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Table of Contents
Pathogenesis
Impact on Treatment
The pathophysiology ofasthma—that is, the processes it entails—involves multiple organs, systems, and mechanisms. While these differ somewhat from onetype of asthmato the next, the end result is the same: bronchoconstriction, inflammation, and mucus overproduction that make it harder for you to breathe. What sets all of this into motion, asthma’s pathogenesis, is equally complex.
Learning more about how asthma comes about can help you better understand how various treatments and management approaches can minimize asthma’s impact on your life and why your healthcare provider recommends certain medications.
Pathophysiology of Asthma
Pathophysiology is the way in which a disease alters the normal function of your body. The term is derived from Greek prefixpathos,meaning “suffering,” and the rootphysiologia,meaning “natural philosophy.”
The pathophysiology of asthma involves:
Hypersensitivity
People with asthma are known to be hypersensitive to things calledtriggers. What this means is that theimmune systemincorrectly perceives certain stimuli, such as dust or pollen, to be harmful. This sensitivity is what causesallergiesand sensitivities.
Common allergens include:
Common sensitivities include:
Hyperresponsiveness to Stimuli
In asthma, the airways narrow after an irritant is breathed in. This is called hyperresponsiveness, and it’s somewhat like a twitch in your airways that’s especially easy to induce.
The narrowing of the airways makes it more difficult to breathe. When you use yourrescue inhaler, you feel better because the medication relaxes your airways and makes them larger so that air can flow more easily.
Hyperresponsiveness occurs soon after exposure to an allergen and is the first part of anasthma attack. Changes that occur later that have more to do withinflammation.
Bronchoconstriction and Inflammation
Hyperresponsiveness causes your bronchial tubes to contract. At the same time, inflammatory cells and chemicals flood your airways and cause inflammation, which further restricts your breathing and can become chronic.
Bronchoconstriction and inflammation combine with excess production of mucus, which exacerbates breathing difficulty and leads to achronic coughthat works to release the mucus.
Bronchospasm typically lasts for one to two hours before resolving. In some cases, however, it may appear to resolve only to have an attack occur up to 12 hours later.
Asthma symptomsmay be present only on occasion or all the time, depending on yourasthma severity. Asthma exacerbations involve a more extreme tightening of the airways that makes it hard to breathe and can be life-threatening.
All About Bronchoconstriction
Airway Remodeling
In more severe cases, chronic inflammation can lead to a process called airway remodeling in which the walls of the air passages thicken and harden, the glands enlarge, and networks of blood vessels grow rapidly and abnormally.
While less severe asthma is considered reversible with proper treatment and management, airway remodeling is currently irreversible. It’s associated with worsened symptoms and more frequent and severe asthma attacks.
Asthma’s Long-Term Impact on Health
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Pathogenesis of Asthma
Taking a step back, all of this begins with a changes that occur at the cellular level.
Hypersensitivity prompts an activation of the immune system and starts a complex chain reaction involving numerous cells and substances. This includes an early phase and a late phase.
The early phase begins when your immune system detects allergens or irritants in your body. In response, plasma cells release an antibody calledimmunoglobulin E (IgE).Antibodiesare specialized cells that attack and try to destroy things your body perceives as threats.
The IgE then attaches itself to several types of white blood cells, which can vary due to the type of asthma.
Mast Cells
Mast cells are especially prevalent in certain areas of your body, including the lungs.
Mast Cells' Role in Your Health
Basophils
Basophilsperform a number of important functions, perhaps the most important of which is in certain inflammatory reactions, particularly those involving allergies.
Basophils are a part of theinnate immune system, which triggers a non-specific reaction to anything the body considers harmful. Unlike adaptive immunity, which elicits a targeted response, innate immunity results in a generalized attack that involves inflammation, swelling, pain, fever, and fatigue.
Basophils, like mast cells, produce histamine, leukotrienes, and PAF. Having too many basophils in your blood (basophilia) can be a powerful driver of asthma symptoms, including:
Basophils are especially implicated inallergic asthma.
