I have seen reports of TLR2 or TLR4 directly interacting with NOX subunits to cause the production of ROS. If anyone has a couple of good articles that speak of this interaction, or of other TLR-dependent intracellular signaling that leads to NOX activation, please post!
Also, if anyone knows how TLR stimulation leads to the production of mitochondrial ROS, please let me know. I am interested in the intracellular signaling processes.
There could be a link between TLR4 activation of pkc, then pkc may is a potent activator of NADPHox.
http://www.plospathogens.org/article/info%3Adoi%2F10.1371%2Fjournal.ppat.1000930#ppat-1000930-g008
http://www.sciencedirect.com/science/article/pii/S1931312812000601
http://www.nature.com/nature/journal/v472/n7344/abs/nature09973.html
http://www.ncbi.nlm.nih.gov/pubmed/25130439
http://www.ncbi.nlm.nih.gov/pubmed/23770291
Dear Reid
Welcome to the central molecular process of inflammation.
Basically TLR activation leads to the release of pro-inflammatory cytokines, e.g. IL-6
The cytokines induce leucocytes like macrophages to release ROS
ROS oxidize also endogenous molecules like lipids, these become DAMPs
DAMPs activate TLRs and other PRRs. The loop closes.
See http://www.ncbi.nlm.nih.gov/pubmed/23436141
Cheers Kurt
Involvement of TLRs or Fcγ receptors (FcγRs) during phagocytosis induces recruitment of the autophagy protein LC3 to phagosomes with similar kinetics. Both receptors are known to activate NOX2 NADPH oxidase, which plays a central role in phagocytic cell killing of microorganisms by generating reactive oxygen species (ROS). Reference: https://sci-hub.wf/10.1016/j.imlet.2010.09.007