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Infection and Immunity > Phagocyte function and macrophages > Flashcards

Phagocyte function and macrophages Flashcards

1
Q

Why is phagocytosis important?

A

Protects against invading organisms
Processes foreign antigens
Presents parts of foreign antigens
Purges debris and damaged/dying host cells

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2
Q

Which cells are phagocytic?

A

Macrophage
Neutrophil
DC
Eosinophil
Basophil

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3
Q

Where do phagocytes act?

A

Sites of infection
Mucosal lymphoid tissue
Lymph nodes
Spleen

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4
Q

Describe the overall process of phagocytosis

A

Activation of resting phagocytes
Chemotaxis
Attachment and signalling
Phagosome maturation
Killing and antigen presentation

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5
Q

What happens in activation of resting phagocytes?

A

Inflammatory mediators activate resting phagocytes
Expression of PRRs and ability to recognise and adhere to microbes increases
Production of ATP, lysosomal enzymes and lethal oxidants increases
Metabolic and microbicidal activity increases

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6
Q

What happens in chemotaxis?

A

Movement towards an increasing concentration of attractant bacterial protein, capsule, cell wall, complement (C5a), chemokine (CXCL-8)

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7
Q

What are the 2 types of attachment?

A

Unenhanced
Enhanced

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8
Q

How does unenhanced attachment occur?

A

Via PRR interaction with PAMPs

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9
Q

How does enhanced attachment occur?

A

Via opsonin recognition receptors interacting with Antibody (Fc) or complement (C5a) fractions previously fixed to microbe components

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10
Q

When does unenhanced attachment occur?

A

In innate immunity - so is antigen non-specific
Designed to recognise a few highly conserved structures (PAMPs)

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11
Q

Name some unenhanced PAMPs

A

Bacteria DNA
Glucans from fungal cell walls
Mannose
LPS from gram negative cell wall
Lipoteichoic acids from gram positive cell wall
N-formylmethionine in bacterial proteins
Microbial peptidoglycans
Viral dsRNA

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12
Q

How can PAMPs be hidden/absent?

A

By pathogen diversity in cell wall structure

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13
Q

Name some unenhanced PRRs

A

Endocytic PRRs
Signalling PRRs

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14
Q

What are some endocytic PRRs?

A

Mannose receptors - bind to mannose and fucose on microbial glycoproteins/lipids
Scavenger receptors - bind to other bacterial cell wall components e.g. LPS, peptidoglycan

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15
Q

How do signalling PRRs work?

A

Binding to bacterial and fungal components
Binding to viral components

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16
Q

What happens if signalling PRRs bind bacterial and fungal components?

A

Transmits a signal to the nucleus, inducing cytokine production e.g. IL-12, TNF-a, IL-6
This leads to innate immune defences such as inflammation, activation of other phagocytes

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17
Q

What happens if signalling PRRs bind viral components?

A

Triggers anti-viral IFNs

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18
Q

Describe enhanced attachment

A

More specific and efficient than unenhanced
Mediated through opsonins
Involves Fc fragments of IgA and IgG
C3b and C5a promote enhanced attachment

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19
Q

What type of attachment do macrophages use?

A

Both enhanced and unenhanced

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20
Q

What type of attachment do neutrophils use?

A

Mainly enhanced

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21
Q

How is the phagosome formed?

A

Microbe attaches to phagocyte
Actin cytoskeleton rearrangement occurs
Forms pseudopods
Membrane remodelling causes phagosome formation
Lysosomes fuse with phagosome and form phagolysosome, allowing for pathogen destruction

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22
Q

What do lysosomes contain?

A

Lysozymes
Cathepsins
Lactoferrin
Defensins

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23
Q

What do lysozymes do?

A

Break down proteoglycans in bacterial cell walls

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24
Q

What are cathepsins?

