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OSU Researchers Discover Marker for Pulmonary Fibrosis

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Posted: 7/24/2007

COLUMBUS, Ohio – Researchers have identified a specific growth factor that appears to contribute to the development of pulmonary fibrosis, suggesting they may be close to finding a cause for even the most puzzling form of the lung disease.

The findings by lung and critical care researchers at Ohio State University Medical Center show the growth factor M-CSF initiates a process that promotes inflammation, producing collagen, or scar tissue, that causes fibrosis. M-CSF was found even in lung fluid from patients with idiopathic pulmonary fibrosis, a form of the lung disease with no known cause.

The study appears in a recent issue of the American Journal of Respiratory and Critical Care Medicine.

The scientists measured lung inflammation and fibrosis in mouse models and studied fluid from the lungs of patients with idiopathic pulmonary fibrosis.

“We wanted to define the role of monocytes and macrophages and the growth factor M-CSF in the initiation and progression of pulmonary fibrosis,” says Dr. Clay B. Marsh, director of OSU Medical Center’s Center for Critical Care and principal investigator of the study.

“Our data shows a connection between M-CSF and other factors that recruit and activate fibroblasts in the lung to make scar tissue.”

The scientists observed that M-CSF works to promote inflammatory cell recruitment and induces proteins that recruit and activate fibroblasts in the lungs, all of which contribute to scarring.

Pulmonary fibrosis is marked by debilitating scarring of the lungs. Early observations suggest that decreasing the risk for scarring is linked to reducing the presence in the lungs of monocytes and macrophages – derivatives of blood cells that are involved in fighting infection. The macrophages are a critical component of this lung disease and appear to direct the recruitment of other cells like fibrosis – the scarring results from the contributions of these cells.

Worldwide, approximately 5 million patients suffer from pulmonary fibrosis, usually because of inflammation caused by various lung conditions. Once scarring occurs, the tissue becomes even thicker, inhibiting the transfer of oxygen into the bloodstream.

Cigarette smoking, environment toxins and autoimmune diseases are associated with development of pulmonary fibrosis, but in a growing number of cases, its cause cannot be determined. Current medications used to treat the scarring include steroids, some cancer drugs and immunotherapy; however, none of these strategies has a predictable protective effect.

The latest observations are significant because there has been no prior reported link for the role of M-CSF in the development of pulmonary fibrosis in animals or humans, Marsh says. In addition, because M-CSF was found in the lung fluid of patients with idiopathic pulmonary fibrosis, researchers are confident that a new direction in treating this disease may be possible.

“This research has identified M-CSF as a new marker for pulmonary fibrosis, as well as a potential new therapeutic target,” adds Marsh.

Along with Marsh, other Ohio State researchers involved in the study were Christopher P. Baran, Benjamin D. Bringardner, Melissa G. Hunter, Sara McMaken, Christie A Newland, James M. O’Brien, Jr., Judy M. Opalek and Paul C. Stromberg, and were joined by investigators from the University of Iowa, Gary W. Hunninghake and Martha M. Monick.

Funding from the National Heart, Lung and Blood Institute supported this research.


Sherri L. Kirk
Medical Center Communications

Lung Diseases; OSU Medical Center