Eosinophils
Eosinophils are less involved in allergic asthma and associated more with their own subtype, called eosinophilic asthma (e-asthma).
E-asthma is often severe and comes on most often in adulthood. While it involves an allergic response, many people with this type of asthma don’t actually have allergies.
Eosinophils:
E-asthma is believed to be associated with a set of symptoms not present with other asthma types, including:
When chronic rhinosinusitis and nasal polyps accompany asthma, they can predispose you to aspirin-induced asthma. When all three conditions are present, they are collectively known as Samter’s Triad.
Understanding E-Asthma
Neutrophils
People with severe asthma that doesn’t respond well to treatment withcorticosteroid medicationsoften have high levels ofneutrophils. Their condition is sometimes referred to as neutrophilic asthma.
Neutrophils are part of an acute inflammatory response. They:
They’re involved in both the innate and adaptive immune response as well.
White Blood Cells and Immunity
T Helper 2 Cells
T helper 2 (Th2) cells do as their name suggests: They support other cells in several ways, including assisting with their activation. Of course, in asthma, these key players in the immune response are what help trigger asthma symptoms:
Macrophages
Like neutrophils,macrophagesare made in your bone marrow and engulf foreign substances to destroy them. In asthma, macrophages release substances that initiate and prolong hyperresponsiveness of the airways, increase mucus production and swelling, and attract eosinophils to the lung.
These substances include:
Macrophages can ultimately increase asthma symptoms.
Late Phase
The late phase of asthma occurs over the next few hours, as many of these cells make their way to the lungs, causing increased bronchoconstriction and inflammation, which makes it harder for you to breathe.
Neutrophils, eosinophils, and Th2 cells are especially believed to be a part of the late-phase response. These cells can be found in the sputum of people with asthma and may be associated with severe exacerbations.
Impact on Asthma Treatment
While there is no cure for asthma, treatment can control its symptoms and slow—if not entirely stop—its progression.
With the pathogenesis and pathophysiology of asthma in mind, healthcare providers can recommend strategies to either minimize or normalize the response, or prevent it from happening altogether. Given the variety of elements involved in these processes, your asthma management plan will very likely be multi-pronged.
Visit your healthcare provider regularly so they can monitor your respiratory health and alter your treatment plan over time, as needed.
Medications
Certain medications target specific cells and the processes they’re involved in, which is why it’s so important for healthcare provider
s to consider all that is happening in the body to cause asthma symptoms.
Some classes of medications used for treating asthma include:
How Asthma Is Treated
Lifestyle
This can include:
A Word From Verywell
The nitty-gritty about what makes asthma come about may ultimately seem most relevant to your healthcare provider. And to a large extent, that is true. That said, it hopefully gives you a better sense of what is happening in your body and why certain treatments and management approaches are working and why others are worth adding on and committing to.
