Investigation of the epithelial-mesenchymal trophic unit in idiopathic pulmonary fibrosis
A fellowship to fill the gap in understanding the factors that drive idiopathic pulmonary fibrosis (IPF).
Dr Franco Conforti’s research has taken on a whole new level of urgency and importance in recent months. His Foundation-funded fellowship examines the factors which drive idiopathic pulmonary fibrosis (IPF), an incurable lung disease which causes shortness of breath, coughing and fatigue.
Before the pandemic, 15,000 people in the UK were thought to be living with IPF. However, there is growing concern that long-term lung damage, as seen in patients with IPF, could now be more widespread.
I’m really thankful to the Medical Research Foundation for allowing me to repurpose my funding, which will help me continue my respiratory research and answer important questions around the long-term impact of SARS-CoV-2 on the lungsDr Franco Conforti
IPF occurs when fragile parts of the lungs become damaged and scarred. This scarring is irreversible and, in some cases, can get worse over time. The causes are unknown and current treatments do not stop the progression of disease – they only slow it down.
Franco, a research fellow from the University of Southampton, is looking at the interaction between cells in the lung; specifically, alveolar cells and fibroblasts. Fibroblasts, which are usually responsible for promoting wound healing, behave abnormally in patients with IPF and produce excess scar tissue. Fibroblasts eliminate the airspaces where alveolar cells would normally allow gas exchanges in respiration. Franco’s work examines whether alveolar cells can be protected from the damaging effects of fibroblasts.
“I’m really thankful to the Medical Research Foundation for allowing me to repurpose my funding, which will help me continue my respiratory research and answer important questions around the long-term impact of SARS-CoV-2 on the lungs,” says Franco.
“Although research into lung damage caused by COVID-19 is only just beginning, we think people with a mild form of the virus are unlikely to suffer long-term damage. However, people with a very strong infection are more vulnerable to the complications we’ve seen in patients with IPF.”
As human alveolar cells are difficult to study, Franco has established new ways to isolate and store them, in order to mimic the effects of SARS-CoV-2 on alveolar cells.
Franco adds: “It’s very important to investigate how the virus finds its way down into the lungs and how it compromises the ability of cells – for example fibroblasts - to heal the lung. We need to know the secondary, long-term impact of the virus. What is the extent of the lung damage, and is it likely to be get worse over time?
“The ultimate aim of my research is to find potential targets to treat COVID-19 and prevent the development of lung fibrosis. We can do this by reproducing the effects of the virus in the lab using human alveolar cells and human lung fibroblasts. Alveolar cells are the bricks that make up the respiratory epithelium. If they are infected by this new coronavirus, the integrity of the respiratory epithelium is compromised. After such injury, fibroblasts step in to support wound healing in the lung.
“Normally, fibroblasts should disappear after they have helped to rebuild cells in the lung but in IPF, fibroblasts aren’t acting in the same way. We think there’s a fault in how alveolar cells and fibroblasts are communicating. When they’re supposed to be switched off, they’re instead proliferating and increasing progression of the scarring.”
Franco is glad to be back in the lab, and hopes his work will benefit COVID-19 patients who have suffered lung damage.
“It’s fantastic seeing more colleagues coming back in the lab, and it feels like things are gradually getting back to normal. The need for social distancing has obviously slowed down my work a little, but everyone has been really supportive.”
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