The Implications Of An Allergic Reaction On Our Health

People living in temperate countries tend to be highly susceptible to the symptoms of hay fever when it comes round to spring time.

The sneezes. The teary eyes. The annoyances of not really feeling unwell, but knowing that there’s something wrong that they can’t pinpoint as yet.

We all know that hay fever is an allergic reaction to the pollen that is produced as flowers bud. They tickle our noses, which then result in the symptoms of the incessant sneezing and the teary eyes, at the very least. We know that histamines are responsible for that, and antihistamine drugs provide some form of relief against those symptoms.

But the question is, how does it all happen?

What immune cells are involved?

An allergic reaction is, as we know it, the effect of excessive histamine production in the body.

These histamines can bind to histamine receptors located in different parts of the body. Histamine receptors in our nose signals the nose to produce excessive amounts of mucus (hypersecretion), as I explain in Unlocking The Lock And Key Mechanism That Governs Our Body’s Cellular Functions:

In an allergic reaction, what we do need to understand is the presence of mast cells. These cells contain many granules that are rich in histamines and interleukin cytokines. When allergens bind to the Immunoglobulin E (IgE) antibodies present on the surface of the mast cell, the mast cell releases its payload of histamines and interleukins to set off the allergic reaction.

However, even before that happens, we do see the effect of an increased activity in the IgE-producing B cells, which stem from an increased activity of the T helper 2 (Th2) cells. Certain interleukins that are released by the mast cell payload also do trigger the B cells to produce more IgE for a more pronounced allergic reaction the next time round. It’s a vicious positive feedback amplification loop that we’re looking at here.

Our T helper (Th) cells are immune cells that operate in a balanced, finite population. These Th cells are responsible for producing cytokines that signal immune responses to viruses, bacteria or fungi. When a new Th cell is synthesised, it is considered a naive (undifferentiated) Th cell, which then differentiates into specific Th cell subsets as and when a stimulus is provided for them to differentiate.

In our immune responses, there are 4 major types of Th cells:

1. Th1, which deals with bacterial and viral invasions.

2. Th2, which deals with parasite invasions.

3. Th17, which deals with fungal invasions.

4. Treg, which balances out the signalling intensity from Th1, Th2 and Th17.

An imbalance of these Th cells would spell trouble, especially when elevated Th2 cell activity contributes to allergic reactions and elevated Th17 activity contributes to the development of autoimmune disorders. The main problem lies in the quantity of the signalling cytokines that the Th cell populations are producing. Treg cells produce cytokines that help to mitigate the cytokine signalling intensity from the Th1, Th2 and Th17 cells.

How does Th2 contribute to the development of an allergic reaction?

The Th2 cell uses IL-4 to signal the B cell to produce Immunoglobulin E (IgE). IgE then binds to the mast cell. When an allergen can interact with IgE according to the lock and key mechanism that I outlined here (Unlocking The Lock And Key Mechanism That Governs Our Body’s Cellular Functions), then a biological response is elucidated from the mast cell. It degranulates, releasing histamine and various other interleukins.

The problem is, mast cell degranulation also releases IL-4, so this additional release of IL-4 can be fed back to the B cell to signal the production of even more IgE. Hence, a subsequent allergic reaction can be even more intense than previously — it is all about a positive amplification feedback loop that we’re looking at here. And that is why some people can have such severe allergic reactions to certain stimulants that they can go into anaphylactic shock - the degranulation and the release of the histamine/cytokine payload is way in excess of what is considered a "normal" response.

Therefore, in an allergic reaction, there can be many things that go wrong. These include:

1. Excessive Th2 activity relative to Th1, Th17 and Treg.

2. Or, the Th2 cells might be working fine, but the B cells just happen to be producing too much IgE.

3. Faulty IgE antibodies getting unlocked by allergens that most other human bodies would consider as safe, for example, in the case of peanut allergies.

Peanuts are not necessarily harmful to us, but yet they are major allergens that can cause serious problems with people who are allergic to them via anaphylactic shock, which in some ways is parallel to a cytokine storm.

I also do highlight here that our gut microbiome also influences Th cell activity (Now, On The Topic Of Those Bugs That Live In Your Intestines…). Meaning that one with digestive health issues, including constipation, small intestine bacterial overgrowth (SIBO), too much antibiotic treatment, or living off a pretty poor quality diet in terms of nutrition may be more susceptible to developing allergies as they grow older.

What’s the main takeaway with regards to allergic reactions?

The key is to understand that allergies can come from many different sources, but how our immune system responds to these allergens is another story together. For the response, we do need to examine the activity of the cells that are involved in expressing the cytokine signallers, and work out a solution from there.

Also, it is important to note that constant irritation and allergic reactions, such as in the case of skin eczema, will result in a chronically elevated release of pro-inflammatory cytokines. These can have a bearing on the development of chronic inflammatory disorders down the line.

For example, we do have the release of interleukin 1-beta (IL-1β) cytokines in an allergic inflammatory reaction. This paper states that:

In autoinflammatory as well as allergic diseases such as contact hypersensitivity, atopic dermatitis and bronchial asthma, dysfunctional inflammasome processing has been demonstrated to account for IL-1β-induced inflammation. IL-1-neutralizing drugs have been shown to completely suppress or markedly reduce inflammatory responses in clinical studies and experimental models of urticarial autoinflammatory diseases as well as common allergic disorders.

And of course, excessive levels of IL-1β cytokines in our blood can result in the development of further health problems in our lives.

For example, as I do highlight in The Delicate Balance Of A Steady State To Maintain A Healthy Body, excessive amounts of IL-1β in our blood can contribute to the equilibrium between bone mineral formation and bone mineral dissolution to favour dissolution, which can lead into osteoporosis in due time. Excessive amounts of IL-1β in our blood can also cause similar problems with the equilibrium between joint cartilage formation and joint cartilage degradation to favour degradation, hence there is also a higher risk of osteoarthritis that is possible.

We may not necessarily feel those effects now as we're sneezing through hay fevers, but the risks of developing degenerative diseases as a result of our body's immune system being unable to regulate the production of these pro-inflammatory cytokines would be problematic in the future!

Joel Yong, PhD, is a biochemical engineer/scientist, an educator and a writer. He has authored 1 ebook (which is available on Amazon.com in Kindle format) and co-authored 6 journal articles in internationally peer-reviewed scientific journals. His main focus is on finding out the fundamentals of biochemical mechanisms in the body that the doctors don’t educate the lay people about, and will then proceed to deconstruct them for your understanding — as an educator should. Do visit his website here or his Patreon website to connect.