The Early Phase Asthma Attack  

Earlier I explained how asthma is an abnormal immune response. Then I showed how this abnormal immune response makes your body sensitized.  In this post, I aim to show you how this abnormal immune response causes asthma attacks. Ready? Here we go!

In the beginning

I want to explain that the biological processes involved in the immune response vary depending on what asthma subgroup you have. For the sake of our example here, we are using an allergic asthmatic sensitized to dust mites. That’s where we are right now.

There are two phases of an asthma attack: the early phase and the late phase. The early phase is your body’s way of dealing with sudden exposure to pathogens. Like, you are inhaling a virus right now. But, with asthma and allergies, your immune system is sensitized to harmless dust mites. Like, you are inhaling dust mites right now. Your sensitized body recognizes this. Your immune system says, “What do we do now?”

Below is what happens during this early phase.  I will discuss the late phase in an upcoming post.

The allergy/asthma attack

It can be days, weeks, months, or years after you were sensitized. Your immune system recognizes the returning offender (those pesky dust mites, in our case).  Immediately, your immune system instigates the…

Early phase

This is the immediate response to an antigen, and causes allergy and/ or asthma symptoms in the matter of seconds or minutes. This response reaches its peak within 15-30 minutes and resolves within 1-2 hours.1 What happens here is dust mite IgE recognize, bind with, and release cytokines that communicate with…

Mast cells. These are white blood cells (leukocytes) that are randomly scattered along connective tissue of your skin, the conjunctiva of your eyes, and your respiratory tract. They were discovered in 1953, and are a special type of leukocyte called a granulocyte.2

Granulocyte. These are leukocytes that contain granules. Stimulation by cytokines causes them to degranulate.

Degranulate. This means they release their contents (their granules) into the bloodstream. Among their contents are the mediators of inflammation.

Mediators of inflammation

They are tiny proteins that mediate inflammation.  Some reduce inflammation, although the ones we are concerned about are the ones that cause inflammation. In our case, they cause airway inflammation. Or, they make inflammation already present worse, thereby causing asthma symptoms.

Some of the most common mediators include histamine, leukotrienes, prostaglandins, cytokines, and chemokines. In previous posts, I have already introduced you to some of them. In my next post I will go into more detail about these mediators and what they do. For now, just know that these all have the potential to cause airway inflammation, which is why they are called mediators (they mediate inflammation. They cause inflammation).

Macrophage. They are the most abundant cells in the airway, and are activated by antigens through the IgE response and by the release of cytokines and chemokines.2

Mast Cell Tryptase. It’s a protein that is also released by mast cells and plays a role in airway inflammation, although this is probably done indirectly by enhancing the effects of other mediators of inflammation, like histamine. They also are responsible for recruiting eosinophils and neutrophils involved in the late phase. There are alpha and beta-tryptase, both made by different genes. Serum tryptase levels in your blood may be elevated within 30-60 minutes after exposure to an antigen.1,3

Conclusion

The early phase is well underway. You may feel allergy symptoms such as an itchy, runny nose, and sneezing. Your eyes may feel itchy and watery. You may feel asthma symptoms such as chest tightness and shortness of breath. These probably respond well to an antihistamine or albuterol. However, little do you know, the reinforcements are on the way.  They will cause the late phase allergy/asthma attack.

In an upcoming post, I will explain a little more about mediators of inflammation. After that, I will discuss the late phase asthma attack. 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 Asthma.net team does not recommend or endorse any products or treatments discussed herein. Learn more about how we maintain editorial integrity here.
View References
  1. Ceislewicz, et al., “The late, but not early, asthmatic response is dependent on IL-5 and correlates with eosinophil infiltration,” Journal of Clinical Investigation, 1999, August 1, https://www.ncbi.nlm.nih.gov/pmc/articles/PMC408423/, accessed 7/11/2017
  2. Asthma Guidelines, National Heart Lung And Blood Institute (NHLBI), https://www.nhlbi.nih.gov/files/docs/guidelines/03_sec2_def.pdf, accessed 7/11/2017
  3.  Zhang, M-O., H. Timmerman, “Mast cell tryptase and asthma,” Mediators of Inflammation, 1997, Dec. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2365873/, accessed 7/11/2017

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