The Elias Laboratory

Jack A. Elias MD.

The Elias Laboratory is intensely interested in chronic inflammatory and remodeling responses in the lung. To optimally address these issues, the lab has established the techniques that allow one to express transgenes in a lung-specific fashion. In addition, the lab established systems that allow transgenes to be eternally regulated giving the investigator the ability to selectively express a gene at a specific point in time during development and the ability to turn a gene on and off at will. Studies in the lab are presently focusing on the inflammation and remodeling in asthma and COPD, the pathogenesis of pulmonary fibrosis and mechanisms of cytoprotection in acute lung injury. These studies are funded by multiple NIH RO1 grants, an NIH Program Project Grant (Dr. Elias is the Principal Investigator) and multiple industrial research awards. Recent scientific highlights include:

(a) The demonstration that chitinases are an essential part of the effector response induced by IL-13 and antigen in the lung that can be detected in the serum of humans with asthma where they correlate with disease severity.

(b) The elucidation of a novel cathepsin-dependent apoptotic pathway that plays a key role in the pathogenesis of emphysema in murine models and in human COPD.

(c) The demonstration that an early growth response gene-1 (Egr-1)-mediated apoptotic response plays a critical role in TGF- b 1 -induced tissue fibrosis.

(d) The demonstration that VEGF is a critical mediator in asthma where it induces tissue inflammation, airway remodeling, airway hyperresponsiveness and links in innate and adaptive immunity.

(e) The demonstration that IL-11 is a critical mediator of IL-13 effects in the lung.

(f) The demonstration that A1 is a critical mediator of tissue cytoprotective responses in the setting of oxidant-induced lung injury.

Many of these findings have led to patentable intellectual property and collaborations between Yale and Pharmaceutical companies developing new pulmonary therapeutics.