18 SourcesVerywell Health uses only high-quality sources, including peer-reviewed studies, to support the facts within our articles. Read oureditorial processto learn more about how we fact-check and keep our content accurate, reliable, and trustworthy.Castillo JR, Peters SP, Busse WW.Asthma exacerbations: Pathogenesis, prevention, and treatment.J Allergy Clin Immunol Pract. 2017;5(4):918-927. doi:10.1016/j.jaip.2017.05.001Zhou-Suckow Z, Duerr J, Hagner M, Agrawal R, Mall MA.Airway mucus, inflammation and remodeling: emerging links in the pathogenesis of chronic lung diseases.Cell Tissue Res. 2017;367(3):537-550. doi:10.1007/s00441-016-2562-zYamauchi K, Inoue H.Airway remodeling in asthma and irreversible airflow limitation-ECM deposition in airway and possible therapy for remodeling.Allergol Int. 2007;56(4):321-9. doi:10.2332/allergolint.R-07-151Ferreira VL, Borba HH, Bonetti ADF, Leonart LP, Pontarolo R.Cytokines and interferons: Types and functions.Autoantibodies and Cytokines. 2019. doi:10.5772/intechopen.74550Yamauchi K, Ogasawara M.The role of histamine in the pathophysiology of asthma and the clinical efficacy of antihistamines in asthma therapy.Int J Mol Sci. 2019;20(7) doi:10.3390/ijms20071733Lee K, Lee SH, Kim TH.The biology of prostaglandins and their role as a target for allergic airway disease therapy.Int J Mol Sci. 2020;21(5):1851. doi:10.3390/ijms21051851Al-Azzam N, Elsalem L.Leukotriene D4 role in allergic asthma pathogenesis from cellular and therapeutic perspectives.Life Sci. 2020;260:118452. doi:10.1016/j.lfs.2020.118452Ulambayar B, Yang EM, Cha HY, Shin YS, Park HS, Ye YM.Increased platelet activating factor levels in chronic spontaneous urticaria predicts refractoriness to antihistamine treatment: an observational study.Clin Transl Allergy. 2019;9:33. doi:10.1186/s13601-019-0275-6Siracusa MC, Kim BS, Spergel JM, Artis D.Basophils and allergic inflammation.J Allergy Clin Immunol. 2013;132(4):789-788. doi:10.1016/j.jaci.2013.07.046de Groot JC, ten Brinke A, Bel EH.Management of the patient with eosinophilic asthma: a new era begins.ERJ Open Res. 2015;1(1):00024-2015-. doi:10.1183/23120541.00024-2015Ray A, Kolls JK.Neutrophilic inflammation in asthma and association with disease severity.Trends Immunol. 2017;38(12):942-954. doi:10.1016/j.it.2017.07.003Mantovani A, Cassatella MA, Costantini C, Jaillon S.Neutrophils in the activation and regulation of innate and adaptive immunity.Nat Rev Immunol. 2011;11(8):519-531. doi:10.1038/nri3024Rucker D, Dhamoon AS.Physiology, thromboxane A2. In:StatPearls. Treasure Island (FL): StatPearls Publishing.Fahy JV.Type 2 inflammation in asthma–present in most, absent in many.Nat Rev Immunol. 2015;15(1):57-65. doi:10.1038/nri3786Quirt J, Hildebrand KJ, Mazza J, Noya F, Kim H.Asthma.Allergy Asthma Clin Immunol. 2018;14(Suppl 2):50. doi:10.1186/s13223-018-0279-0Price D, Fletcher M, Van der molen T.Asthma control and management in 8,000 European patients: the REcognise Asthma and LInk to Symptoms and Experience (REALISE) survey.NPJ Prim Care Respir Med. 2014;24:14009. doi:10.1038/npjpcrm.2014.9Finn DF, Walsh JJ.Twenty-first century mast cell stabilizers.Br J Pharmacol. 2013;170(1):23-37. doi:10.1111/bph.12138Singh RK, Tandon R, Dastidar SG, Ray A.A review on leukotrienes and their receptors with reference to asthma.J Asthma. 2013;50(9):922-931. doi:10.3109/02770903.2013.823447Additional ReadingLynn S, Kushto-Reese K.Understanding asthma pathophysiology, diagnosis, and management.American Nursing Today.2015;10(7):49-51.
