Yes, sort of.

I think you are combining damage release triggers (DAMP ligands) and cytokine/chemokines (DAMP signalling) produced by pathways.  HMGB1, S100, heat shock proteins, advanced glycation end products (AGE), and even uric acid are triggers for DAMP receptors. Many of the DAMP receptors are shared with PAMP signalling. Binding to the receptors causes release of the cytokines/chemokines of the immune system,(e.g. TNFa, TGFb, etc.)

Here is a pretty good paper on it that covers much more than I mentioned. The area is still being worked out. DAMP signalling is not completely understood, but a lot of progress is happening.

http://jasn.asnjournals.org/content/22/3/416.full

When TLR4 gets overstimulated by injury (large radiation burn for instance) it will do the same thing as it does in sepsis.

Thank you Mr. Hanley. Your contribution will be of great value to my work.

Thank you Mónica!