Research focuses on the effects of cigarette smoke and e-cigarette aerosols on susceptibility to acute respiratory distress syndrome (ARDS), a major cause of respiratory failure in critically ill patients.
ARDS remains a frequently fatal cause of acute respiratory failure, with an estimated U.S. incidence of nearly 200,000 cases per year and a mortality of 30%; no specific therapies beyond supportive measures have been demonstrated to be beneficial. Our research is focused on both improving our understanding of the pathogenesis of ALI and on developing novel biomarker-based strategies for diagnostic and prognostic purposes, with the ultimate goal of developing new preventative and therapeutic strategies for this devastating syndrome. To this end we have developed animal models of how smoke exposure affects the trajectory of viral and bacterial lung injury. More recently we have begun studying e-cigarette aerosols and their toxicity to human lung cells, exposing cultures of alveolar and airway epithelia (derived from human lungs declined for transplantation) in a novel aerosol generating machine.
Since their introduction a decade ago, e-cigarettes (e-cigs), which use a heated coil to aerosolize nicotine-containing e-liquids, have been aggressively promoted by tobacco companies as safe alternatives to cigarettes. The use of these devices has increased at an alarming rate across all segments of society and especially among adolescents, with 13% of US high school students reporting recent use in 2014.
The health consequences of smoking are primarily perceived to be cancer, cardiovascular disease, and chronic pulmonary disease, but acute pulmonary consequences of exposure to cigarette smoke are likely to be as or more important. However, there has been little research on smoking and acute lung injury a common cause of acute respiratory failure in critically ill patients.
University of Texas at Austin, BA, 1992-1997; University of California, Los Angeles MD/PhD, 1997-2006; University of California, San Francisco Internal Medicine Internship/Residency, 2006-2009; University of California, San Francisco Pulmonary & Critical Care Fellowship, 2010-2013
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Gotts JE, Matthay MA. Cell therapy for lung disease: a step forward. Chest 2013 Jun;143(6):1525–1527.
Gotts JE, Abbott J, Matthay MA. Influenza causes prolonged disruption of the alveolar-capillary barrier in mice unresponsive to mesenchymal stem cell therapy. Am. J. Physiol. Lung Cell Mol. Physiol. 2014 Sep;307(5):L395-406.
Gotts JE, Matthay MA. Endogenous and Exogenous Cell-Based Pathways for Recovery from Acute Respiratory Distress Syndrome. Clin. Chest Med. 2014 Dec;35(4):797–809.
Gotts JE, Matthay MA. Treating ARDS: new hope for a tough problem. Lancet Respir Med 2014 Feb;2(2):84–85.
Liu KD, Wilson JG, Zhuo H, Caballero L, McMillan ML, Fang X, Cosgrove K, Calfee CS, Lee J-W, Kangelaris KN, Gotts JE, Rogers AJ, Levitt JE, Wiener-Kronish JP, Delucchi KL, Leavitt AD, McKenna DH, Thompson BT, Matthay MA. Design and implementation of the START (STem cells for ARDS Treatment) trial, a phase 1/2 trial of human mesenchymal stem/stromal cells for the treatment of moderate-severe acute respiratory distress syndrome. Ann Intensive Care 2014;4:22.
Vaughan AE, Brumwell AN, Xi Y, Gotts JE, Brownfield DG, Treutlein B, Tan K, Tan V, Liu FC, Looney MR, Matthay MA, Rock JR, Chapman HA. Lineage-negative progenitors mobilize to regenerate lung epithelium after major injury. Nature 2015 Jan;517(7536):621–625.
Gotts JE, Matthay MA. Sepsis: pathophysiology and clinical management. BMJ 2016;353:i1585.