Immunity against infection - bacteria Flashcards

lecture 8

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1
Q

What are the key features of innate defence mechanisms?

A

Rapid
Include barriers, complement (alternative pathway), phagocytes, NK cells, antimicrobial peptides
Act early as the first line of defence
Non-specific
Ineffective against many pathogens

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2
Q

What are the features of acquired/adaptive defence mechanisms?

A

Involve antibodies and cell-mediated immunity
Take longer to develop
Exhibit memory
Enhance and focus innate defences
Less easily evaded by pathogens
Involve cross-talk with innate immunity

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3
Q

What is the role of TH1 cells?

A

Active against intracellular pathogens
Activate macrophages
Stimulate cytotoxic T cells (CD8+)

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4
Q

What is the role of TH2 cells?

A

Active against extracellular pathogens
Support antibody production (especially IgE class-switching)
Activate eosinophils, basophils, and mast cells

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5
Q

What is the role of TH17 cells?

A

Active against extracellular bacteria and fungi
Attract inflammatory cells like neutrophils
Induced early in infection

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6
Q

What are examples of Gram-positive bacteria?

A

Staphylococcus aureus
Streptococcus spp.

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7
Q

What are examples of Gram-negative bacteria?

A

Campylobacter
Salmonella
Shigella
Haemophilus
Neisseria

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8
Q

What components of bacterial cell walls can induce innate responses?

A

LPS (lipopolysaccharides)
Peptidoglycan

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9
Q

How do bacterial components like LPS interact with the immune system?

A

Bind to Toll-like receptors (TLRs) on macrophages
Activate NOD-like receptors (intracellular sensors) in the cytoplasm

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10
Q

What are Toll-like receptors (TLRs) and their effects?

A

Recognise pathogen-associated molecular patterns (PAMPs)
Promote inflammation
Stimulate dendritic cell maturation
Influence T cell differentiation
Activate B cells

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11
Q

How do bacteria evade phagocytosis?

A

Some have protective capsules (e.g., Streptococcus pneumoniae)
Can be opsonised by antibody/complement for effective phagocytosis

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12
Q

What roles do antibodies play in bacterial infections?

A

Opsonisation: Bind Fc receptors on phagocytes
Complement activation: Promote inflammation, opsonise, or lyse Gram-negative bacteria
Neutralise toxins (e.g., tetanus, diphtheria)
Prevent mucosal adherence by binding surface structures

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13
Q

How do Gram-negative bacteria die via complement?

A

Killed by complement lysis (via the membrane attack complex, MAC)
Defects in terminal complement components increase susceptibility to Neisseria spp.

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14
Q

How do some bacteria survive within phagocytes?

A

Mycobacterium tuberculosis inhibits lysosome-phagosome fusion

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15
Q

What is the role of TH1 cells against intracellular bacteria?

A

Secrete cytokines like TNF-α and IFN-γ to activate macrophages
Enhance phagocytosis and antigen presentation

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16
Q

What are the outcomes of responses to Mycobacterium leprae?

A

Tuberculoid leprosy: Strong TH1 response, slow progression, granuloma formation
Lepromatous leprosy: Strong TH2 response, disseminated infection, fatal. widespread infection due to ineffective macrophage activation by TH2 responses

17
Q

What protects against extracellular and intracellular bacterial infections?

A

Extracellular bacteria: Antibodies (e.g., against Streptococcus pneumoniae, Clostridium tetani)
Intracellular bacteria: T cell effector mechanisms (e.g., TH1 for Mycobacterium tuberculosis)

18
Q

What are the key differences between innate and adaptive immunity?

A

Innate Immunity: Rapid, non-specific, includes barriers, complement, phagocytes, NK cells, antimicrobial peptides.
Adaptive Immunity: Slower to develop, specific, includes antibodies and cell-mediated immunity, exhibits memory.

19
Q

How do CD8+ T cells contribute to bacterial defence?

A

Kill infected cells displaying bacterial antigens via MHC class I.
Release perforins and granzymes to induce apoptosis in infected cells.

20
Q

: What are immune-privileged sites, and why are they important?

A

Sites like the eye, testis, and CNS have barriers that limit immune responses.
Reduce inflammation and damage in sensitive areas but can allow persistent infections.

21
Q

Why are TH17 cells critical in immune defence?

A

Recruit neutrophils early in infection.
Effective against extracellular bacteria and fungi.
Secrete IL-17 to promote inflammation.

22
Q

How do antibodies neutralise bacterial toxins?

A

Bind directly to toxins, preventing them from interacting with host cells.
Examples: Tetanus and diphtheria toxins.

23
Q

What is the vaccine for Streptococcus pneumoniae?

A

Composed of 23 polysaccharide serotypes.
Conjugate vaccine available to provide broader and longer-lasting immunity.

24
Q

How does Mycobacterium tuberculosis evade immune defences?

A

Inhibits lysosome-phagosome fusion within macrophages.
Survives and replicates inside phagocytes.

25
Q

What are the effects of complement activation against bacteria?

A

Promotes inflammation via C3a, C5a.
Opsonisation via C3b binding.
Direct lysis of Gram-negative bacteria through the Membrane Attack Complex (MAC).

26
Q

How do different antibodies contribute to bacterial defence?

A

IgG: Opsonises bacteria for phagocytosis.
IgA: Prevents bacterial adherence to mucosal surfaces.
IgE: Involved in responses to parasites and allergies but supports TH2 against extracellular pathogens.