NIH Funds Research Into Immune Mechanisms to Reverse Fibrosis

Marisa Wexler, MS avatar

by Marisa Wexler, MS |

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The National Institutes of Health (NIH) has awarded a grant to support research into immune mechanisms that could allow for the reversal of fibrosis, or tissue scarring, in idiopathic pulmonary fibrosis (IPF).

The $469,034 award went to Narendiran Rajasekaran, PhD, and Archana Varadaraj, PhD, both of whom are assistant professors in the department of chemistry and biochemistry at Northern Arizona University.

The team plans to build on prior research that focused on the role of a protein called fibronectin in certain kinds of cancers. Fibronectin is a key component of the extracellular matrix, or ECM, which is the mesh of proteins and other substances that helps to support cells in the body’s tissues.

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IPF and other forms of pulmonary fibrosis are characterized by lung tissue scarring. Biologically, scarring is driven by the excessive production of ECM components, resulting in tissue being abnormally hard, stiff, and inflexible. Fibrosis often is accompanied by inflammation.

Fibrosis and inflammation in IPF are both coordinated by the activity of signaling molecules called cytokines. Some cytokines are pro-inflammatory, meaning they promote inflammation, while others suppress the activity of the immune system.

In prior work, researchers have shown that targeting fibronectin using a conserved immunosuppressive protein domain — a small piece of protein with a particular structure that is commonly found in immune-suppressing cytokines — can reverse fibrosis in mouse models of the disease.

The new funding from the NIH will allow researchers to conduct further tests with the hope of understanding exactly which immune mechanisms are responsible for this reversal. Ultimately, they hope to uncover new strategies for stopping fibrosis that could be translated into treatments.

“Like numerous disease states, IPF develops from the contribution of the microenvironment such as the extracellular matrix and immune milieu and defects within the cells that are intrinsic. Hopefully the NIH funding will allow us to identify the contribution of each of these factors with a goal of targeting it,” Varadaraj said in a press release.

“Ultimately, we hope to provide therapeutic agents that can be used either on their own or in combination with existing therapies to reverse fibrosis and restore lung function,” Varadaraj added.

Rajasekaran and Varadaraj will work closely with Megha Padi, PhD, director of the Bioinformatics Shared Resource at the University of Arizona Cancer Center, who is an expert in computational genomics and will serve as a collaborator in the project. The team also will mentor several students over the course of the project, instructing them about how to carry out experiments using several techniques, analyze the results and present findings at national conferences.

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