What does COVID-19 do to the lungs? What is a Surfactant?
Let me try to answer these questions.
We see below the alveoli, the respiratory part of our lungs.
We can see the alveolar sacs.
These are our main focus. Because in this Covid19 disease, deterioration occurs on the surface of these sacs.
Let’s take a closer look at their structure:
The inside of these alveolar sacs are covered with two different types of cells. We will examine these two different types called Type 1 and Type 2.
In their normal structure, the alveoli are covered with 93% type 1 cells and 7% type 2 cells. These cells form the inner surface of the alveolus. Oxygen enters from these cells.
These alveoli are shaped like a sac and are hollow. Air gets filled in there. But there is a surfactant substance between these cells and inside the sac, and it covers the cells.
The purpose of the surfactant is to ‘reduce surface tension’. This means that the lung can open and close like a sponge, thanks to this surfactant. If it wasn’t for the surfactant, the lungs would sink down and remain deflated.
The surfactant is very fatty. Therefore, it is slippery and solvent, just like detergent.
The fats inside are called phospholipids. They have different names like phosphatidylcholine or phosphatidylinositol.
We need to understand that the more phospholipids there are, the more slippery and flexible it becomes.
Even babies have the surfactant upon birth. But if the surfactant is not produced in some preterm babies, they will have respiratory distress in 24–48 hours after birth. This is called ARDS, acute respiratory distress syndrome. As can be seen, respiration becomes insufficient in just 24–48 hours. In other words, not having the surfactant causes trouble very quickly. So doctors fix the condition immediately by giving surfactant to the babies and doing some additional treatments. Our subject is respiratory distress in adults. We wonder, is this covid19 ARDS condition similar to that in children?
Let’s step back and see how we produce this surfactant in the alveoli:
Type 1 cells:
As the majority in the alveoli, type 1 cells are responsible for gas exchange. They are flat cells. They cover the inside of the alveolar sac in a line next to each other. They are easily damaged, so they are constantly renewed. Just like in our intestinal epithelium. This is their main responsibility.
Type 2 cells:
Type 2 cells deserve all the praise. They are very small in numbers, but they are the main keepers of the lung.
Type 2 cells are only 7% of the cells. They are less in infants, but they get to this rate in adults.
These are not flat but rather elliptical and pointed.
Type 2 cells are actually some kind of stem cells of the lung. They allow the formation of type 1 cells. If there are damaged type 1 cells in the lung, they renew these.
Type 2 cells are not just ordinary flat cells. They are secretory cells. Which means they produce and release substances. And the surfactant comes first among these. Yes, they produce our key substance.
Another feature of type 2 cells is they have these ‘water gates’ (aquaporin) and ion pumps. They prevent the accumulation of fluid in the lungs.
Type 2 cells are also involved in the immunity war. In viral or bacterial defense, in the first stage called innate immunity, they defend with the ‘collectins’ they produce. Collectins bind to pathogens and present to the alveolar macrophages that they are harmful. The alveolar macrophages are the frontline soldiers in case of any type of infection in the lung. The collectins in type 2 cells mark the enemy for the macrophages.
Type 2 cells are not only responsible for fighting viruses or bacteria, but also for cleaning toxin. They detoxify harmful chemicals called xenobiotics in the lung, which mimic human hormones, just like the liver. With this method, they try to clean substances in polluted air or cigarette smoke and plastic or chemical substances that enter us through tiny breaths.
Other benefits of surfactant:
While type 2 cells do all these things we mentioned, the surfactant they produce also has its own duty.
Surfactant is more than just a fatty substance that makes the lung slippery.
The surfactant has SOD and Catalase enzymes. These two enzymes are antioxidant enzymes. We need these enzymes to clear the area after a war in the lung.
Let’s elaborate a little more: When viruses enter the lung, alveolar macrophages absorb them and try to kill them with chemical free radicals like hydrogen peroxide, superoxide and peroxynitrite, which are like the bleach we use. (See my old articles for a detailed explanation of this subject.)
In this virus war, this bleach can damage the lung while killing the viruses. These two enzymes in antioxidant defense are also present in the surfactant so that this doesn’t happen.
Surfactant provides extra antioxidant capacity here.
So far, we have seen the importance of type 2 cells and the surfactant they produce.
Now let’s link them to viruses:
ACE2 Receptor:
You learned that this coronavirus holds on to the ACE2 receptor as it enters the lung, right?
Well, ACE2 is right on top of these type 2 cells….
Now you will begin to connect the dots.
The virus neutralizes ACE2 and type 2 alveolar cells.
In this case, we can understand that type 2 cells can produce nothing.
We can link this information to:
- Decreased surfactant,
- Decreased type 2 cells, lack of discharge of the fluid in the lung through the water gates, lung edema,
- Type 1 cells not being renewed since type 2 cells are decreased, the inability of oxygen to get in
- and other things.
There is an additional point to this. It looks like a tiny detail, but it is very important.
The name ACE2 stands for Angiotensin-Converting Enzyme 2.
What it does: There is a substance called angiotensin 1. This angiotensin 1 needs be converted to angiotensin 2.
See diagram below.
Our subject is ACE2, which converts ANG1 to ANG2.
Without ACE2, these angiotensin 1 and 2 don’t get converted to the most harmless form angiotensin, 1–9 and 1–7. You can see the mechanism above.
If you’re asking why it matters, because…
If this doesn’t happen, LUNG FIBROSIS occurs. Without ACE2, the lung suffers from proliferation and fibrosis. This is what brings death.
- The ACE2 receptor on top of type 2 cells
- The lack of surfactant without type 2 cells
- The tendency to fibrosis without ACE2
The question is, should we consider to use Angiotensin 2 blockers in order to prevent lung fibrosis???
Corona adheres to this ACE2, reducing both ACE2 and type2 cells, as well as all the benefits they provide.
Intensive caregivers have recently put the use of surfactant in their agenda. but what about Losartan type antihypertensives?
Corona adheres to this ACE2, reducing both ACE2 and type2 cells, as well as all the benefits they provide.
Intensive caregivers have recently put the use of surfactant in their agenda. but what about Losartan type antihypertensives?
Kind regards…
Aysegul Coruhlu MD. PhD
MD-Biochemist-Biomedical Engineer