18 Sources
Verywell Health uses only high-quality sources, including peer-reviewed studies, to support the facts within our articles. Read oureditorial processto learn more about how we fact-check and keep our content accurate, reliable, and trustworthy.Castillo JR, Peters SP, Busse WW.Asthma exacerbations: Pathogenesis, prevention, and treatment.J Allergy Clin Immunol Pract. 2017;5(4):918-927. doi:10.1016/j.jaip.2017.05.001Zhou-Suckow Z, Duerr J, Hagner M, Agrawal R, Mall MA.Airway mucus, inflammation and remodeling: emerging links in the pathogenesis of chronic lung diseases.Cell Tissue Res. 2017;367(3):537-550. doi:10.1007/s00441-016-2562-zYamauchi K, Inoue H.Airway remodeling in asthma and irreversible airflow limitation-ECM deposition in airway and possible therapy for remodeling.Allergol Int. 2007;56(4):321-9. doi:10.2332/allergolint.R-07-151Ferreira VL, Borba HH, Bonetti ADF, Leonart LP, Pontarolo R.Cytokines and interferons: Types and functions.Autoantibodies and Cytokines. 2019. doi:10.5772/intechopen.74550Yamauchi K, Ogasawara M.The role of histamine in the pathophysiology of asthma and the clinical efficacy of antihistamines in asthma therapy.Int J Mol Sci. 2019;20(7) doi:10.3390/ijms20071733Lee K, Lee SH, Kim TH.The biology of prostaglandins and their role as a target for allergic airway disease therapy.Int J Mol Sci. 2020;21(5):1851. doi:10.3390/ijms21051851Al-Azzam N, Elsalem L.Leukotriene D4 role in allergic asthma pathogenesis from cellular and therapeutic perspectives.Life Sci. 2020;260:118452. doi:10.1016/j.lfs.2020.118452Ulambayar B, Yang EM, Cha HY, Shin YS, Park HS, Ye YM.Increased platelet activating factor levels in chronic spontaneous urticaria predicts refractoriness to antihistamine treatment: an observational study.Clin Transl Allergy. 2019;9:33. doi:10.1186/s13601-019-0275-6Siracusa MC, Kim BS, Spergel JM, Artis D.Basophils and allergic inflammation.J Allergy Clin Immunol. 2013;132(4):789-788. doi:10.1016/j.jaci.2013.07.046de Groot JC, ten Brinke A, Bel EH.Management of the patient with eosinophilic asthma: a new era begins.ERJ Open Res. 2015;1(1):00024-2015-. doi:10.1183/23120541.00024-2015Ray A, Kolls JK.Neutrophilic inflammation in asthma and association with disease severity.Trends Immunol. 2017;38(12):942-954. doi:10.1016/j.it.2017.07.003Mantovani A, Cassatella MA, Costantini C, Jaillon S.Neutrophils in the activation and regulation of innate and adaptive immunity.Nat Rev Immunol. 2011;11(8):519-531. doi:10.1038/nri3024Rucker D, Dhamoon AS.Physiology, thromboxane A2. In:StatPearls. Treasure Island (FL): StatPearls Publishing.Fahy JV.Type 2 inflammation in asthma–present in most, absent in many.Nat Rev Immunol. 2015;15(1):57-65. doi:10.1038/nri3786Quirt J, Hildebrand KJ, Mazza J, Noya F, Kim H.Asthma.Allergy Asthma Clin Immunol. 2018;14(Suppl 2):50. doi:10.1186/s13223-018-0279-0Price D, Fletcher M, Van der molen T.Asthma control and management in 8,000 European patients: the REcognise Asthma and LInk to Symptoms and Experience (REALISE) survey.NPJ Prim Care Respir Med. 2014;24:14009. doi:10.1038/npjpcrm.2014.9Finn DF, Walsh JJ.Twenty-first century mast cell stabilizers.Br J Pharmacol. 2013;170(1):23-37. doi:10.1111/bph.12138Singh RK, Tandon R, Dastidar SG, Ray A.A review on leukotrienes and their receptors with reference to asthma.J Asthma. 2013;50(9):922-931. doi:10.3109/02770903.2013.823447Additional ReadingLynn S, Kushto-Reese K.Understanding asthma pathophysiology, diagnosis, and management.American Nursing Today.2015;10(7):49-51.
Verywell Health uses only high-quality sources, including peer-reviewed studies, to support the facts within our articles. Read oureditorial processto learn more about how we fact-check and keep our content accurate, reliable, and trustworthy.
