Silicosis-induced PF Rats Went Into Remission After Fat Stem Cell Transplant, Study Shows

Iqra Mumal, MSc avatar

by Iqra Mumal, MSc |

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Transplantation of stem cells derived from adipose (fat) tissue in an animal model of silica dust-induced pulmonary fibrosis led to remission of the disease, as well as a reduction in inflammation and cell death, a new study shows.

The study reporting the findings, “Transplantation of adipose-derived mesenchymal stem cells attenuates pulmonary fibrosis of silicosis via anti-inflammatory and anti-apoptosis effects in rats,” was published in the journal Stem Cell Research & Therapy.

Silicosis — the inhalation and retention of silica dust in the lungs — can lead to lung epithelial cell injury and development of pulmonary fibrosis. While the mechanisms that lead to silica-induced fibrosis are not fully clear, it is likely related to the inflammatory and apoptosis (cell death)-inducing properties of silica dust.

Many attempts have been made to treat silicosis by repairing the injured cells. However, these attempts have not been successful and show limited effectiveness. This has lead researchers to investigate the use of stem cell transplantation.

Recently, many studies have explored the role of mesenchymal stem cells (MSCs) in the regulation of immunity and tissue remodeling in animal models of lung fibrosis. MSCs are a promising therapeutic option in the field of regenerative medicine, as they secrete anti-inflammatory molecules called cytokines and growth factors, they migrate to the site of injury when administered, and they can rescue dysfunctional cells.

However, the use of adipose-derived MSCs (AD-MSCs) has not been investigated in the treatment of silicosis. As a result, this study set out to determine the therapeutic effect of AD-MSC transplantation in a rat model of silica-induced lung fibrosis.

The animals underwent silica exposure for 24 hours, after which AD-MSCs were given to the treatment group; 28 days after AD-MSC transplantation researchers examined organ damage, inflammatory cytokines, levels of apoptosis, and pathological and fibrotic changes in lung tissue.

As expected, results demonstrated that exposure to silica led to significant pulmonary fibrosis. Importantly, treatment with AD-MSC transplantation led to a remission of pulmonary fibrosis. In fact, researchers determined that after AD-MSC transplantation, the inflammatory response induced by silica significantly decreased.

Additionally, levels of an indicator of apoptosis — Caspase-3 protein — significantly decreased. This was accompanied by a concurrent increase in the Bcl-2/Bax ratio, another indicator of reduced apoptosis. Thus, AD-MSC transplantation not only counteracts the silica-induced inflammatory response, but also cell death.

“Anti-inflammatory and anti-apoptosis of AD-MSCs may play important roles in their anti-pulmonary fibrosis effect. Our data suggest that AD-MSCs may have a beneficial effect on pulmonary fibrosis and may represent the basis of a new treatment for patients with silicosis,” the team concluded. “Ongoing behavioral and biochemical assessment of long-term positive effects of AD-MSCs will provide further insight regarding the therapeutic potential of AD-MSCs for silicosis.”

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