Steplewski, A., Fertala, J., Arita, M., Romero, F., Summer, R., Fertala, R. Target-Specific Delivery of an Antibody That Blocks the Formation of Fibrotic Deposits in Keloid and Lung Fibrosis Models, Monoclon Antib Immunodiagn Immunother. 
This study demonstrates our ability to deliver a novel antifibrotic antibody to the lung and provides preliminary evidence that this biologic may be effective in the treatment of pulmonary fibrosis.
Freddy Romero, Xu Hong, Dilip Shah, Caleb B. Kallen, Ivan Rosas, Zhi Guo, DeLeila Schriner, Julie Barta, Hoora Shaghaghi, Jan B. Hoek, Clementina Mesaros, Augustine M. Choi, Nathaniel W. Snyder, and Ross Summer, Lipid synthesis is required to resolve ER stress and limit fibrotic responses in the lung Am J Respir Cell Mol Biol. 2018.
This study provides a unifying mechanism linking ER stress to the development of pulmonary fibrosis. We show that metabolic dysfunction, namely the impairment of lipid synthesis, reduces the capacity of alveolar epithelial cells to resolve ER stress, leading to sustained cellular dysfunction and induction of fibrotic responses. We also provide evidence that pharmacological or dietary approaches to increasing lung lipids could be effective in treating pulmonary fibrosis.
Shah, D., Romero, R., Duong, M., Wang, N., Paudyal, B., Suratt, B., Kallen, C.B., Sun, J., Walsh, K., Summer., R. Obesity-induced adipokine imbalance impairs mouse pulmonary vascular endothelial function and primes the lung for injury. Sci Rep. 2015 Jun 12;5:11362. PMID: 26068229.
This study uncovers a novel mechanism that appears to explain why obesity predisposes patients to developing ARDS, and in the process, might have discovered a novel strategy for preventing ARDS in obese individuals.
Romero F, Shah D, Duong M, Penn RB, Fessler MB, Madenspacher J, Stafstrom W, Kavuru M, Lu B, Kallen CB, Walsh K, Summer R. A Pneumocyte-macrophage Paracrine Lipid Axis Drives the Lung Toward Fibrosis. Am J Respir Cell Mol Biol. 2014 Nov 19. E-pub ahead of print [PMID:25409201].
This study is the first to suggest that macrophage foam cells play a causal role in the development of pulmonary fibrosis and that strategies aimed at blocking their formation might be effective in limiting the onset and progression of disease.
Romero, F., Shah, D., Duong, M., Stafstrom, W., Hoek, JB., Kallen, CB., Lang, CH. , Summer, R. Chronic alcohol ingestion in rats alters lung metabolism, promotes lipid accumulation and impairs alveolar macrophage functions. Am J Respir Cell Mol Biol 2014 Jun 8 [PMID: 24940828].
This work demonstrates that chronic alcohol exposure induces significant metabolic changes in the lung, including marked accumulation of triglycerides and free fatty acids within distal airspaces and alveolar macrophages (AMs). Furthermore, this study provides evidence linking these lipid abnormalities to phenotypic and functional impairments in AMs, suggesting that metabolic disturbances may be contributing to the pathogenesis of alcohol-related inflammatory lung diseases.