Castillo JR, Peters SP, Busse WW.Asthma exacerbations: Pathogenesis, prevention, and treatment.J Allergy Clin Immunol Pract. 2017;5(4):918-927. doi:10.1016/j.jaip.2017.05.001Zhou-Suckow Z, Duerr J, Hagner M, Agrawal R, Mall MA.Airway mucus, inflammation and remodeling: emerging links in the pathogenesis of chronic lung diseases.Cell Tissue Res. 2017;367(3):537-550. doi:10.1007/s00441-016-2562-zYamauchi K, Inoue H.Airway remodeling in asthma and irreversible airflow limitation-ECM deposition in airway and possible therapy for remodeling.Allergol Int. 2007;56(4):321-9. doi:10.2332/allergolint.R-07-151Ferreira VL, Borba HH, Bonetti ADF, Leonart LP, Pontarolo R.Cytokines and interferons: Types and functions.Autoantibodies and Cytokines. 2019. doi:10.5772/intechopen.74550Yamauchi K, Ogasawara M.The role of histamine in the pathophysiology of asthma and the clinical efficacy of antihistamines in asthma therapy.Int J Mol Sci. 2019;20(7) doi:10.3390/ijms20071733Lee K, Lee SH, Kim TH.The biology of prostaglandins and their role as a target for allergic airway disease therapy.Int J Mol Sci. 2020;21(5):1851. doi:10.3390/ijms21051851Al-Azzam N, Elsalem L.Leukotriene D4 role in allergic asthma pathogenesis from cellular and therapeutic perspectives.Life Sci. 2020;260:118452. doi:10.1016/j.lfs.2020.118452Ulambayar B, Yang EM, Cha HY, Shin YS, Park HS, Ye YM.Increased platelet activating factor levels in chronic spontaneous urticaria predicts refractoriness to antihistamine treatment: an observational study.Clin Transl Allergy. 2019;9:33. doi:10.1186/s13601-019-0275-6Siracusa MC, Kim BS, Spergel JM, Artis D.Basophils and allergic inflammation.J Allergy Clin Immunol. 2013;132(4):789-788. doi:10.1016/j.jaci.2013.07.046de Groot JC, ten Brinke A, Bel EH.Management of the patient with eosinophilic asthma: a new era begins.ERJ Open Res. 2015;1(1):00024-2015-. doi:10.1183/23120541.00024-2015Ray A, Kolls JK.Neutrophilic inflammation in asthma and association with disease severity.Trends Immunol. 2017;38(12):942-954. doi:10.1016/j.it.2017.07.003Mantovani A, Cassatella MA, Costantini C, Jaillon S.Neutrophils in the activation and regulation of innate and adaptive immunity.Nat Rev Immunol. 2011;11(8):519-531. doi:10.1038/nri3024Rucker D, Dhamoon AS.Physiology, thromboxane A2. In:StatPearls. Treasure Island (FL): StatPearls Publishing.Fahy JV.Type 2 inflammation in asthma–present in most, absent in many.Nat Rev Immunol. 2015;15(1):57-65. doi:10.1038/nri3786Quirt J, Hildebrand KJ, Mazza J, Noya F, Kim H.Asthma.Allergy Asthma Clin Immunol. 2018;14(Suppl 2):50. doi:10.1186/s13223-018-0279-0Price D, Fletcher M, Van der molen T.Asthma control and management in 8,000 European patients: the REcognise Asthma and LInk to Symptoms and Experience (REALISE) survey.NPJ Prim Care Respir Med. 2014;24:14009. doi:10.1038/npjpcrm.2014.9Finn DF, Walsh JJ.Twenty-first century mast cell stabilizers.Br J Pharmacol. 2013;170(1):23-37. doi:10.1111/bph.12138Singh RK, Tandon R, Dastidar SG, Ray A.A review on leukotrienes and their receptors with reference to asthma.J Asthma. 2013;50(9):922-931. doi:10.3109/02770903.2013.823447
Castillo JR, Peters SP, Busse WW.Asthma exacerbations: Pathogenesis, prevention, and treatment.J Allergy Clin Immunol Pract. 2017;5(4):918-927. doi:10.1016/j.jaip.2017.05.001
