Lec 32 Immune Response to Infectious Pathogens Flashcards
What is host response to extracellular bacteria [innate and adaptive]?
innate: phagocytosis, alternative complement activation, inflammation
adaptive: same effector mech as innate but initiated by antibodies that also neutralize microbes/toxins
What is the body’s response to superantigen? What are examples of these antigens?
- systemic inflammatory response
- superantigens bind to Class II MHC randomly on any APC and bind T cell, trigger T cells to respond as if were interacting with their specific antigen even though they aren’t, get polyclonal activation of T cells and cytokine storm
- examples: exotoxins like SEA [staph aureus], SEB [staph aureus], TSST [staph aureus], TSLS [strep pyogenes]
What is the local and systemic protective response of the immune system to LPS [on gram neg] or lipoteichoic acid [on gram pos]?
local: microbe comes along, triggers endothelial cells to release cytokines [TNF, IL-1, IL-6] which cause inflammatory response, increased blood flow, changed in vascular permeability, etc
cytokines then recruit other leukocytes to site of infection
systemic:
- trigger fever
- acute phase proteins release from liver [C reacitve protein, mannan binding lectin, serum amyloid protein]
- leukocyte production in bone marrow
what are the potential pathologic effects of endotoxin LPS [on gram -] or lipoteichoic acids [on gram +]?
- can cause septic shock
- lead to release of acute phase cytokines which have some protective and some pathologic effects
- ex. the pathologic effects of TNF
- — decrease cardiac function
- — increased vascular leakage and potential thrombus formation
- — metabolic abnormalities –> insulin resistance, wasting syndrome
What are the pathologic effects of TNF that we talked about?
- — decrease cardiac function
- — increased vascular leakage and potential thrombus formation
- — metabolic abnormalities –> insulin resistance, wasting syndrome
What are 3 examples of acute phase proteins released from liver in response to IL-1/IL-6 in infection
- C reactive protein
- mannan binding lectin
- serum amyloid protein
N. gonorrhoeae: what is mech of immune evasion?
- antigenic variation
Strep pyogenes: what is mech of immune evasion?
- M protein resists phagocytosis
- resists alternative path of complement
Strep aureus: what is mech of immune evasion?
- catalase: inhibits ROS from phagosome so avoids digestion
- coagulase: causes clot formation
Strep epidermidis: what is mech of immune evasion?
- biofilm formation
Where do intracellular bacteria replicate? Why is this beneficial for them?
- survive or replicate in phagocytes
- means they are not susceptible to circulating antibodies –> thus recovery depends solely on cellular immunity and cytokine production
What is host response to intracellular bacteria [adaptive and innate]?
innate: first response, NK cells and phagocytes control bacterial growth in absence of adaptive
adaptive: starts at 7 days, T cells release cytokines [IL-12] trigger Th1 response that activates phagocytes
What are 3 examples of intracellular bacteria?
- mycobacteria
- listeria
- legionella
How do intracellular microbes survive in phagocytes?
- some survive within phagolysosomes
- some escape from phagolysosome into cytoplasm
What is immune mech for killing microbes located within vesicles [phagolysosomes]?
- cytokines [mainly IFN gamma] secreted form TH1 and TH17 act on cells that have phagocytosed microbes
this: - upregulates their ROS activity so they kill ingested microbes
- causes them to secrete TNF, IL-1, IL-12 [inflammation, TH1 differentiation]
- causes them to increase expn MHC and costimulators [so more susceptible targets of killer cells, amplify T cell response]
What is immune mech for killing microbes located in cytoplasm?
- CD8 T cells kill phagocytes that are expressing MHC and costimulators
Is TB in phagolysosome or in cytoplasm?
phagolysosome
Is listeria in phagolysosome or cytoplasm?
cytoplasm
