Immunity against infection - bacteria Flashcards
lecture 8
What are the key features of innate defence mechanisms?
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
What are the features of acquired/adaptive defence mechanisms?
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
What is the role of TH1 cells?
Active against intracellular pathogens
Activate macrophages
Stimulate cytotoxic T cells (CD8+)
What is the role of TH2 cells?
Active against extracellular pathogens
Support antibody production (especially IgE class-switching)
Activate eosinophils, basophils, and mast cells
What is the role of TH17 cells?
Active against extracellular bacteria and fungi
Attract inflammatory cells like neutrophils
Induced early in infection
What are examples of Gram-positive bacteria?
Staphylococcus aureus
Streptococcus spp.
What are examples of Gram-negative bacteria?
Campylobacter
Salmonella
Shigella
Haemophilus
Neisseria
What components of bacterial cell walls can induce innate responses?
LPS (lipopolysaccharides)
Peptidoglycan
How do bacterial components like LPS interact with the immune system?
Bind to Toll-like receptors (TLRs) on macrophages
Activate NOD-like receptors (intracellular sensors) in the cytoplasm
What are Toll-like receptors (TLRs) and their effects?
Recognise pathogen-associated molecular patterns (PAMPs)
Promote inflammation
Stimulate dendritic cell maturation
Influence T cell differentiation
Activate B cells
How do bacteria evade phagocytosis?
Some have protective capsules (e.g., Streptococcus pneumoniae)
Can be opsonised by antibody/complement for effective phagocytosis
What roles do antibodies play in bacterial infections?
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
How do Gram-negative bacteria die via complement?
Killed by complement lysis (via the membrane attack complex, MAC)
Defects in terminal complement components increase susceptibility to Neisseria spp.
How do some bacteria survive within phagocytes?
Mycobacterium tuberculosis inhibits lysosome-phagosome fusion
What is the role of TH1 cells against intracellular bacteria?
Secrete cytokines like TNF-α and IFN-γ to activate macrophages
Enhance phagocytosis and antigen presentation
What are the outcomes of responses to Mycobacterium leprae?
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
What protects against extracellular and intracellular bacterial infections?
Extracellular bacteria: Antibodies (e.g., against Streptococcus pneumoniae, Clostridium tetani)
Intracellular bacteria: T cell effector mechanisms (e.g., TH1 for Mycobacterium tuberculosis)
What are the key differences between innate and adaptive immunity?
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.
How do CD8+ T cells contribute to bacterial defence?
Kill infected cells displaying bacterial antigens via MHC class I.
Release perforins and granzymes to induce apoptosis in infected cells.
: What are immune-privileged sites, and why are they important?
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.
Why are TH17 cells critical in immune defence?
Recruit neutrophils early in infection.
Effective against extracellular bacteria and fungi.
Secrete IL-17 to promote inflammation.
How do antibodies neutralise bacterial toxins?
Bind directly to toxins, preventing them from interacting with host cells.
Examples: Tetanus and diphtheria toxins.
What is the vaccine for Streptococcus pneumoniae?
Composed of 23 polysaccharide serotypes.
Conjugate vaccine available to provide broader and longer-lasting immunity.
How does Mycobacterium tuberculosis evade immune defences?
Inhibits lysosome-phagosome fusion within macrophages.
Survives and replicates inside phagocytes.
What are the effects of complement activation against bacteria?
Promotes inflammation via C3a, C5a.
Opsonisation via C3b binding.
Direct lysis of Gram-negative bacteria through the Membrane Attack Complex (MAC).
How do different antibodies contribute to bacterial defence?
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.