Zhou-Suckow Z, Duerr J, Hagner M, Agrawal R, Mall MA.Airway mucus, inflammation and remodeling: emerging links in the pathogenesis of chronic lung diseases.Cell Tissue Res. 2017;367(3):537-550. doi:10.1007/s00441-016-2562-z
Yamauchi K, Inoue H.Airway remodeling in asthma and irreversible airflow limitation-ECM deposition in airway and possible therapy for remodeling.Allergol Int. 2007;56(4):321-9. doi:10.2332/allergolint.R-07-151
Ferreira VL, Borba HH, Bonetti ADF, Leonart LP, Pontarolo R.Cytokines and interferons: Types and functions.Autoantibodies and Cytokines. 2019. doi:10.5772/intechopen.74550
Yamauchi K, Ogasawara M.The role of histamine in the pathophysiology of asthma and the clinical efficacy of antihistamines in asthma therapy.Int J Mol Sci. 2019;20(7) doi:10.3390/ijms20071733
Lee K, Lee SH, Kim TH.The biology of prostaglandins and their role as a target for allergic airway disease therapy.Int J Mol Sci. 2020;21(5):1851. doi:10.3390/ijms21051851
Al-Azzam N, Elsalem L.Leukotriene D4 role in allergic asthma pathogenesis from cellular and therapeutic perspectives.Life Sci. 2020;260:118452. doi:10.1016/j.lfs.2020.118452
Ulambayar B, Yang EM, Cha HY, Shin YS, Park HS, Ye YM.Increased platelet activating factor levels in chronic spontaneous urticaria predicts refractoriness to antihistamine treatment: an observational study.Clin Transl Allergy. 2019;9:33. doi:10.1186/s13601-019-0275-6
Siracusa MC, Kim BS, Spergel JM, Artis D.Basophils and allergic inflammation.J Allergy Clin Immunol. 2013;132(4):789-788. doi:10.1016/j.jaci.2013.07.046
de Groot JC, ten Brinke A, Bel EH.Management of the patient with eosinophilic asthma: a new era begins.ERJ Open Res. 2015;1(1):00024-2015-. doi:10.1183/23120541.00024-2015
Ray A, Kolls JK.Neutrophilic inflammation in asthma and association with disease severity.Trends Immunol. 2017;38(12):942-954. doi:10.1016/j.it.2017.07.003
Mantovani A, Cassatella MA, Costantini C, Jaillon S.Neutrophils in the activation and regulation of innate and adaptive immunity.Nat Rev Immunol. 2011;11(8):519-531. doi:10.1038/nri3024
Rucker D, Dhamoon AS.Physiology, thromboxane A2. In:StatPearls. Treasure Island (FL): StatPearls Publishing.
Fahy JV.Type 2 inflammation in asthma–present in most, absent in many.Nat Rev Immunol. 2015;15(1):57-65. doi:10.1038/nri3786
Quirt J, Hildebrand KJ, Mazza J, Noya F, Kim H.Asthma.Allergy Asthma Clin Immunol. 2018;14(Suppl 2):50. doi:10.1186/s13223-018-0279-0
Price D, Fletcher M, Van der molen T.Asthma control and management in 8,000 European patients: the REcognise Asthma and LInk to Symptoms and Experience (REALISE) survey.NPJ Prim Care Respir Med. 2014;24:14009. doi:10.1038/npjpcrm.2014.9
Finn DF, Walsh JJ.Twenty-first century mast cell stabilizers.Br J Pharmacol. 2013;170(1):23-37. doi:10.1111/bph.12138
Singh RK, Tandon R, Dastidar SG, Ray A.A review on leukotrienes and their receptors with reference to asthma.J Asthma. 2013;50(9):922-931. doi:10.3109/02770903.2013.823447
Lynn S, Kushto-Reese K.Understanding asthma pathophysiology, diagnosis, and management.American Nursing Today.2015;10(7):49-51.
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