Effects of Medication Use on Small Airway Function and Airway Inflammation in Patients with Clinically Controlled Asthma

Objective To observe effects of medication use on small airway function,airway inflammation and acute exacerbations in patients with clinically controlled asthma.Methods Forced expiratory flow over the middle half of the forced expiratory curve(FEF25%–75%),percentage of eosinophil,concentrations of eosinophil cationic protein(ECP)and interleukin(IL)-5 in induced sputum were assessed in patients with clinically controlled asthma who were given oral anti-inflammatory agents alone or in combination with inhaled therapy and inhaled therapy alone.Subsequently,acute exacerbations were compared between two groups during the 24-week follow-up period.Results FEF25%–75%in 43 patients with clinically controlled asthma given oral anti-inflammatory agents alone or in combination with inhaled therapy was significantly higher than that in 49 patients given inhaled therapy alone.Meanwhile,the percentage of eosinophils and levels of IL-5 and ECP in patients with clinically controlled asthma given oral anti-inflammatory agents alone or in combination with inhaled therapy were significantly lower than those in patients given inhaled therapy alone.Additionally,the patients with clinically controlled asthma given inhaled therapy were likely to have more acute exacerbation than the patients given oral anti-inflammatory agents alone or in combination with inhaled therapy during the 24-week follow-up period.Conclusion Systemic anti-inflammatory agents may have a greater effect on parameters reflecting small airway patency and reducing acute exacerbations,presumably secondary to reduction in airway inflammation.

Effects of Shenmai and Aminophylline on Apoptosis of Small Airway Smooth Muscle Cells and the Expression of Relevant Genes in Rats with Emphysema

The effects of Shenmai injection (SMI) and am inophylline on apoptosis of sm all airway smooth muscle cells (SASMC) and the Fas/ Fas L expression in rats with papain- induced em physe- ma were investigated.Rat emphysema model was established by a single intratracheal instillation of papain.Apoptosis and Fas/Fas L expression of SASMC were detected by im munohistochemistry SABC and TU NEL assay at day1,3,5 ,7,15 ,30 after modeling,and the effect of SMI and am inophylline on them were observed.The results indicated that the Fas/Fas L expression positive rate in SASMC was2 .31± 0 .5 5 /1.2 8± 0 .4 7respectively.After a single intratracheal instillation of papain,the expression of Fas/Fas L positive rate in the placebo group was increased in a tim e- dependent manner.SMI could inhibit the expression of Fas/ Fas L ,but aminophylline couldn't. The positive rate of apoptosis in the control group was 0 .87± 0 .32 .After a single intratracheal in- stillation of papain,the SASMC apoptosis positive rate in the placebo group was increased in a tim e- dependent manner.The SASMC apoptosis rate in all groups was declined after treatment with SMI,but the effect of am inophylline was notobvious.Itwas dem onstrated thatin the patho- genesis of emphysem a Fas/Fas L played an important role in the regulation of SASMC apoptosis. SMI influenced the expression of Fas/ Fas L and declined SASMC apoptosis by inhibiting the releas- ing of inflamm atory m edia and played an im portant role in the therapy of em physema.

Small airways in asthma:Pathophysiology,identification and management

Background:The aim of this review is to summarize the current evidence regarding small airway disease in asthma,focusing on recent advances in small airway pathophysiology,assessment and therapeutic implications.Methods:A search in Medline was performed,using the keywords“small airways”,“asthma”,“oscillometry”,“nitrogen washout”and“imaging”.Our review was based on studies from adult asthmatic patients,although evidence from pediatric populations is also discussed.Results:In asthma,inflammation in small airways,increased mucus production and airway wall remodelling are the main pathogenetic mechanisms of small airway disease.Small airway dysfunction is a key component of asthma pathophysiology,leading to increased small airway resistance and airway closure,with subsequent ventilation inhomogeneities,hyperresponsiveness and airflow limitation.Classic tests of lung function,such as spirometry and body plethysmography are insensitive to detect small airway disease,providing only indirect measurements.As discussed in our review,both functional and imaging techniques that are more specific for small airways,such as oscillometry and the multiple breath nitrogen washout have delineated the role of small airways in asthma.Small airways disease is prevalent across all asthma disease stages and especially in severe disease,correlating with important clinical outcomes,such as asthma control and exacerbation frequency.Moreover,markers of small airways dysfunction have been used to guide asthma treatment and monitor response to therapy.Conclusions:Assessment of small airway disease provides unique information for asthma diagnosis and monitor-ing,with potential therapeutic implications.

Computed tomography-identified phenotypes of small airway obstructions in chronic obstructive pulmonary disease

Chronic obstructive pulmonary disease(COPD)is a heterogeneous disease characteristic of small airway inflammation,obstruction,and emphysema.It is well known that spirometry alone cannot differentiate each separate component.Computed tomography(CT)is widely used to determine the extent of emphysema and small airway involvement in COPD.Compared with the pulmonary function test,small airway CT phenotypes can accurately reflect disease severity in patients with COPD,which is conducive to improving the prognosis of this disease.CT measurement of central airway morphology has been applied in clinical,epidemiologic,and genetic investigations as an inference of the presence and severity of small airway disease.This review will focus on presenting the current knowledge and methodologies in chest CT that aid in identifying discrete COPD phenotypes.

The sounds of small airways： emerging role in pathogenesis and clinical expression of asthma

Asthma is a heterogeneous disease that involves a complex interplay of genetic and environmental factors, leading to＇chronicinflammation and airway remodeling. The major features that lead to clinical symptoms are infiltration of inflammatory cells, epithelial shedding, mucous gland hyperplasia, increased airway smooth muscle mass and contraction,

Idiopathic airway-centered interstitial fibrosis:report of two cases

Airway-centered interstitial fibrosis （ACIF）, a novel .form of diffuse interstitial lung disease （ILD） of unknown cause, was recently presented. There is no final conclusion on its property and denomination, and it might be a new type of idiopathic interstitial pneumonia （IIP）. Histopathologically, it was characterized by progressive lobular or small ACIF, and neither similar to any known category of airway disease and ILD, nor similar to known subtype of HE It showed a poor response to corticosteroids and poor progrnosis. It has been reported in Caucasian patients, here, we utilized the term idiopathic airway-centered interstitial fibrosis （IAIF） for the disease to report 2 Chinese patients, in order to improve understanding and diagnosis of this disease.

Hydrogen Sulfide Inhibits Transforming Growth Factor Beta-1 Induced Bronchial Epithelial-mesenchymal Transition

INTRODUCTION Chronic obstructive pulmonary disease （COPD） is one of the leading causes of death in the developed world and associated with a high individual and socioeconomic burden. It is characterized by persistent airflow limitation that is usually progressive and associated with an enhanced chronic inflammatory response in the airways and the lung to noxious panicles or gases. Peri-bronchiolar fibrosis was occurred in small airways in the early state of COPD, and then followed by structure changes, and finally became persistent airflow limitation？21 Recent researches have shown that epithelial-mesenchymal transition （EMT） is one of the leading causes of fibrosis in various diseases.