Bacterial Infection

Question 1

Time scale of infection

Answer 1

0-12h innate. 12h - 7 days adaptive

Question 2

PAMPs

Answer 2

pathogen-associated molecular patterns. recognised by PRR

Question 3

PRRs

Answer 3

pattern recognition receptors that recognise PAMPs, e.g. TLR

Question 4

TLR

Answer 4

toll-like receptors (type of PRR)

Question 5

Effector functions of complement cascade

Answer 5

C3a and C5a bind to receptors on the cell surface of a mast cell, promoting degranulation and release of histamine to vasodilate. C5a can also act as a chemoattractant to bring in neutrophils and macrophages

Question 6

recognition of bacterium by phagocyte

Answer 6

Direct: PAMPs recognised by PRR (e.g. TLR). Indirect: C3b recognised by C3bR and antibody-antigen complex recognised by antibody receptors (e.g. FcR)

Question 7

TLR4

Answer 7

Homodimer (2 TLR4 molecules form a pair) and recognise lipopolysachharide (gram -ve bacteria)

Question 8

TLR5

Answer 8

flagellin (motile bacteria)

Question 9

TLR1/2

Answer 9

Heterodimer of 1 subunit of TLR1 and 1 subunit of TLR2. Recognise peptidoglycan and triacyl lipopeptides (bacteria)

Question 10

TLR7, TLR8

Answer 10

Recognise ssRNA (viruses)

Question 11

TLR10

Answer 11

recognise NK

Question 12

TLR3

Answer 12

recognise dsRNA of viruses

Question 13

TLR signalling

Answer 13

Recognition of bacterial molecule by TLR. Dimerisation of TLR which brings together two signalling domains. Signal down either a MyD88 pathway of TRIF pathway. MyD88 pathway activates NFkB transcription factor whereas TRIF pathway activates IRFs (interferon regulatory factors). Switch on genes within the phagocyte that produce cytokines or iterferons

Question 14

Cytokines prduced due to TLR activation

Answer 14

IL-1 activates endothelial cells (fever). IL-6 activates antibody-producing B cells. TNF-a activates endothelial (fever) and neutrophils.

Question 15

Interferons produced due to TLR activation

Answer 15

IFN-a and IFN-b promote CD4+ and CD8+ T cell responses in antiviral responses.

Question 16

Phagocytosis after TLR activation

Answer 16

Bacteria get ingested into phagosome, might escape into the cytosol. Or phagosome fuses with lysosome to form phagolysosome (toxic) to break up the bacteria, exocytosis of debris.

Question 17

If bacteria is in cytosol of phagocyte

Answer 17

Enter the MHCI pathway where they a processed by the proteasome and form a complex with MHCI at cell surface. Activate CD8+ T cells to kill the host cell by releasing perforin and granzymes and granulin. Important for diseases where bacteria live in host cells e.g. salmonellosis, tuberculosis, listerosis.

Question 18

When bacteria is within the phagolysosome of the phagocyte

Answer 18

Bacterial proteins enter endocytic pathway with MHCII and are presented on phagocyte cell surface. Activate CD4+ T cell which releases cytokines. IL-17 and TNF lead to inflammation. IFN-gamma activate macrophages. Various other cytokines promote antibody production.

Question 19

opsonisation

Answer 19

coat antigen with antibodies to enhance phagocytosis.

Question 20

agglutination

Answer 20

enhances phagocytic and by clumping bacteria, there’s less infectious units to deal with. e.g. Ab 1E2 can but 5F6 cannot.

Question 21

neutralisation

Answer 21

blocks adhesion of bacteria/viruses to mucosa. blocks active site of toxin. e.g. Diphtheria antitoxin (1981 onwards) - raised in horses and serum used to treat disease BUT foreign protein may cause serum sickness - not used anymore due to unrpredictable

Question 22

inflammation

Answer 22

disruption of cell by complement/reactive protein attracts phagocytic and other immune cells

Question 23

complement

Answer 23

cell lysis

Question 24

ADCC

Answer 24

antibody attaches to target cell and cause destruction by non specific immune cells.

Question 25

Bacterial diseases where antibody plays a key role in protection.

Answer 25

Tetanus, plague and anthrax: antibody neutralises toxin. Streptococcul pneumoniae, meningitis and pertussis: Ab agglutinates, opsonises, complement activating.