Luis Ulloa

TL;DR: It is reported that the nicotinic acetylcholine receptor α7 subunit is essential for inhibiting cytokine synthesis by the cholinergic anti-inflammatory pathway.

TL;DR: The authors showed that nicotine attenuates serum HMGB1 levels and improves survival in experimental models of sepsis, even when treatment is started after the onset of the disease and suggest that selective nicotinic agonists for the α7nAChR might have therapeutic potential for the treatment of septicemia.

TL;DR: Observations demonstrate that specific inhibition of endogenous HMGB1 therapeutically reverses lethality of established sepsis indicating thatHMGB1 inhibitors can be administered in a clinically relevant time frame.

TL;DR: The results indicate a mechanism of transmodulation between the STAT and SMAD signal-transduction pathways that prevents the interaction of Smad3 with the TGF-β receptor.

TL;DR: It is shown that vagus nerve stimulation fails to inhibit tumor necrosis factor (TNF) production in splenectomized animals during lethal endotoxemia, revealing a specific, physiological connection between the nervous and innate immune systems that may be exploited through either electrical vagu nerve stimulation or administration of α7 agonists to inhibit proinflammatory cytokine production during infection and tissue injury.