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

Theme 2- innate 2b Flashcards by P Sreekumar

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

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

How well did you know this?

Not at all

Perfectly

what has to happen for cytoskeletal rearrangement to occur

phagocyte receptors bind particle

- surface receptors are CLUSTERED

How well did you know this?

Not at all

Perfectly

in pseudopodia formation, what helps

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

How well did you know this?

Not at all

Perfectly

which organelle has a role in phagosome formation

phagocytic and endocytic vesicle membranes are recycled

How well did you know this?

Not at all

Perfectly

what are the 2 types of digestion in phagocytosis

oxygen dependent

oxygen independent

How well did you know this?

Not at all

Perfectly

what can be involved in oxygen independent digestion

Acidification
•Lysozyme
•Other enzymes
•Defensins 
•Lactoferrin
•Cathelicidins
•S100 proteins

How well did you know this?

Not at all

Perfectly

what can be involved in oxygen dependent digestion

Reactive oxygen intermediates
Reactive nitrogen intermediates

in the RESPIRATORY BURST

How well did you know this?

Not at all

Perfectly

how is acidification used in ox independent digestion

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

How well did you know this?

Not at all

Perfectly

how is lysozyme used in ox independent digestion

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

How well did you know this?

Not at all

Perfectly

how are other enzymes used in ox independent digestion

acid hydrolases:
phosphatases, sulphatases, glycosidases, deoxyribonucleases

lipases: phospholipase A2

neutral proteases: collagenases, elastase, cystein proteases

How well did you know this?

Not at all

Perfectly

how is lactoferrin used in ox independent digestion

binds to essential nutrients, inhibiting bacterial and fungal growth

How well did you know this?

Not at all

Perfectly

how are defensins used in ox independent digestion

+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

How well did you know this?

Not at all

Perfectly

how are cationic proteins used in ox independent digestion

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)

How well did you know this?

Not at all

Perfectly

how is TNF alpha used in ox independent digestion

secreted by macrophages

- cytotoxic to tumour cells

How well did you know this?

Not at all

Perfectly

describe the ox dep of digestion in phagocytosis

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

How well did you know this?

Not at all

Perfectly

describe ROI

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

How well did you know this?

Not at all

Perfectly

describe RNI

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

most microbial mediators are prod where

where do they produce microbial mediators

MC/MFs and Neu
(professional phagocytes)

lysosomes- mc and macrophages
primary and secondary granules- neus

neutrophils are more likely to kill how

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

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

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

what are the hallmarks of inflammation

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

acute phase response in inflammation lasts how long

0-24hours

what is the aim of inflammation

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

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

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

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

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

what are ways of destroying an organism

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

inflammatory mediators

- 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

what do cytokines do | eg

- 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)

what are the alarm cytokines

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

what do anti-inflammatory cytokines do

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

what do IL-12 and IL-18 do

induce DIFFERENTIATION of PRO INFLAMMATORY T cells | IL-8 is a potent chemokine for neutrophils

what does IFNγ do

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

what are type I interferons

IFNalpha and beta

what do Type I interferons do

have antiviral properties

whaat are the 2 major families of chemokines

CC and CXC

what is chemokine structure what is chemotaxis give examples

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

Prostaglandins, Leukotrienes and Thromboxanes are all what

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

how are prostaglandins made

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

what does histamine cause

acts to inc vascular permeability and smooth muscle contraction

what is EXTRAVASATION

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