Asthma Lexicon: Mediators of Inflammation
In respiratory therapy (RT) school, I learned that asthma is caused by an overactive immune response. It begins with your immune system identifying something as harmful. Then it releases mediators of inflammation that cause airway inflammation. This is what causes asthma symptoms.
Even in the short 20 years since I graduated, researchers have learned a ton about what causes airway inflammation. So much so that they have identified specific mediators that contribute to asthma. Even better, they have identified drugs to block their effects. This has helped so many of us asthmatics obtain better asthma control.
Below is a basic lexicon about inflammatory mediators. These are terms that are often used in asthma-related articles and communities like ours. I figured it would be neat to have a place where they are all defined. So, let us begin.
Asthma lexicon: Inflammatory mediators
Mediators of inflammation
These are small proteins that mediate inflammation. You can learn more by reading my post "What are mediators?"1
"Mediators of inflammation may be responsible for asthma."
It’s red and inflamed tissue. Mediators of inflammation cause cells to release some of their fluid. This fluid gets into spaces between cells, thereby causing the tissue to become inflamed. With asthma, this inflammation occurs along airway walls.2
"One theory is that all asthmatics have some degree of airway inflammation."
This basically means that they cause or impact inflammation in some way.3
“Inflammatory mediators mediate inflammation.”
These are small proteins released by cells. They tell other cells what to do. They are neat in that they allow cells to communicate with each other.4
“Some cytokines are inflammatory mediators.”
They are a group of small cytokines. You don’t hear this term used as much as cytokines. But, it is a term used in some research articles about our disease. They are basically specialized cytokines that attract white blood cells. They enter your blood. They then tell white blood cells to come to the area of infection.5
"Chemokines are a special type of cytokine."
These include a group of cytokines that are released by leukocytes. They are also released from epithelial tissue, or tissues lining blood vessels.6,7
“Singulair is a medicine that blocks the effects of leukotrienes.”
These are white blood cells.
These are types of leukotrienes. There are many of them.7
“Researchers have identified 15 types of interleukins. Two interleukins believed to contribute to asthma are Interleukin 5 (IL5) and Interleukin 13 (IL13).7
It travels through the bloodstream to recruit reinforcements. The reinforcements, in our case, are eosinophils. They arrive 3-4 hours after exposure to your allergy or asthma trigger. They are responsible for more aggressive inflammation. They are also responsible for your more severe asthma attacks.9
This is a response by your immune system. Immune cells called white blood cells play a major role. They release interleukins that cause inflammation. The role of this inflammation is to trap and kill pathogens.10
Abnormal immune response
It is when immune cells act abnormally. They become overactive. This is what is believed to be responsible for asthma and allergy symptoms. Instead of just responding to pathogens, they respond to otherwise innocuous (harmless) substances, such as your common allergens. Inflammation, in our case, occurs in the airways. It causes allergy and asthma symptoms.11 Learn more in my post, "Asthma is an Overactive Immune Response."
It is a leukotriene antagonist. It blocks the effects of leukotrienes. It prevents them from causing inflammation. It thereby prevents allergy and asthma symptoms.12
"Singulair is another option to try for asthma."
These are drugs that block the effects of certain biological processes. In our case, biologics called Cinqair, Fasenra, Nucala, and Dupixent block the effects of IL5.13
"Biologics are a good medicine to try for severe, persistent asthma."
Always hunting for more asthma wisdom
It’s a hobby of mine to research asthma. Sometimes, this research gets pretty deep. And some of it is very complex stuff. So, my attempt in these articles is to make the complex seem easy to understand. I hope I accomplished that here.
These are just some basic definitions. For those seeking to learn more, you can check out the links throughout this article. I have, at times, delved pretty deep into what scientists are learning about our disease. It will be neat to see how much more they learn in the next 20 years.
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