W2 Flashcards
(15 cards)
Q: What are the usual routes of infection for pathogens?
A:
Respiratory: Inhalation (e.g., influenza).
Gastrointestinal: Ingestion (e.g., Salmonella).
Urogenital: Sexual or urinary transmission (e.g., Chlamydia).
Skin: Cuts or wounds (e.g., Staphylococcus).
Vector-borne: Transmitted by insects (e.g., malaria).
Q: What is a PAMP?
A: Pathogen-Associated Molecular Patterns are molecular structures shared by pathogens (e.g., LPS in Gram-negative bacteria, peptidoglycan in Gram-positive bacteria) recognized by the immune system via Pattern Recognition Receptors (PRRs).
Q: How do exotoxins differ from endotoxins?
A:
Exotoxins: Secreted proteins that directly damage host cells (e.g., diphtheria toxin).
Endotoxins: Lipopolysaccharides (LPS) released during bacterial lysis, causing systemic inflammation.
Q: What are neutrophil NETs?
A: Neutrophil Extracellular Traps (NETs) are webs of DNA, histones, and proteins released by dying neutrophils to trap and kill pathogens.
Q: What is an opportunistic pathogen?
A: Normally harmless microbes (e.g., commensals) that cause disease under certain conditions, such as weakened immunity or disrupted microbiota.
Q: What are the roles of complement proteins in immunity?
A: Complement proteins enhance phagocytosis (opsonization), lyse pathogens (via membrane attack complex), and recruit immune cells.
Q: What are innate lymphoid cells (ILCs), and how do they differ from T and B cells?
A: ILCs are lymphocyte-like cells without antigen-specific receptors. They rapidly respond to infection and produce cytokines to shape immune responses.
Q: What is the “BAM model” for bacteriophages in immunity?
A: Bacteriophages (phages) may protect humans by targeting bacterial pathogens, crossing epithelial barriers, and potentially regulating immune tolerance.
Q: How do pathogens evade the immune system?
A:
Disrupting NETs: Using nucleases to degrade NET DNA.
Producing adenosine: Inhibits macrophages and dampens immune responses.
Mimicking host molecules: Reduces immune recognition.
Q: What is Chronic Granulomatous Disease (CGD)?
A: A genetic disorder where NADPH oxidase dysfunction impairs ROS production, reducing the ability of phagocytes to kill pathogens.
Q: Explain the process of phagocytosis and its role in combating infection.
A:
Steps: Pathogen recognition → engulfment into a phagosome → fusion with lysosome to form a phagolysosome → digestion using ROS, nitric oxide, and enzymes.
Role: Clears pathogens, presents antigens to T cells, and produces inflammatory signals to recruit more immune cells.
Q: Discuss the differences between innate and adaptive immune responses to extracellular and intracellular pathogens.
A:
Extracellular pathogens: Handled by phagocytes, complement, and antibodies.
Intracellular pathogens: Targeted by NK cells, cytotoxic T lymphocytes, and macrophage activation. Innate immunity provides immediate defense, while adaptive responses offer specificity and memory.
Q: How do pathogens cause damage during infection? Provide examples.
A:
Exotoxins: Damage host cells (e.g., cholera toxin disrupts ion balance).
Endotoxins: Trigger systemic inflammation (e.g., LPS-induced sepsis).
Cytopathic effects: Viral replication destroys host cells (e.g., lysis in influenza).
Immune system hijacking: SARS-CoV-2 induces excessive NETs and inflammation, causing tissue damage.
Q: Describe the roles and activation of neutrophils during an innate immune response.
A:
Neutrophils rapidly migrate to infection sites, engulf pathogens via phagocytosis, and release antimicrobial molecules (ROS, defensins).
Activation: PAMP recognition via PRRs triggers cytokine release and formation of NETs to trap and kill pathogens.
Q: What are the mechanisms by which bacteriophages and the “BAM model” contribute to innate immunity?
A:
Bacteriophages kill bacterial pathogens by infecting and lysing them.
Transcytosis: Phages cross epithelial barriers to target microbes.
Immune tolerance: Regulate host immune responses by modulating bacterial populations in mucosal areas.
