Mechanism of action of BET bromodomain inhibitor JQ1 in treating airway remodeling in asthmatic mice / 中国当代儿科杂志

<p><b>OBJECTIVE</b>To investigate the molecular mechanism of action of BET bromodomain inhibitor JQ1 in treating airway remodeling in asthmatic mice.</p><p><b>METHODS</b>A total of 24 mice were randomly divided into control group, ovalbumin (OVA)-induced asthma group (OVA group), and JQ1 intervention group (JQ1+OVA group), with 8 mice in each group. OVA sensitization/challenge was performed to establish a mouse model of asthma. At 1 hour before challenge, the mice in the JQ1+OVA group were given intraperitoneal injection of JQ1 solution (50 μg/g). Bronchoalveolar lavage fluid (BALF) and lung tissue samples were collected at 24 hours after the last challenge, and the total number of cells and percentage of eosinophils in BALF were calculated. Pathological staining was performed to observe histopathological changes in lung tissue. RT-PCR and Western blot were used to measure the mRNA and protein expression of E-cadherin and vimentin during epithelial-mesenchymal transition (EMT).</p><p><b>RESULTS</b>Compared with the control group, the OVA group had marked infiltration of inflammatory cells in the airway, thickening of the airway wall, increased secretion of mucus, and increases in the total number of cells and percentage of eosinophils in BALF (P<0.01). Compared with the OVA group, the JQ1+OVA group had significantly alleviated airway inflammatory response and significant reductions in the total number of cells and percentage of eosinophils in BALF (P<0.01). Compared with the control group, the OVA group had significant reductions in the mRNA and protein expression of E-cadherin and significant increases in the mRNA and protein expression of vimentin (P<0.01); compared with the OVA group, the JQ1+OVA group had significant increases in the mRNA and protein expression of E-cadherin and significant reductions in the mRNA and protein expression of vimentin (P<0.01); there were no significant differences in these indices between the JQ1+OVA group and the control group (P>0.05).</p><p><b>CONCLUSIONS</b>Mice with OVA-induced asthma have airway remodeling during EMT. BET bromodomain inhibitor JQ1 can reduce airway inflammation, inhibit EMT, and alleviate airway remodeling, which provides a new direction for the treatment of asthma.</p>

Exhaled Air Molecules and Chronic Obstructive Pulmonary Disease / 中国医学科学院学报

Chronic airway inflammation,a main pathologic process of chronic obstructive pulmonary disease (COPD),can trigger inflammation cells and airway structure cells to produce bioactive molecules,which play key roles in the pathogenesis of COPD and are also an efficient indicators for the diagnosis and treatment of COPD. This article reviews the important roles of these exhaled air molecules in the diagnosis and treatment of COPD,with an attempt to offer new strategies in the management of COPD.

Immunological mechanism of wheezing attack in children with cytomegalovirus infection / 中国当代儿科杂志

<p><b>OBJECTIVE</b>To study the possible immunological mechanism of wheezing attack in children with cytomegalovirus (CMV) infection.</p><p><b>METHODS</b>A total of 25 under-5-year-old children with wheezing following CMV infection were enrolled. The expression of serum regulatory T cells (Treg)/T helper 17 (Th17) cytokines interleukin (IL)-10, IL-6, and IL-17, and peripheral blood lymphocyte subsets were determined. Twenty age-matched healthy children were selected as the control group.</p><p><b>RESULTS</b>The wheezing group had a significantly reduced serum IL-10 level, significantly increased IL-6 and IL-17 levels, significantly reduced levels of natural killer cells, and significantly increased levels of CD8+ T cells and CD19+ B cells, as compared with the control group.</p><p><b>CONCLUSIONS</b>Wheezing children with CMV infection have Treg/Th17 imbalance and cellular immune dysfunction, which may be an important immunological mechanism of the development of wheezing in children after CMV infection.</p>