Distinct functions of eosinophils in severe asthma with type 2 phenotype: clinical implications

Abstract

Asthma is commonly recognized as a heterogeneous condition with a complex pathophysiology. With advances in the development of multiple medications for patients with asthma, most asthma symptoms are well managed. Nevertheless, 5% to 10% of adult asthmatic patients (called severe asthma) are in uncontrolled or partially controlled status despite intensive treatment. Especially, severe eosinophilic asthma is one of the severe asthma phenotypes characterized by eosinophilia in sputum/blood driven by type 2 immune responses. Eosinophils have been widely accepted as a central effector cell in the lungs. Some evidence has demonstrated that persistent eosinophilia in upper and lower airway mucosa contributes to asthma severity by producing various mediators including cytokines, chemokines and granule proteins. Moreover, extracellular traps released from eosinophils have been revealed to enhance type 2 inflammation in patients with severe asthma. These novel molecules have the ability to induce airway inf lammation and hyperresponsiveness through enhancing innate and type 2 immune responses. In this review, we highlight recent insight into the function of eosinophil extracellular traps in patients with severe asthma. In addition, the role of eosinophil extracellular vesicles in severe asthma is also proposed. Finally, current biologics are suggested as a potential strategy for effective management of severe eosinophilic asthma.

Titanium Dioxide Nanoparticles Exacerbate Allergic Airway Inflammation via TXNIP Upregulation in a Mouse Model of Asthma

“…It is characterized by excessive inflammation of bronchi and obstruction of the airflow due to increased immune responses, resulting in varying respiratory symptoms, mainly difficulty in breathing, wheezing, coughing, and tightness in the chest [ 3 , 8 , 9 ]. Based on its main characteristics, asthma has been divided into molecular pathways/clinical presentations or atopic/non-atopic asthma and more recently, into eosinophilic or non-eosinophilic phenotypes based on biological mechanisms [ 10 ]. Proinflammatory cytokines are key players in the development and progression of asthma, and they induce elevated immune responses, resulting in characteristic asthmatic responses such as eosinophilia, airway hyperresponsiveness (AHR), airway remodeling, and mucus production [ 11 ].…”

Effect of TGF-β1 on eosinophils to induce cysteinyl leukotriene E4 production in aspirin-exacerbated respiratory disease

“…Eosinophilia in peripheral blood and upper/lower airway mucosa are commonly found in AERD patients [ 3 ]. Although both mast cells and eosinophils are critical for inducing airway inflammation in the pathogenesis of AERD, emerging evidence supports an important role of eosinophils in its pathogenesis [ 4 , 5 ]. AERD patients have shown that significantly elevated levels of eosinophil-derived granule proteins, such as eosinophil cationic protein (ECP) and eosinophil-derived neurotoxin (EDN), compared to aspirin-tolerant asthma (ATA) patients [ 6 , 7 ].…”

Early Prediction of Severe COVID-19 in Patients by a Novel Immune-Related Predictive Model

“…Recent reports suggested that during virus infection and lung injury, circulating EOS are recruited to the lung tissue to mediate the antiviral response, and this might lead to the decreased amount of EOS in the circulatory system ( 15 , 16 ). Other studies also showed that EOS were recruited to the lungs during the development of asthma ( 17 ). On the other hand, viral infection caused disturbance of the homeostasis of bone marrow, which might further lead to aberrant hematopoiesis ( 18 ) and abnormal production of EOS ( 19 ).…”