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What Are Mediators Of Inflammation?  Part 1

Asthma is an “Abnormal Immune Response.” Your immune cells recognize one of your asthma triggers and immediately releases chemicals. Many of the chemicals are called mediators of inflammation. They “mediate” inflammation and are responsible for asthma. That said, here’s all you need to know about these mediators.

Mediators of inflammation

They are tiny proteins that mediate inflammation. Some cause inflammation and others reduce inflammation. But, for our purposes, we are mainly concerned with mediators that cause it. Some cause it directly, while others do so by recruiting or communicating with other immune cells. Mediators are in various cells of your body, but for our purposes we will just consider those stored in airway epithelial cells and granulocytes.

The cells where inflammation mediators are found

Airway Epithelial Cells. These are cells that line the surfaces of your airways. When foreign invaders (like viruses) come into contact with them, they release mediators of inflammation.

Granulocytes. These are white blood cells (leukocytes) that contain granules. Examples of granulocytes include mast cells that are randomly scattered throughout your airways. Other examples include eosinophils, neutrophils, and basophils that circulate your bloodstream. When told to do so, granulocytes release their contents (their granules).

What happens after exposure to an asthma trigger.

For the sake of simplicity, let’s assume our subject has allergic asthma with an allergy to dust mites. While other cells also release mediators, we’ll just discuss the ones released by mast cells here.

Early Phase Asthma Attack. After you are sensitized to dust mites, the next time you are exposed to dust mites your immune system recognizes them as harmful. This begins the early phase asthma attack. Mast cells are told to release their contents, which include various mediators of inflammation.

What do mediators do?

They travel to cells lining airways to mediate inflammation. Some reduce inflammation and others increase inflammation. The ones we are concerned about here are the ones that increase inflammation.

They do this by irritating cells (airway epithelial cells, in our case), causing tiny blood vessels (arterioles) around these cells to dilate. This causes an increase of blood flow to capillaries. Their walls become permeable, and some of their fluid leaks into interstitial spaces. This causes redness and swelling of airway walls. Some call it airway edema. Others call it airway inflammation. Whatever you choose to call it, this swelling delays the spread of foreign invaders; it traps them.1,3

Furthermore, this irritation causes bronchial smooth muscles to spasm and constrict (bronchospasm), causing shortness of breath (dyspnea). It irritates goblet cells causing them to secrete excessive mucus to trap pathogens (but, in our case, our body is attacking harmless dust mites). This further blocks airways and may cause a cough.

This irritation also irritates nerve endings causing an itching or burning sensation (chest tightness or pain).3

So, that’s what mediators of inflammation do.

They cause airway inflammation. This inflammation is responsible for asthma symptoms. So, that’s enough to grasp for now. In part 2 I will list some mediators of inflammation that are responsible for asthma. It’s important to know them because some of our newer medicines and biologics work to block their effects. So, if you want to understand these medicines, it’s good to have at least a basic understanding of the mediators of inflammation.

So, stay tuned!

This article represents the opinions, thoughts, and experiences of the author; none of this content has been paid for by any advertiser. The team does not recommend or endorse any products or treatments discussed herein. Learn more about how we maintain editorial integrity here.

  1. Shier, David, Jackie Butler, Ricki Lewis, editors, “Holes Human Anatomy & Physiology,” 7th edition, 1996, page 541, 645
  2. Gurish, et al., “Mast Cell Derived Mediators,”, accessed 7/11/17
  3. Riley, James F., “Histamine and Sir Henry Dale,” 1965, June 5,, accessed 7/11/17
  4. Hammarastrom, S., “Leukotrienes,” Annual Review of Biochemistry, 1983,, accessed 7/11/17
  5. Asthma Guidelines, National Heart Lung And Blood Institute (NHLBI), 2007,, accessed 7/11/17
  6. Ricciotti, Emanuela, Garret A. FitzGerald, “Prostaglandins and Inflammation,” Arteriosclerosis, Thrombosis, and Vascular Biology, 2012, May 1,, accessed 10/25/16
  7. Masafumi, et al., “Prostaglandin D2 and TH2 Inflammation in the Pathogenesis of Bronchial Asthma,” Korean Journal of Internal Medicine, 2011, March,, accessed 7/11/17
  8. CCL11 Gene,,, accessed 10/24/16
  9. CCL17 Gene,,, accessed 10/24/16
  10. CCL22 Gene,,, accessed 10/25/16


  • krishwaecosse
    10 months ago

    What an interesting article. I never really thought about how the process our bodies go through when meeting a trigger before .

  • Leon Lebowitz, RRT moderator
    10 months ago

    Hi krishwaecosse and thanks for your post. I’m sure the author, John Bottrell, will be pleased you felt this article was so helpful, when he sees what you wrote. All the best, Leon (site moderator)

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