Pulmonary Fibrosis Patient’s Age May Affect Stem Cells’ Ability to Prevent Damage

Patricia Inácio, PhD avatar

by Patricia Inácio, PhD |

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A team of researchers report that a mouse’s age influences the ability of its mesenchymal stem cells to repair pulmonary fibrosis-induced damage, a finding with significant implications for stem cell therapies. The study, “Therapeutic benefits of young, but not old, adipose-derived mesenchymal stem cells in a chronic mouse model of bleomycin-induced pulmonary fibrosis,” was published in the Translational Research journal.

Previous studies have shown that while pulmonary fibrosis-induced injuries can spontaneously resolve in young mice, they remain irreversible in the lungs of old mice, suggesting that the efficiency of pulmonary regeneration and repair pathways is linked to age.

Since there currently are no drugs that can reverse pulmonary fibrosis damage, a team of researchers from the Miller School of Medicine, University of Miami, hypothesized that a patient’s own mesenchymal stem cells (MSCs) could promote repairing mechanisms in the lungs and that age may influence the MSCs efficiency (MSCs are adult stem cells traditionally found in the bone marrow). To this end, the team investigated the potential of donor MSCs, obtained from young and old mice, in inhibiting bleomycin-induced pulmonary fibrosis (the most common experimental study model of human lung fibrosis) in older mice.

Scientists observed that lung tissue from older bleomycin-induced pulmonary fibrosis mice infused with young adipose-derived MSCs (ASCs) exhibited decreased fibrosis, reduction of oxidative stress, and markers of cell death. However, mice lungs treated with ASCs from older mice showed no decrease in fibrosis or cell death markers.

Marilyn K. Glassberg, MD, study lead author and Professor of medicine, surgery and pediatrics, Director of the Interstitial Lung Disease Program, Director of Pulmonary Diseases at the Interdisciplinary Stem Cell Institute, and Vice-Chair of Medicine for Diversity and Innovation, said in a press release, “Donor stem cells from younger mice were effective in preventing damage when infused into older mice at the same time as a disease-causing agent. However, donor MSCs from older mice had virtually no effect.”

Dr. Glassberg added, “Our study found that the age of the donor animal is important. This would indicate that it’s unlikely that infusions of autologous stem cells from the body of an older patient would be effective in treating pulmonary disease.”

The findings carry a significant relevance for clinical-based stem cell therapies in older patients with damaged lungs.

“We plan to continue to develop more representative models of human pulmonary fibrosis. Our goal is not only to develop a preventive model of disease but also to search for a way to offer safe and effective clinical treatments for patients with this deadly disease,” concluded Dr. Glassberg.