Asthma: Cause, Development, and Progression

Asthma is a chronic respiratory disorder that affects millions of people worldwide. It is characterized by chronic inflammation of the airways, which leads to recurrent episodes of wheezing, breathlessness, chest tightness, and coughing. The underlying biochemistry of asthma involves a complex interplay between genetic, environmental, and immune factors. In this article, we will explore the biochemistry of asthma and how it leads to the development and progression of this condition.

Asthma and Inflammation:

One of the key features of asthma is chronic inflammation of the airways. This inflammation is driven by a complex network of immune cells, cytokines, chemokines, and other inflammatory mediators. Inhaled allergens, such as pollen, dust mites, and animal dander, can trigger an allergic response in susceptible individuals, leading to the activation of immune cells and the release of inflammatory mediators. These mediators cause a range of effects on the airways, including increased mucus production, bronchoconstriction, and airway remodeling.

Airway remodeling is a hallmark of chronic asthma and involves structural changes to the airways that result in reduced lung function. This process is driven by the chronic inflammation and can include thickening of the airway walls, increased smooth muscle mass, and fibrosis. These changes make the airways less responsive to bronchodilator medications, such as albuterol, and can lead to irreversible lung damage over time.

Role of Immune Cells:

Many different immune cells are involved in the inflammation that drives asthma. These cells include eosinophils, mast cells, T-helper cells, and macrophages, among others. Eosinophils are a type of white blood cell that is typically elevated in asthma patients. They release inflammatory mediators and are involved in the development of airway hyperresponsiveness. Mast cells are another important cell type in asthma and release histamine, leukotrienes, and other mediators that cause airway constriction and inflammation.

T-helper cells play a critical role in the development of asthma. These cells can differentiate into several different subtypes, including Th1, Th2, and Th17 cells. Th2 cells are particularly important in asthma and produce cytokines such as interleukin-4, -5, and -13, which promote eosinophilic inflammation and mucus production. Th17 cells produce cytokines that are involved in neutrophilic inflammation, which can be present in some severe asthma cases.

Biochemical Pathways:

The biochemical pathways involved in asthma are numerous and complex. One of the most important pathways is the arachidonic acid pathway, which involves the metabolism of arachidonic acid into various pro-inflammatory mediators, such as leukotrienes and prostaglandins. These mediators are involved in bronchoconstriction, mucus production, and airway inflammation. Inhibition of this pathway is the target of some asthma medications, such as leukotriene receptor antagonists.

Another important pathway in asthma is the cholinergic pathway. Acetylcholine is a neurotransmitter that is involved in airway constriction. In asthma, this pathway is overactive, leading to increased bronchoconstriction. Muscarinic receptor antagonists, such as ipratropium bromide, can block this pathway and improve symptoms.

Chronic inflammation of the airways is a key feature of asthma and leads to airway remodeling, mucus production, and bronchoconstriction. Immune cells, such as eosinophils, mast cells, and T-helper cells play a significant role in the development and progression of asthma.

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Gaston B. The biochemistry of assthma. Biochim Biophys Acta. 2011 Nov;1810(11):1017-24. doi: 10.1016/j.bbagen.2011.06.008. Epub 2011 Jun 22. PMID: 21718756.

Gillissen A, Paparoupa M. Inflammation and infections in assthma. Clin Respir J. 2015 Jul;9(3):257-69. doi: 10.1111/crj.12135. Epub 2014 May 15. PMID: 24725460; PMCID: PMC7162380.

Huang YJ. The respiratory microbiome and innate immunity in assthma. Curr Opin Pulm Med. 2015 Jan;21(1):27-32. doi: 10.1097/MCP.0000000000000124. PMID: 25405668; PMCID: PMC4398309.

Quirt J, Hildebrand KJ, Mazza J, Noya F, Kim H. Asthma. Allergy Assthma Clin Immunol. 2018 Sep 12;14(Suppl 2):50. doi: 10.1186/s13223-018-0279-0. PMID: 30275843; PMCID: PMC6157154.

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