The microRNAs (miRNAs/miRs) are a class of short non-coding RNAs regulating protein translation via mRNAs silencing. Studies have shown that microRNAs play critical roles in allergic diseases, tumors, and infections. The allergic airway diseases are characterized by inflammation and hyperresponsiveness of the respiratory tract. Several miRNAs are found to be involved in a series of pathophysiologic processes in allergic airway diseases including inflammatory cells infiltration, cytokines' expressions, airway hyperresponsiveness, and proliferation and change in phenotype of smooth muscle cells. Therefore, miRNAs may be new therapeutic targets for these allgeric diseases. This article reviews the roles of miRNAs in asthma and allergic rhinitis and their molecular biological mechanisms.
Asthma ; physiopathology ; Humans ; MicroRNAs ; metabolism ; Rhinitis ; physiopathology

Animals ; Humans ; Thymic Stromal Lymphopoietin ; Pyroglyphidae/metabolism* ; Cytokines/metabolism* ; Asthma/metabolism* ; Respiratory System ; Epithelial Cells/metabolism*

Asthma ; diagnosis ; Exhalation ; Humans ; Nitric Oxide ; metabolism ; Respiratory Function Tests

Helper T cell (Th) has been identified as a critical immune cell for regulating immune response since 1980s. The type 2 helper Tcell (Th2), characterized by the production of interleukin-4 (IL-4), IL-5 and IL-13, plays a critical role in immune response against helminths invading cutaneous or mucosal sites. It also has a functional role in the pathophysiology of allergic diseases such as asthma and allergic diarrhea. Currently, most studies have shed light on Th2 cell function and behavior in specific diseases, such as asthma and helminthes inflammation, but not on Th2 cell itself and its differentiation. Based on different cytokines and specific behavior in recent research, Th2 cell is also regarded as new subtypes of T cell, such as IL-9 secreting T cell (Th9) and CXCR5(+) T follicular helper cells. Here, we will discuss the latest view of Th2 cell towards their function and the involvement of Th2 cell in diseases.
Animals ; Asthma ; immunology ; metabolism ; Cell Differentiation ; physiology ; Humans ; Interleukin-9 ; metabolism ; Th2 Cells ; cytology ; immunology ; metabolism

It is widely known that the cockroach is an inhalant allergen in atopic asthma and allergic rhinitis. Even though Bla g I and Bla g II are considered as the major allergens, several relatively high-molecular weight (MW) cockroach allergens have also been recently identified by IgE-immunoblot in western countries. However, the environmental control and diagnostic tests mainly focussed on Bla g I and Bla g II. Furthermore there is no data about major IgE-binding cockroach antigens in Korea. We performed this study to identify the major German cockroach allergens in Korean atopic children. By the results of allergy skin tests, 14 children with atopic asthma (9 were cockroach-sensitive and 5 were cockroach-nonsensitive atopics) were enrolled in this study. We conducted IgE immunoblot and autoradiographic analysis using Yonsei-extract of German cockroach antigen produced in our laboratory, individual sera from 9 cockroach- sensitive children, and the pooled sera of 5 house-dust-mites-only-sensitive children. We performed an allergic skin test to cockroach mix, and a radioallergosorbent test (RAST) using German cockroach crude extract on all subjects. German cockroach-specific IgE was detected in 6 out of 9 subjects by RAST. We identified at least 15 IgE-binding protein bands, and among them, the components of MWs of 76, 64, 50, 38, and <14 kilodaltons (kDa) were the major German cockroach allergens in study subjects. Therefore, Bla g I (25-30 kDa) and Bla g II (36 kDa) could not be the absolute indicators of German cockroach sensitization and parameters of environmental control.
Adolescence ; Allergens/analysis ; Animal ; Asthma/metabolism* ; Asthma/immunology ; Asthma/complications ; Child ; Child, Preschool ; Cockroaches/immunology ; Cockroaches/chemistry* ; Female ; Human ; Hypersensitivity/metabolism* ; Hypersensitivity/immunology ; Hypersensitivity/complications ; IgE/metabolism* ; Korea ; Male ; Tissue Extracts/metabolism*

OBJECTIVEAsthma and chronic obstructive pulmonary disease (COPD) are representative chronic inflammatory airway diseases responsible for a considerable burden of disease. In this article, we reviewed the relationship between neutrophil extracellular traps (NETs) and chronic inflammatory airway diseases.

DATA SOURCESArticles published up to January 1, 2017, were selected from the PubMed, Ovid Medline, Embase databases, with the keywords of "asthma" or "pulmonary disease, chronic obstructive", "neutrophils" and "extracellular traps."

STUDY SELECTIONArticles were obtained and reviewed to analyze the role of NETs in asthma and COPD.

RESULTSNETs are composed of extracellular DNA, histones, and granular proteins, which are released from activated neutrophils. Multiple studies have indicated that there are a large amount of NETs in the airways of asthmatics and COPD patients. NETs can engulf and kill invading pathogens in the host. However, disordered regulation of NET formation has shown to be involved in the development of asthma and COPD. An overabundance of NETs in the airways or lung tissue could cause varying degrees of damage to lung tissues by inducing the death of human epithelial and endothelial cells, and thus resulting in impairing pulmonary function and accelerating the progress of the disease.

