Listen to the article here:
They say in stressful situations you should take a breath and calm down, but what if you literally can’t? Asthma is a common disease that affects around 25 million Americans. It results in several million ER visits and hundreds of thousands of hospitalizations yearly. It can also get worse over time. So what is asthma, how does it cause trouble, and what can we do about it? Take a deep breath as we dive in.
To start, asthma is a medley of several related conditions that can be divided in many ways. Into allergic and non-allergic, eosinophilic and neutrophilic, adult onset, asthma with persistent airflow, asthma with obesity, and severe asthma. Several of these categories overlap and make a big mess of everything. The common threads between all types of asthma are the symptoms. Asthma is defined by its symptoms:
- Shortness of breath
- Chest tightness
A collection of symptoms are needed to diagnose asthma; a single symptom isn’t enough. Symptoms are also variable, getting worse at night, in the morning, or in response to a stimulus. Stimuli include irritants, allergens, exercise, infection, and weather. A pattern of symptoms in response to irritants may lead to an asthma diagnosis.
Our need to breathe makes this a dangerous disease. Asthma symptoms are variable, but they all involve the airway. The airway is affected in three ways: inflammation, bronchial hyperresponsiveness, and structural remodeling.
Inflammation is complicated. In allergic asthma, immune cells respond to dust, pollen, and other airborne items. These are detected by defense cells in our windpipe which mistake them as dangerous. Immune cells act quickly to try and kill the “invaders”. In asthma, the big guns are brought in. Eosinophils and neutrophils are like a bazooka: highly effective at killing invaders, but can cause area-of-effect damage when used improperly. Eosinophils cause bronchial hyperresponsiveness, impaired throat function, inflammation, phlegm, and long-term allergen sensitivity. Eosinophils can also occur in non-allergic asthma. They might get involved because of genetic predisposition, polyps, viruses, and fungi. Neutrophils are similar to eosinophils in causing inflammation, but cause more severe symptoms. They generally need more irritants to activate and can be triggered by tobacco smoke, pollutants, microbes, and obesity. You can have eosinophilic or neutrophilic asthma, or both at the same time. Whatever the flavor, inflammation is the result.
One of the effects of inflammation from eosinophils and neutrophils in the throat is bronchial hyperresponsiveness. Bronchial refers to the windpipe, hyper- means abnormally high, and responsiveness in this case refers to how narrow the throat gets. Bronchial hyperresponsiveness is an abnormally high constriction of the throat in response to stimuli, such as irritants. The responsiveness is temporary, leading to the characteristic variability in symptoms. Long term inflammation can cause persistent damage, called airway structural remodeling. This is when the cells of the airway grow in different ways. The walls of the airway are thickened, there is more muscle mass in the throat, the throat contracts harder, and the airway is reduced in size. This is a more permanent change in our throat, making this a long-term effect.
The symptoms are very constricting, is there relief? Yes! Eosinophils respond well to anti-inflammatory medicines known as corticosteroids, like cortisone. These are used for both long-term control and for asthma attacks. Unfortunately, these don’t work on neutrophils, and can actually prolong their lifespan, exacerbating symptoms. Bronchodilators open airways and reduce swelling. Allergy-induced asthma may also be alleviated using allergy shots, tablets, or medications. Newer medicines include monoclonal antibodies that target allergens or specific cells for destruction. Medicines that directly target eosinophils or neutrophils might provide a deeper relief from asthma. Don’t hold your breath, but keep an eye out for new research opportunities!
Written By Benton Lowey-Ball, BS Behavioral Neuroscience
Cockcroft, D. W., & Davis, B. E. (2006). Mechanisms of airway hyperresponsiveness. Journal of allergy and clinical immunology, 118(3), 551-559. https://www.jacionline.org/article/S0091-6749(06)01511-9/fulltext
Global Initiative for Asthma. (2000). Global Strategy for Asthma Management and Prevention updated 2022. www.ginasthma.org.
Pate, C. A., Zahran, H. S., Qin, X., Johnson, C., Hummelman, E., & Malilay, J. (2021). Asthma surveillance—United States, 2006–2018. MMWR Surveillance Summaries, 70(5), 1. https://www.cdc.gov/mmwr/volumes/70/ss/ss7005a1.htm?s_cid=ss7005a1_w
Pelaia, G., Vatrella, A., Busceti, M. T., Gallelli, L., Calabrese, C., Terracciano, R., & Maselli, R. (2015). Cellular mechanisms underlying eosinophilic and neutrophilic airway inflammation in asthma. Mediators of inflammation, 2015. https://www.hindawi.com/journals/mi/2015/879783/