Content area

Full text

Youngwoo Choi [1] and Le Duy Pham [1; 2; 3] and Dong-Hyun Lee [2] and Ga-Young Ban [1] and Ji-Ho Lee [1] and Seung-Hyun Kim [4] and Hae-Sim Park [1; 2; 4]

Academic Editor: Younghyo Kim

1, Department of Allergy and Clinical Immunology, Ajou University School of Medicine, Suwon, Republic of Korea, ajou.ac.kr

2, Department of Biomedical Sciences, Graduate School of Ajou University, Suwon, Republic of Korea, ajou.ac.kr

3, Faculty of Medicine, University of Medicine and Pharmacy, Ho Chi Minh City, Vietnam, yds.edu.vn

4, Clinical Trial Center, Ajou University Medical Center, Suwon, Republic of Korea, ajou.ac.kr

Received May 30, 2017; Revised Jul 20, 2017; Accepted Aug 1, 2017

This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

1. Introduction

Asthma is a chronic inflammatory disease of the airways. Approximately 5%–10% of patients with asthma exhibit severe symptoms that are not easily controlled by regular medication [1–3]. Severe neutrophilic asthma is a major phenotype of severe asthma (SA), in which neutrophils significantly contribute to the exacerbation of symptoms and airway remodeling [4]. However, the role of neutrophils in pathophysiological mechanisms responsible for SA has not been fully determined.

Recent studies have demonstrated that neutrophils participate in autoimmune disease [5, 6]; furthermore, autoimmune mechanisms, such as the deposition of autoantibodies in specific tissues, are known to play a role in asthma [7]. Our group previously found circulating autoantibodies, such as anti-cytokeratin (CK) 18, anti-CK19, and anti-α-enolase antibodies, against proteins expressed by airway epithelial cells (AECs) in patients with SA [8, 9]. Moreover, antibodies against tissue transglutaminase (tTG) were detected in patients with toluene diisocyanate-induced occupational asthma, which is generally associated with a neutrophilic phenotype [10]. Although autoimmune responses are associated with the pathogenesis of asthma [11], the mechanisms by which these autoantigens are generated in SA remain poorly understood.

Neutrophils, which are the most abundant leukocytes in humans, produce cytotoxic granule proteins [12]. Recently, it has been suggested that activated neutrophils undergo a novel form of cell death during which a meshwork of chromatin with bound granule proteins, known as neutrophil extracellular DNA traps (NETs), is released [13, 14]. A previous study demonstrated high...

Show less