CONCLUSIONSExcessive NETs accumulate in the airways of asthmatics and COPD patients. Although NETs play an essential role in the innate immune system against infection, excessive components of NETs can cause lung tissue damage and accelerate disease progression in asthmatics and COPD patients. These findings suggest that administration of NETs could be a novel approach to treat asthma and COPD. Mechanism studies, clinical practice, and strategies to regulate neutrophil activation or directly interrupt NET function in asthmatics and COPD patients are desperately needed.

Animals ; Asthma ; metabolism ; pathology ; Extracellular Traps ; metabolism ; physiology ; Humans ; Neutrophils ; metabolism ; pathology ; Pulmonary Disease, Chronic Obstructive ; metabolism ; pathology

OBJECTIVE: To explore the role of heat shock protein 90α (HSP90α) and endoplasmic reticulum (ER) stress pathway in allergic airway inflammation induced by house dust mite (HDM) in bronchial epithelial cells. METHODS: A HDM- induced asthmatic cell model was established in human bronchial epithelial (HBE) cells by exposure to a concentration gradient (200, 400 and 800 U/mL) of HDM for 24 h. To test the effect of siHSP90α and HSP90 inhibitor 17-AAG on HDM-induced asthmatic inflammation, HBE cells were transfected with siHSP90α (50 nmol, 12 h) or pretreated with 17-AAG (900 nmol, 6 h) prior to HDM exposure (800 U/mL) for 24 h, and the changes in the expression of HSP90α and ER stress markers were assessed. We also tested the effect of nasal drip of 17-AAG, HDM, or their combination on airway inflammation and ER stress in C57BL/6 mice. RESULTS: In HBE cells, HDM exposure significantly up-regulated the expression of HSP90α protein (P=0.011) and ER stress markers XBP-1 (P=0.044), ATF-6α (P=0.030) and GRP-78 (P=0.027). Knocking down HSP90α and treatment with 17-AAG both significantly inhibited HDM-induced upregulation of XBP-1 (P=0.008). In C57BL/6 mice, treatment with 17-AAG obviously improved HDM-induced airway inflammation and significantly reduced the number of inflammatory cells in the airway (P=0.014) and lowered the levels of IL-4 (P=0.030) and IL-5 (P=0.035) in alveolar lavage fluid. Immunohistochemical staining showed that the expressions of XBP-1 and GRP-78 in airway epithelial cells decreased significantly after the treatment of 17-AAG. CONCLUSIONS HSP90α promotes HDM-induced airway allergic inflammation possibly by upregulating ER stress pathway in bronchial epithelial cells.
Animals ; Asthma/metabolism* ; Endoplasmic Reticulum Stress ; Epithelial Cells ; Inflammation/metabolism* ; Mice ; Mice, Inbred C57BL ; Pyroglyphidae

Asthma ; metabolism ; therapy ; Breath Tests ; Child ; Child, Preschool ; Female ; Humans ; Male ; Nitric Oxide ; metabolism

OBJECTIVETo study the utility of fractional exhaled nitric oxide (FeNO) in young children at different stages of asthma.

METHODSFifty-eight children with newly diagnosed asthma (aged 1-3 years) at the acute exacerbation stage between April and June, 2014 were recruited. After 3 months' treatment, the children switched into the chronic persistent stage (n=34) or remission stage (n=24). Thirty aged-matched healthy children served as controls. FeNO levels and lung function were measured for all subjects. The best cut-off value of FeNO for the diagnosis of asthma was evaluated by receiver operating characteristic (ROC) curve.

RESULTSThe FeNO levels in children with asthma at various stages were higher than controls (P<0.05). The FeNO levels in the acute exacerbation stage were highest, followed by the chronic persistent stage (P<0.05). FeNO level was correlated to the stages of asthma (r=-0.382, P<0.001). The cut-off value of FeNO for the diagnosis of asthma was 22.75 ppb by ROC curve, with the sensitivity of 0.933 and the specificity of 0.388.

CONCLUSIONSThe children with asthma at different stages have different FeNO levels. Measurement of FeNO is useful in the diagnosis of asthma in young children.

Asthma ; diagnosis ; metabolism ; Breath Tests ; Humans ; Nitric Oxide ; metabolism ; ROC Curve

Coronavirus disease 2019 (COVID-19) caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) has affected 660 million people and resulted in 6.7 million deaths. At present, a variety of risk factors related to the severity of COVID-19 have been identified, but whether allergic rhinitis and asthma will affect SARS-CoV-2 infection remains controversial. In general, there is no sufficient evidence to support that allergic rhinitis or asthma is a risk factor for increasing the rate of SARS-CoV-2 infection or aggravating the disease. Some studies even show that atopy may be a protective factor to alleviate SARS-CoV-2 infection, which is related to the decreased expression of angiotensin-converting enzyme 2, the receptor required for SARS-CoV-2 to enter cells, in atopic individuals. This paper reviews the influence of the severity and treatment of allergic rhinitis and asthma on SARS-CoV-2 infection, in order to provide some references for establishing strategies for prevention, risk stratification and treatment of COVID-19.
Humans ; COVID-19 ; SARS-CoV-2/metabolism* ; Peptidyl-Dipeptidase A/metabolism* ; Asthma/therapy* ; Rhinitis, Allergic