New model shows promise to treat lung fibrosis in Covid-19 patients

A new study published in the journal Science Advances revealed a promising molecular target to improve pulmonary fibrosis. Read on to find out more.

By: Arushi Bidhuri | | Updated: December 8, 2020 9:00 am

A new study published in the journal Science Advances revealed a promising molecular target to improve pulmonary fibrosis. Read on to find out more.

As Covid-19 continues to affect millions worldwide, many breakthroughs studies have surfaced, linking coronavirus with other diseases. In a recent study published in the journal Science Advances analyzed lung tissues from patients with different types of pulmonary fibrosis – including cases triggered by Covid-19 – has revealed a promising molecular target to improve the chronic and irreversible disease. Also Read - COVID-19 Live Updates: Cases in India surge to 10,571,773 while death toll reaches 1,52,419

Pulmonary fibrosis is a lung disease that happens lung tissues become damaged and scarred. This makes it harder for the lunge to work properly. Symptoms of the disease include shortness of breath, a dry cough, feeling tired, and weight loss. Also Read - Adverse events post Covid-19 vaccination: AIIMS' security guard admitted to ICU

The findings

For the study, researchers studied mouse models and patients of pulmonary fibrosis. Also Read - Delhi health workers suffer mild reaction post COVID-19 vaccine: What you should expect

Experiments in mouse models of lung fibrosis showed that administering blockers of an epigenetic regulator called MBD2 via intratracheal inhalation protected the mice against fibrotic lung injury, highlighting a potentially viable therapy.

A poor understanding of what causes pulmonary fibrosis has greatly hindered the development of treatments, and to this day, no effective therapy is available other than lung transplantation.

The researchers from Shenzhen University in China studied lung samples from patients with pulmonary fibrosis triggered by one of three causes: SARS-CoV-2 infection, systemic sclerosis-associated interstitial lung disease, or an unknown factor.

The researchers also studied mouse models of pulmonary fibrosis, which they induced in the animals by administering the compound bleomycin.

All cases of pulmonary fibrosis, they found, were characterized by overexpression of MBD2.

This activity localised in areas occupied by macrophages – known contributors to the development of pulmonary fibrosis.

To investigate this further, the scientists depleted the Mbd2 gene in macrophages of mice, which protected the animals against pulmonary fibrosis, characterized by markedly reduced macrophage accumulation in the lung following administration of bleomycin.

As well, direct administration of liposomes — established carriers of inhaled drugs — loaded with MBD2 silencer RNA into the trachea of mice protected them from lung injuries and fibrosis.

“Since MBD2 itself does not affect the essential epigenetic process of DNA methylation, inhibiting the molecule could prove to be a safe way to treat pulmonary fibrosis,” the study authors wrote.

“However, future studies will first need to assess the impact of altered MBD2 expression in other types of cells relevant to pulmonary fibrosis, they noted.

(with inputs from IANS)

Published : December 7, 2020 3:08 pm | Updated:December 8, 2020 9:00 am

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