COMBINED USE OF ACUPUNCTURE AND BLOOD- INJECTION AT THE BACK-SHI; POINTS FOR TREATMENT OF ALLERGIC ASTHMA -A Report of 80 Cases

Allergic asthma is a chronic inflammation of anaphylactic reaction of the respiratory tract. Based on this knowledge, the treatment is given aiming at relieving bronchial spasm or antianaphylaxis and the control of inflammation. A large amount of     

Achieving therapeutic benefits of inhaled corticosteroids/beta2 agonist in chronic obstructive airway disease

Asthma and chronic obstructive pulmonary disease t（COPD） are the two commonest causes of adultairflow obstruction. The fundamental dltterences anti similarities between the pathological mechanisms of asthma and COPD are well recognized.^1 Both asthma and COPD involve inflammation of airway, but the pattern and distribution of inflammation markedly differ between typical patients with asthma and COPD. Chronic lung disease is now the most important long-term pulmonary complication in daily practice, and is associated with prolonged hospitalization and long-term pulmonary and clinical problems.^2     

Pollen Extract of Populus deltoides Stimulates Lung Inflammation in a Mouse Model

<正>Allergic asthma is an inflammatory disease of the airways characterized by recurrent episodes of wheezing,bronchoconstriction,and airway hyperresponsiveness (AHR)^[1].In recent years,allergic asthma has become a heated public health problem because of the highly increased incidence and prevalence^[2].The main pathogenesis of asthma is airway inflammation and AHR.AHR is caused by an imbalance of Th1/Th2 cells with predominance to Th2,whereas airway inflammation is cau...     

Research on airway inflammation: present status in Mainland China

Airway inflammation involving activated eosinophils, mast cells and T lymphocytes is an established feature of asthma and has been the key target to treatment. Airway structural changes thatoccur in patients with asthma in response to persistent inflammation are termed airway remodeling.     

Involvement and therapeutic implications of airway epithelial barrier dysfunction in type 2 inflammation of asthma

Type 2 inflammation is a complex immune response and primary mechanism for several common allergic diseases including allergic rhinitis, allergic asthma, atopic dermatitis, and chronic rhinosinusitis with nasal polyps. It is the predominant type of immune response against helminths to prevent their tissue infiltration and induce their expulsion. Recent studies suggest that epithelial barrier dysfunction contributes to the development of type 2 inflammation in asthma, which may partly explain the...     

Inhibition of interleukin-13 gene expression in T cells through GATA-3 pathway by arsenic trioxide

Aarsenic trioxide （AT） has a long history of use in both traditional Chinese medicine and in modem medicine in asthma therapy. Recently, Yin et al＇ found that AT even at small doses reduced the airway inflammation of sensitized guinea pigs. However the mechanism underlying this is still largely unknown. Interleukin 13 （IL-13）, as one of the important TH2 cytokines, plays an important role in asthma pathogenesis through promoting eosinophilic inflammation,     

Do neutrophils actively participate in airway inflammation and remodeling in asthma?

Previous studies have demonstrated an increase of neutrophils in lung tissues, bronchoalveolar lavage fluid (BALF), and sputum of subjects with severe, often glucocorticoid (GC)-dependent asthma, but the mechanisms behind this are not clear.1-3 Whether neutrophils function to worsen the disease or they are simply 'bystanders' in the process of severe asthma is not certain. However, recent studies suggest a possibly active role of neutrophils in the airway inflammation and potentially in the airway remodeling of asthma.4,5     

Therapeutic potential of antibodies against interleukin 5 in asthma

Bronchial asthma is characterized by chronic recruitment of eosinophils in the airways. It has been reported that bronchial eosinophil recruitment and activation may even occur in mild-moderate stable asthma and that bronchial epithelium damage and airway responsiveness may be partially associated with the eosinophilic inflammatory reaction.1 There is increasing evidence that the eosinophil-rich bronchial inflammation characteristic of asthma is orchestrated, at least partly,     

Persistent asthma increases the risk of chronic kidney disease: a retrospective cohort study of 2354 patients with asthma

Background Chronic kidney disease （CKD） is a growing public health problem with well-established risk factors. Other contributing factors, however, remain to be identified. Systemic inflammation in asthma plays a significant role in the development of other diseases. We therefore initiated a study to assess whether the growing prevalence of asthma is associated with an increase in the risk of CKD.     

Inhibitory effects of sunitinib on ovalbumin-induced chronic experimental asthma in mice

Background Tyrosine kinase signaling cascades play a critical role in the pathogenesis of allergic airway inflammation. Sunitinib, a multitargeted receptor tyrosine kinase inhibitor, has been reported to exert potent immunoregulatory, anti-inflammatory and anti-fibrosis effects. We investigated whether sunitinib could suppress the progression of airway inflammation, airway hyperresponsiveness （AHR）, and airway remodeling in a murine model of chronic asthma.
Methods Ovalbumin （OVA）-sensitized mice were chronically challenged with aerosolized OVA for 8 weeks. Some mice were intragastrically administered with sunitinib （40 mg/kg） daily during the period of OVA challenge. Twelve hours after the last OVA challenge, mice were evaluated for the development of airway inflammation, AHR and airway remodeling. The levels of total serum immunoglobulin E （IgE） and Th2 cytokines （interleukin （IL）-4 and IL-13） in bronchoalveolar lavage fluid （BALF） were measured by ELISA. The expression of phosphorylated c-kit protein in the lungs was detected by immunoprecipitation/Western blotting （IP/WB） analysis.
Results Sunitinib significantly inhibited eosinophilic airway inflammation, persistent AHR and airway remodeling in chronic experimental asthma. It reduced levels of total serum IgE and BALF Th2 cytokines and also lowered the expression of phosphorylated c-kit protein in remodelled airways.
Conclusions Sunitinib may inhibit the development of airway inflammation, AHR and airway remodeling. It is potentially beneficial to the prevention or treatment of asthma.