A

Proteolytic enzymes that degrade enzymes

25
What does lactoferrin do?
Deprives bacteria of iron
26
What are defensins?
Small peptides that form channels in lipid bilayers
27
What are lysosomes a form of?
Oxygen-independent killing
28
Describe oxygen-dependent killing
O2 forms O2- (superoxide) via NADPH oxidase H20 + superoxide forms hydrogen peroxide and hydroxyl radicals via dismutase Arginine + O2 forms NO and citrulline via inducible NO synthase (iNOS) NO + hydrogen peroxide forms peroxynitrite radicals All these oxygen-containing radicals go on to kill the phagocytosed bacteria
29
How does oxidation kill bacteria?
Oxidation of proteins, carbs and DNA destroys function Oxidation lipids can destabilise cytoplasmic membrane structure
30
How do microbes evade immune response?
Block phagocytes Block engulfment Block phagolysosome killing Kill phagocytes
31
What microbe blocks phagocytes?
Strep pneumoniae has a capsule so is able to resist unenhanced attachment by preventing binding of PRRs Resists C3b opsonisation
32
What microbe blocks engulfment?
Yernisia depolymerises actin, preventing engulfment
33
What microbe blocks phagolysosome killing?
Salmonella - more resistant to toxic ROS and defensins Mycobacterium - blocks phagosome fusing with lysosome
34
What microbe kills phagocytes?
Staph aureus produces leukocidin (a toxin which damages membranes)
35
Why do apoptotic cells need to be phagocytosed?
Important for regulation of immune responses Prevents leakage of cytotoxic or antigenic contents Rapid, efficient and silent (no inflammation)
36
Which phagocytes engulf apoptotic cells?
Professional phagocytes - macrophages because they are mobile and can infiltrate tissues Amateur phagocytes - essentially any cell can take up a neighbouring dying cell; slower kinetics than the professional phagocytes
37
What are the signals for phagocytosis of apoptotic cells?
Signals attracting phagocytes - soluble and secreted by apoptotic cells Signals activating phagocytes - expressed on the apoptotic cell surface Signals preventing phagocytosis - not expressed by dying cells
38
What are the signals attracting phagocytes?
Chemoattractants: - Lysophosphatidylcholine (LPC) - ATP - Chemokines e.g. CX3CL1
39
What are signals activating phagocytes?
Phosphatidylserine (PtdSer) Recognition tethering Promotes engulfment
40
Describe PtdSer
Normally expressed on inner leaflet of plasma membrane In apoptosis PtdSer is translocated to outer part of the lipid bilayer Involves flipase and scramblase enzyme
41
Describe host cell housekeeping
RPE (retinal epithelial cells) in the eye remove fragments of photoreceptors that die by apoptosis in response to light - essential for maintaining vision Microglia in the brain help trim and drive neuronal structuring by 'nibbling' them (trogocytosis)
42
What are signals preventing phagocytosis?
CD47 CD31
43
Describe CD47
Ubiquitously expressed in human cells and overexpressed in many different tumour cells Interfere with actin engulfment pathway
44
Describe CD31
Expressed on endothelial cells, platelets, macrophages, Kupffer cells, granulocytes, lymphocytes, megakaryocytes and osteoclasts Binding leads to repulsion signals
45
What happens to CD31 signalling during apoptosis?
It is disabled so the phagocyte is not actively rejected
46
What are consequences of apoptotic cell removal?
Secretion of pro-healing anti-inflammatory cytokine e.g. IL-10, TGF-b Presentation of antigens
47
What does secretion of anti-inflammatory cytokines do?
Reduces inflammation Promotes wound healing
48
What does presentation of antigens allow?
Maintenance of self tolerance Release of unprocessed pathogens/antigens
49
What are some defects that can occur in apoptotic cell clearance?
Leakage of content from non-cleared apoptotic cells act as inflammatory factors Lack of suppression of inflammatory and immune responses - no release of anti-inflammatory cytokines Onset of autoimmune disorders linked to inefficient removal of apoptotic cells - knock-out mice studies SLE
50
What are some diseases associated with defects in phagocytosis?
Chronic granulomatous disease - missing NAPH oxidase components Chediak-Higashi syndrome, hyperpigmentation/albinism - delayed phagosome-lysosome fusion, low chemotaxis Both lead to recurrent infections
51
What are the macrophage subsets?
M1- inflammatory M2 - healing Regulatory/suppressive
52
How do macrophages get the M1 phenotype?
Monocytes recruited from circulation/BM Monocytes differentiate into macrophages that can help activate DCs to stimulate Th1/NK cells which release IFN-g IFN-g promotes macrophages to become M1-phenotype
53
What does the M1 inflammatory phenotype produce?
NO ROS IL-1 TNF MMPs Causes inflammatory microbial response
54
How does the M2 phenotype develop?
Alarmins (IL-25, IL-33, TSLP) stimulate Th2 cells and other cell subsets to release IL-4 and IL-13 Macrophages develop M2 and later regulatory phenotypes which begin to accumulate
55
What do M2 macrophages do?
Antagonise M1 and promote wound healing
56
What do regulatory macrophages do?
Stop wound healing when complete
57
What promotes macrophage proliferation in situ?
Helminth infection
58
Give an example of helminth infection promoting macrophage proliferation
Nematode worm infection drive high levels of IL-4 through Th2 and other cells types High IL-4 promotes M2 macrophage proliferation in situ M2 macrophages kill pathogen High IL-4 and M2 macrophage presence can also produce a M1/M2 combined phenotype that is proliferative

Infection and Immunity (33 decks)

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