Notes 3.6

e. Diseases associated with NODs
> Crohn’s disease
-chronic bowel inflammation
-mutation to NODs—inability of cells to respond to peptidoglycan
>Blau syndrome
-chronic organ inflammation
**over-active NOD proteins, so concentration too high
III. Nuclear factor kappa-B (NF-kappa-B) and cytokine gene expression
>transcription factor: protein that binds to particular sequences of DNA
(promoter, enhancer) that enables RNA polymerase to transcribe that gene
a. MyD88 and TRIF
>TLR binds to microbial motif w/ extracellular domain thisinteraction
With MyD88 or TRIF
**both examples of signal transduction proteins
>most TLRs interact with MyD88
>TLR3 interacts with TRIF
>TLR4 interacts w/ bothactivate a more aggressive inflammatory
response
b. Phosphorylation cascade
>common way of signal transduction
-TLRMyD88phosphorylation of many signaling proteins
phosphorylation of I-kappa-B(inhibitor of NF-kappa-B)
destruction of I-kappa-Bactivate NF-kappa-B, moves to
nucleusactivates transcription of cytokines

Inflammation
I. Inflammation overview
a. TLRs and NODs
b. NF-kappa-B
c. Expression of inflammatory cytokines
d. rubor, calor, tumor dolor
>symptoms from making vessels leaky so immune cells (like
neutrophils) can get to infection site
II. Mediators of inflammation
a. Cytokines
i. Inflammatory cytokines
1. IL-1-beta
>attracts neutrophils, makes endothelia stickier
2. TNF-alpha
>increase catabolism in cells to get energy
>makes endothelia stickier

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