Philadelphia University + Thomas Jefferson University


Highlighted Publications

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. [201728972447]

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 SummerLipid 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.

Recent Publications

Silicosis decreases bone mineral density in rats

Severe airflow obstruction in a man with stomatitis and lymphadenopathy

Muc1 deficiency exacerbates pulmonary fibrosis in a mouse model of silicosis

Protein folding and the challenges of maintaining endoplasmic reticulum proteostasis in idiopathic pulmonary fibrosis

Target-Specific Delivery of an Antibody That Blocks the Formation of Collagen Deposits in Skin and Lung

Obesity-induced endoplasmic reticulum stress causes lung endothelial dysfunction and promotes acute lung injury

An official American thoracic society workshop report: Obesity and metabolism an emerging frontier in lung health and disease

Binding of CIB1 to the aIIb tail of aIIbβ3 is required for FAK recruitment and activation in platelets

T-cadherin deficiency increases vascular vulnerability in T2DM through impaired NO bioactivity

Chronic Obstructive Pulmonary Disease

Surfactant lipids at the host-environment interface metabolic sensors, suppressors, and effectors of inflammatory lung disease

Therapeutic advances in idiopathic pulmonary fibrosis

Pulmonary alveolar proteinosis: Pathogenesis, diagnosis, and management

C1q deficiency promotes pulmonary vascular inflammation and enhances the susceptibility of the lung endothelium to injury

Systemic Inflammatory Response Syndrome Criteria for Severe Sepsis

A pneumocyte-macrophage paracrine lipid axis drives the lung toward fibrosis

Obesity-induced adipokine imbalance impairs mouse pulmonary vascular endothelial function and primes the lung for injury

Direct effects of leptin and adiponectin on peripheral reproductive tissues: A critical review

Role of Angiotensin II type 1 receptor on renal NAD(P)H oxidase, oxidative stress and inflammation in nitric oxide inhibition induced-hypertension

To the editor