to chronic inflammation by recruiting macrophages to inf/damage

33
Q

what are type I interferons

A

IFNalpha and beta

34
Q

what do Type I interferons do

A

have antiviral properties

35
Q

whaat are the 2 major families of chemokines

A

CC and CXC

36
Q

what is chemokine structure
what is chemotaxis
give examples

A

4 cysteine residues and seq of aa
- when they bind they stimulate MIGRATION and ACTIVATION of cells towards the source along conc gradient (CHEMOTAXIS)
eg IL-8, MCP-1

37
Q

Prostaglandins, Leukotrienes and Thromboxanes are all what

A

all Eicosanoids- INFLAMMATORY MEDIATORS-unsaturated fatty acids derived from arachidonic acid

38
Q

how are prostaglandins made

A

by enzymes inc cyclooxygenases (COX-1, COX-2) a target of anti inflammatory pain killers

  • hormone like effects
  • Act on vascular permeability and leucocyte migration to tissues
  • PGE2 acts on hypothalamus to induce fever
39
Q

what does histamine cause

A

acts to inc vascular permeability and smooth muscle contraction

40
Q

what is EXTRAVASATION

A

Movement (or migration) of white blood cells or fluid from the lumen of blood vessels into tissues

YEAR 2 S2 IMMUNO (14 decks)

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