Exam 1: Chapters 2 and 3 Flashcards
What is septic shock?
Cardiovascular collapse due to a body-wide increase in vascular permeability
Fill in the blanks.
- Phosphocholine; 2. C-reactive protein (CRP); 3. C1 complex; 4. C4; 5. C4a; 6. C4b; 7. C2; 8. C2b; 9. C2a; 10. C3; 11. C2aC4b; 12. C3a; 13. C3b
What are the functions of protease inhibitors in the innate response?
Protease inhibitors trick proteases into cleaving their covalent bonds rather than those of C3b on the pathogen surface, thus activating the protease inhibitor to enclose the protease and prevent it from deactivating complement
What are the three responses to infection?
Immediate Innate Response, Mobilized Innate Response, Adaptive Response
What mechanism(s) protect human cells from complement?
Factor H and Factor I; MCP and DAF
What are the three ways that complement can be activated?
Alternative pathway, classical pathway, lectin pathway
Fill in the blanks.
- C3; 2. iC3; 3. Factor B; 4. Factor D; 5. iC3Bb; 6. Bb; 7. Ba; 8. C3; 9. C3a; 10. C3b; 11. C3b; 12. Factor B; 13. Factor D; 14. C3bBb; 15. C3; 16. C3a; 17. C3b
What are defensins and how do they work?
Defensins are amphipathic proteins that insert themselves into pathogen membranes, which disrupts membrane integrity by forming a pore
How are INF-B (Interferon Beta) and INF-a (Interferon Alpha) activated?
RLR binds to viral RNA, activating IRF-3, which produces IFN-B. An autocrine signal initiated by IFN-B activates IRF-7, which produces IFN-a. A paracrine signal by IFN-B warns other cells.
How does complement fight infection?
Coats pathogens and makes them easier to identify and phagocytose; pokes holes through pathogen membranes
How does interferon affect NK cells?
Interferon recruits NK cells to sites of infection and increases their killing ability
How are complement coated pathogens recognized?
Complement receptors (CR1, CR2, CR3, CR4) on the surface of the macrophages
What are chemokines and how do they work?
Chemokines are a specific type of cytokine that recruit cells via a chemokine gradient; neutrophils, NK cells, etc. follow the gradient to find the greatest amount of infection
What are the three functions of the immediate innate immune system?
Identify pathogen, induce inflammation, kill pathogen/prevent pathogen from causing damage
Are the receptors on macrophages pathogen specific?
No, they recognize broad classes of pathogens
Fill in the blanks.
- Mannose Binding Lectin (MBL); 2. Mannose; 3. C4; 4. C4a; 5. C4b; 6. C2; 7. C2b; 8. C2a; 9. C2aC4b; 10. C3; 11. C3a; 12. C3b
How are pathogens opsonized with complement destroyed?
Macrophages and neutrophils recognize opsonized pathogens and phagocytose them
What other serum proteins function in the innate immune response?
Proteins of the coagulation cascade and proteins of the kinin system
What is the consequence of interferon signaling?
The anti-viral state will activate, which prevents viral replication, alerts other cells that they are infected, and improves the adaptive immune response
How do Nod-Like Receptors (NLRs) recognize pathogens and send a signal?
NLRs function similar to TLRS, except they bind to bacterial components within the cytoplasm
How does the complement system induce inflammation?
The C3a and C5a fragments (anaphalatoxins) induce an inflammatory response by inducing vascular permeability and acting as a chemoattractant for neutrophils and macrophages
How does the barrier function work?
A combination of mechanical, microbial, and chemical defenses in the skin, gut, lungs, and eyes/nose/mouth
What is the role of platelets in innate immunity?
Platelets release inflammatory mediators
How do neutrophils kill pathogens?
Respiratory burst, low pH, defensins, anti-microbial peptides, withholding nutrients from pathogens
What are acute phase proteins and how do they work?
Acute phase proteins are produced by the liver and function by marking pathogens for destruction
How are macrophages and neutrophils different?
Neutrophils are short-lived, are produced in response to inflammation, and are eaten by the macrophages once they die. Macrophages are long lived and reside in the tissues.
How do TLRs recognize pathogens and produce a signal?
The extracellular portion of the TLR recognizes the pathogen ligand; the inner portion of the TLR interacts with proteins to build a signaling complex, which amplifies the signal and activates gene transcription
How do pentraxins work?
Pentraxins bind to pathogens with one domain and interact with phagocyte receptors with the other, inducing phagocytosis
How does macrophage activation lead to inflammation?
It leads to the expression of pro-inflammatory cytokines and chemokines
What is the role of inflammation in the innate immune response?
Inflammation increases vascular permeability, activates endothelium, mobilizes fat metabolism to generate heat, and recruits/activates NK cells
How do pathogens damage tissues?
Exotoxins, endotoxins, direct cytopathic effect
What are the receptors on macrophages and what do they recognize?
The receptors are Pattern Recognition Receptors, and they recognize Pathogen Associated Molecular Patterns (PAMPs)
What causes fever and why is it good?
Pyrogens (mainly IL-6) induce fever in response to pyrogenic pathogens. Fever is good because it slows down pathogen growth/replication, makes the innate response work better, and makes healthy cells more resistant to the effects of TNF-a and other molecules
How is the membrane attack complex assembled?
C3b attaches to C3bBb to form C3b2Bb. This complex cleaves C5 into C5a and C5b. C5b recruits C6 and C7, and C7 gets stuck in the membrane. C7 recruits C8, which imbeds in the membrane and recruits C9. C9 recruits more C9 to form a pore in the membrane.
What are NK cells and how do they function during innate response?
NK cells are lymphoid cells that kill other cells infected with viruses and produce signals that can activate macrophages
What mechanism(s) prevent pathogens from inactivating complement?
Factor P
How do neutrophils find infected tissues?
Neutrophils express adhesion molecules that interact with complementary adhesion molecules on infected cells; neutrophils then migrate into the infected tissue via extravasation and follow the chemokine gradient
What are the steps of extravasation?
Rolling adhesion, tight binding, diapedesis, migration
How does the inflammasome work to amplify IL-1B?
The inflammasome activates caspase 1 from the inactive form procaspase 1, which cleaves inactive pro-IL-1B to form active IL-1B
