Does intestinal ischemia/reperfusion injury trigger activation of innate toll-like receptor 4 and adaptive chemokine programs?
This study is the first to demonstrate increased expression of TLR4 and NF-kappaB after warm intestinal IRI. This detrimental cascade may be initiated by TLR4 via NF-kappaB signaling pathways, implicating TLR4 as a potential therapeutic target for the prevention of intestinal IRI.
The present study demonstrates that there is no shift in cytokine balance towards a Th2 profile in former UNTAC soldiers with symptoms similar to those of the Gulf War syndrome.