Teachable moment in classrooms:
- tissues chapter – elastin and collagen fibers in connective tissues
- respiratory system chapter – microscopic structure of alveoli
- respiratory system chapter – changes in lung volume during ventilation
- cellular basis of life chapter – general action of receptors on cell surface
The news item: Recently the following article appeared online:
Overactive genes contribute to long COVID lung fibrosis
A handful of overactive genes that regulate the immune response cause debilitating lung fibrosis, researchers find.
The article describes research that identified interleukin 6, CD47 and pJUN genes that make COVID-19 survivors’ lungs resemble the lungs with pulmonary fibrosis. The article also states that those three genes are active in scar formation, and that in mice the fibrosis was stopped by blocking interleukin 6 and CD47 action.
So, Why Do I Care?? Currently, approximately 23 million people in the US have long-COVID (defined by having disease symptoms longer than 3 months after the initial infection). Many of these people have respiratory symptoms such as debilitating shortness of breath and difficulty breathing. Research into the causes into the molecular details of the chronic fibrosis might lead to remedies that greatly improve the quality of life of long-COVID patients.
Plain English, Please!!! Let’s talk about what the nature of the fibrosis is seen in the lungs of long-COVID patients. In the walls of alveoli, away from the respiratory membrane, there is a layer of connective tissue normally dominated by the stretchable elastic fibers. In lung fibrosis the elastin fibers are degraded and replaced with collagen fibers that are not stretchable. The cells that make the connective tissue are called fibroblasts. The increased volume of collagen-rich connective tissue and increased number of fibroblasts is the hallmark of fibrosis we observe in the lungs of long-COVID patients. Apparently, this process is similar to scar formation in the skin.
Second, let’s talk about how fibrosis limits lung function. The accumulation of fibrotic tissue in the lung doesn’t affect the gas exchange process in the alveoli, but, rather, it makes ventilation more difficult.