Respiratory Infection and Hstopathology (Xiao Su)
Severe pneumonia caused by bacterial (E. coli, Pseudomonas) or viral (influenza virus) infection can evolve into the clinical syndrome of acute lung injury (ALI), a major cause of respiratory failure that requires intensive care and life support (Matthay and Su, Nature Med, 2007). The mortality of ALI remains high (~40%) despite the best supportive care. Therefore, better understanding the mechanisms and new potential therapies are urgently needed to combat this deadly disease. This commitment leads us to exploring novel mechanisms and therapeutic targets for ALI.
In the past decade, we have investigated the role of alveolar fluid clearance and pulmonary barriers in acute lung inflammation and injury (Su, Intensive Care Med 2003& 2004; Su, Am J Physiol Lung Cell Mol Physiol 2006); the role of protease activated receptor 1 and 2 during lung neurogenic inflammation and ventilator induced ALI (Su, JI 2005; Looney, JCI 2006); the role of neutrophils in acute lung inflammation and injury (Su, JI 2007; Su, Am J Respir Crit Care Med 2012); using mesenchymal stem cells as a therapy for ALI (Gupta, JI 2007; Su, Am J Physiol Lung Cell Mol Physiol 2009); the effects of CFTR on neutrophils and platelets in the development of acute lung infection and inflammation (Su, Inflam Res 2011; Zhao, PLoS One 2013; Wu, PLoS One 2014). More importantly, we have found that activation of vagus nerve-α7 nAChR pathway could regulate acute lung infection and inflammation (Su, Am J Respir Cell Mol Biol 2007; Su, JI, 2010; Su, Mol Med, 2013; Wu, Biomed Res Int 2014; Yang, QJM 2014).
Our ongoing projects aim at: (1) To study how vagus nerve-α7 nAChR pathway regulates the host inflammatory response to bacterial or viral lung infection; (2) To investigate how this pathway affects anti-inflammatory memory of macrophages during infection and inflammation, and (3) To test whether and how activation of this pathway could regulate function of proinflammatory cells and stem cells and determine outcome of acute lung infection and immunity. We have opened a new field in neuroimmune regulation of acute lung infection and inflammation.