Bacterial Infection Flashcards

1
Q

Time scale of infection

A

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

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2
Q

PAMPs

A

pathogen-associated molecular patterns. recognised by PRR

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3
Q

PRRs

A

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

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4
Q

TLR

A

toll-like receptors (type of PRR)

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5
Q

Effector functions of complement cascade

A

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

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6
Q

recognition of bacterium by phagocyte

A

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

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7
Q

TLR4

A

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

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8
Q

TLR5

A

flagellin (motile bacteria)

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9
Q

TLR1/2

A

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

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10
Q

TLR7, TLR8

A

Recognise ssRNA (viruses)

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11
Q

TLR10

A

recognise NK

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12
Q

TLR3

A

recognise dsRNA of viruses

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13
Q

TLR signalling

A

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

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14
Q

Cytokines prduced due to TLR activation

A

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

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15
Q

Interferons produced due to TLR activation

A

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

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16
Q

Phagocytosis after TLR activation

A

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.

17
Q

If bacteria is in cytosol of phagocyte

A

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.

18
Q

When bacteria is within the phagolysosome of the phagocyte

A

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.

19
Q

opsonisation

A

coat antigen with antibodies to enhance phagocytosis.

20
Q

agglutination

A

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

21
Q

neutralisation

A

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

22
Q

inflammation

A

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

23
Q

complement

A

cell lysis

24
Q

ADCC

A

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

25
Q

Bacterial diseases where antibody plays a key role in protection.

A

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