What happens in the lungs when symptoms begin—and why.

All About Inflammation how an attack occurs

The shortness of breath experienced by the 25 million Americans who suffer from asthma is the result of chronic inflammation of the lungs and the airways, the breathing passages into and out of the lungs.

Inflammation, which is the body’s natural response to protect itself from harm, causes the lining of the airways to swell and excess mucus to be produced. Over time, this inflammation (or airway remodeling, as it’s often called) can trigger long-term damage to the tissues and muscles in the lungs and airways. This inflammation makes wheezing common and breathing difficult. Here’s what you need to know about inflammation—and how it contributes to asthma symptoms, such as shortness of breath, and asthma attacks.

What is inflammation?

Inflammation is an essential protective tool of the immune system to fight off what it considers to be harmful invaders, or anything that can potentially cause injury to the body— from a virus to air pollution. In those who suffer from asthma, these invaders are your particular triggers—everything from dust and pollution to pollen and cat or dog dander.

When the immune system senses this invader, it begins to fight it off, just as it would a virus or bacteria. To aid in this fight, immune cells at the scene of the invasion (in the case of asthma, this is the airways and lungs) release natural chemicals called cytokines. It’s these chemicals—which go by names like IL-4 and IL-13 (though there are many others)—that trigger symptoms of inflammation. These symptoms include swelling and constriction of the airways and excess mucus production in the lungs and the airways—all common in those with asthma.

Inflammatory symptoms are all an attempt by the immune system to rid the body of the invader. Sneezing, for example, is meant to force it out of the body, as is coughing. (Coughing can also be a sign of airway constriction in those who have asthma.) Production of sticky mucus is another symptom of immune-system-triggered inflammation. Mucus is designed to attach itself to the invader and pull it out of the body. Swelling is meant to draw more “fighting” reinforcements (e.g., blood and immune cells) to the area.

The more inflammation in the airways, the more sensitive they become to potential triggers, with hypersensitivity occurring often in those with asthma.

Acute inflammation vs. chronic inflammation

Inflammation with all its symptoms is meant to be short term: it’s designed to turn on to get rid of the offending substance and turn off once it achieves this goal, with symptoms going away until the next invader appears on the scene. In those with asthma, however, this inflammation is chronic, meaning it’s happening all the time and is not ever fully turning off. This is why asthma is referred to as a chronic inflammatory disease.

This chronic inflammation causes the immune system to be on hyper alert all the time, making the lungs and airways more sensitive. (Imagine a rash that you keep itching; it just keeps getting worse until you can calm it down.) Turning off this inflammation—which is the aim of many asthma medications today—helps calm the immune system and the body, reducing hypersensitivity, and allowing everything (including breathing) to relax and become more balanced. When it comes to inflammation and asthma, however, there are specialized immune cells that are involved.

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Immune Cells on the Attack

When you have symptoms of asthma, these immune cells are hard at work:

Mast cells are white blood cells found in tissue throughout the body, including under the skin, in the nasal passages, and in the lungs. They are the first line of defense against invaders, or triggers, entering the body. These cells are activated by invaders and initiate inflammation by secreting natural chemicals, or cytokines, like histamine and IL-4 and IL-13.

Basophils are immune cells involved in allergic  inflammation. When an allergen enters the body (e.g., cat or dog dander, pollen, or pollution), basophils are sent to the sites of entry in the body—such as the nose, the eyes, and the airways— where they release histamine. It’s this natural chemical that contributes to sneezing, itchy eyes, coughing, skin rashes, and difficulty breathing.

Eosinophils (e-o-SIN-o-phils) are other important immune cells when it comes to allergic asthma. They can accumulate in large numbers when allergic inflammation is present, why the blood count of these white blood cells is often high in patients with allergies and certain types of asthma.

Over time, too-high numbers of these eosinophils—present in atopic asthma and eosinophilic asthma (characterized by wheezing, coughing, shortness of breath, chest tightness, and inflamed mucous membranes)—can cause tissue damage.

T cells are the most abundant white blood cells in the body. In the case of asthma, these cells trigger what’s called Th2, or Type 2, inflammation, which is linked to moderate to severe asthma. It causes increased sensitivity and reactivity of the airways (called hyperresponsiveness) and can cause permanent cellular changes to the airways, if asthma goes untreated. These changes—which include thickened and scarred bronchial tissue and permanently enlarged muscle tissue—can cause reduced lung function that can’t ever be healed. This is why taking control of your asthma before it gets to this point is critical.

Type 2 Inflammation and Asthma

Type 2 inflammation is involved in allergic asthma, exercise-induced asthma, and eosinophilic asthma (the asthma mentioned earlier that’s characterized by too-high numbers of immune cells called eosinophils). It tends to run in families: studies show that if one or both parents have Type 2 inflammation and asthma, their child is four times more likely to have asthma or an allergic disease. This Type 2 inflammation is characterized by:

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Increased blood levels of IgE, a protein. When the immune system encounters an allergen, it produces immunoglobulin E, or IgE. It’s this protein, or antibody, that triggers the symptoms of inflammation. People with Type 2 asthma tend to have high blood levels of IgE.

Increased activity of eosinophils. Too many of these immune cells in the blood is associated with increased inflammation. Elevated blood levels can cause swelling of the airways that can lead to asthma attacks.

Activity of specific cytokines called IL-4 and IL-13. These natural chemicals trigger the symptoms of inflammation that are characteristic of Type 2 asthma, such as the excessive secretion of mucus (that causes you to cough and wheeze) and hyper sensitivity of the airways. These cytokines are also involved in airway scarring and long-term tissue damage.

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The Gut’s Role in Inflammation

The gut, or microbiome as it’s also called, does much more than just digest your food.

It contains trillions of bacteria—both good and bad—along with fungi and parasites living together happily in a mutually beneficial environment. Also, 70 percent of our immune cells are found in the gut. This is why, when the gut is in balance, our immune system is functioning well and, as research shows, we have little chronic inflammation and/or fewer allergies.

Any imbalance (or dysbiosis as it’s often referred to), however, in this microbiome—be it bacterial, fungal, and/or parasitic—causes immune problems and subsequent inflammation. In fact, an imbalanced gut is behind almost all chronic inflammation and chronic ailments today, including asthma. An imbalance in the fungal community, in particular, has been shown to trigger allergic inflammation. (Keep in mind that mold, a common allergen, is a fungus. See page 27.)

A healthy diet, including plenty of fiber and fermented foods (see page 23), steering clear of foods and ingredients that don’t agree with you, cutting back on processed sugar (which bacteria and fungi love to feed on), drinking plenty of water, and living a healthy lifestyle all work to keep your gut, and everything living in it, in balance. This is one reason why revamping your lifestyle has often been associated with reduced asthma symptoms (see pages 13-14).