Lecture 18

1.
What are the activities of different cells during a bacterial infection?
Platelets form closts, mast cells induce inflammation, neutrophils lyse pathogens, macrophages release chemokines
2.
What causes vasodilation?
Histamines, heparin
3.
What are common PAMPs?
DNA, LPS, flagellin, peptidoglycons
4.
Which PAMPS are unique to Gram negative bacteria?
LPS
5.
6.
Why is LPS only in gram negative bacteria?
The outer lipid membrane makes them negative to gram staining
7.
What are the regions of lipopolysaccharide?
Lipid A, inner core, outer core, O antigen
8.
Which region of LPS is recognised by TLR4?
Lipid A
9.
What type of toxin is LPS?
Endotoxin
10.
What coreceptor is associated with TLR4?
CD14
11.
What facilitates binding of LPS to TLR4?
LBP
12.
What is activated by LPS binding to TLR4?
NF-kβ
13.
What does NF-kβ do?
Transcription factor to produce IL-1β, TNF-⍺
14.
What is the progression of bacterial infection to septic shock?
Infection -> bacteremia -> lysis/endotoxins -> cytokine storm
15.
What are the results of TNF⍺ secretion?
decrease appetite, fever, vasodilation, sitmulation of macrophages
16.
What are the results of IL-1β secretion?
Vasodiltation, macrophages
17.
How do immune responses to meningococcus affect blood vessels?
Alteration of coagulation pathways, intravascular coagulation, damage to weakened endothelium
18.
What causes rash from meningococcus infection?
Bleeding into tissues
19.
What does progression of meningococcus infection lead to?
Necrosis, multi organ failure
20.
What bacteria affect MHC complexes (superantigens)?
S. aureus, S. pyogenes
21.
What makes superantigens more disruptive than peptides that activate MHC?
Superantigens can bind 20% of immune T cells
22.
What do superantigens activate?
NF-kβ