Journal of Allergy & Therapy

Mechanisms Involving in Development of Airway Inflamation

¹Department of Infectious Diseases, Lovely Professional University, Gujarat, India
^*Correspondence: Thoma Mizutani, Department of Infectious Diseases, Lovely Professional University, Gujarat, India, Email:

Received: 02-Jun-2022, Manuscript No. JAT-22-17405; Editor assigned: 06-Jun-2022, Pre QC No. JAT-22-17405 (PQ); Reviewed: 20-Jun-2022, QC No. JAT-22-17405; Revised: 30-Jun-2022, Manuscript No. JAT-22-17405 (R); Published: 07-Jul-2022, DOI: 10.35248/2155-6121.22.13.289

Description

The pathophysiology of asthma is heavily influenced by inflammation, bronchial inflammation and airflow restriction, which cause recurrent episodes of cough, wheeze, and shortness of breath. Our study is currently being done to determine the mechanisms by which these interacting events take place and cause clinical asthma. In addition, airway inflammation continues to be a common pattern even when there are different phenotypes of asthma (such as intermittent, persistent, exerciseassociated, aspirin-sensitive, or severe asthma). However, the severity, persistence, and duration of the disease do not always affect the pattern of airway inflammation in asthma.

Lymphocytes

Following the identification and description of the lymphocyte subpopulations known as T helper 1 cells and T helper 2 cells (Th1 and Th2), which have different inflammatory mediator profiles and effects on airway function, there has been a greater understanding of the development and regulation of airway inflammation in asthma. Evidence showed that the eosinophilic inflammation characteristic of asthma was caused by a change, or inclination, toward the Th2-cytokine profile in human asthma when these unique lymphocyte subpopulations were identified in animal models of allergic inflammation.

Mast cells

Bronchoconstrictor mediators (histamine, cysteinyl-leukotrienes, prostaglandin D2) are released when mucosal mast cells are activated. Although allergen activation via high-affinity IgE receptors is likely the most important reaction, osmotic stimuli may also activate sensitised mast cells to account for Exercise- Induced Bronchospasm (EIB). Airway hyperresponsiveness may be connected to an increased number of mast cells in the smooth muscle of the airway. Even if allergen exposure is limited, mast cells can release a high number of cytokines to alter the airway environment and induce inflammation.

Eosinophils

Most, but not all, people with asthma have an increased amount of eosinophils in their airways. Inflammatory enzymes, leukotrienes, and a wide range of pro-inflammatory cytokines are all present in these cells. Increases in eosinophils are frequently linked to increased asthma severity. Furthermore, multiple studies suggest that corticosteroids lower circulating and airway eosinophils in tandem with clinical improvement in asthma patients. However, based on studies with an anti-IL-5 medication that greatly reduced eosinophils while having little effect on asthma control, the role and contribution of eosinophils to asthma is being re-evaluated. Although the eosinophil may not be the only major effector cell in asthma, it is thought to have a unique role at different stages of the disease.

Neutrophils

People with severe asthma have more neutrophils in their airways and sputum, especially during acute exacerbations and when they smoke. Their pathophysiological role is unknown, however they could be a factor in the lack of responsiveness to corticosteroid therapy.

Dendritic cells

These cells serve as crucial antigen-presenting cells, interacting with allergens on the airway surface before migrating to regional lymph nodes, where they interact with regulatory cells and trigger Th2 cell production from naive T cells.

Macrophages

Macrophages are the most numerous cells in the airways, and allergens can activate them via low-affinity IgE receptors, causing them to release inflammatory mediators and cytokines that increase the inflammatory response.

Resident cells of the airway

The smooth muscle of the airway is not only a target of the asthma response (by contracting to impede airflow), but it also contributes to it (via the production of its own family of proinflammatory mediators). The airway smooth muscle cell can experience proliferation, activation, contraction, and hypertrophy as a result of airway inflammation and the production of growth factors-events that can impact asthmatic airway dysfunction. Another important airway lining cell in asthma is the airway epithelium. Inflammatory mediator production, inflammatory cell recruitment and activation, and respiratory virus infection can all induce epithelial cells to create more inflammatory mediators or harm the epithelium.