Search

Background ： L ysophosphatidylcholine ( LPC ) is generated through the hydrolysis of phospha-tidylcholine (PC) by phospholipase A2 and is converted back to PC by lysophosphatidylcholine acyltransferase 1 (LPCAT1). E levated levels of (LPC) are known to play a pathogenic role in the inflammatory injury of asthma. However, the role of LPCAT1 in asthma has not yet been reported. Objective : T o determine whether the e xogenous expression of LPCAT1, delivered by using a recombinant lentiviral vector, could att enuate airway inflammation in asthmatic mice. Methods : Recombinant lentivirus carrying cDNA encoding LPCAT1 ( Lenti-LPCAT1 ), or EGFP (Lenti-EGFP) as a control, was constructed. BALB/c mice were sensitised with ovalbumin (OVA), and intratracheally pre-treated with an endobronchial administration of the recombinant lentivirus intratracheally 72 hours before the first challenge. After the last OVA challenges, the mice were assessed for airway inflammation, airway hyper-responsiveness and lipid levels. Results : Lenti -LPCAT1-infected HEK 293 T cells expressed exogenous recombinant LPCAT1 protein that showed high activity of the LPC acyltransferase. OVA sensitisation and challenge significantly increased the levels of saturated species LPC 16:0 and LPC 18:0 levels in the bronchoalveolar lavage fluid (BALF) compared with wild-type mice respectively. The intratracheal Lenti-LPCAT1 instillation obviously down-regulated the OVA-induced release of LPC 16:0 and LPC 18:0. Treatment with Lenti-LPCAT1 ameliorated OVA-induced airway hyper-responsiveness and reduced airway eosinophilia infiltration in lung tissue. Furthermore, the secretion of eotaxin and Th2-associated cytokines IL-5 and IL-13 were inhibited in BALF. The level of OVA-specific IgE in serum was suppressed. Conclusions: These results suggested that the exogenous expression of LPCAT1 may attenuate eosinophil inflammation in the airway by down-regulating the LPC 16:0 and LPC 18:0 BALF levels in asthmatic mice.

Background: IL-35 has been found to be involved in many inflammatory diseases in humans but its role in asthma and chronic obstructive pulmonary disease (COPD) is not clear. The plasma level of IL-35 in patients with asthma and COPD needs to be measured. Objective: The aim of this study was to examine the plasma concentrations of IL-35 in newly diagnosed asthmatic and COPD patients and control subjects and investigate correlations of lung function, age, sex, smoking history with the levels of IL-35 in plasma in these diseases. Methods: Blood samples were collected from patients with newly diagnosed asthma (44, 12 males, aged 33.75±8.94), newly diagnosed COPD (36, 36 males, aged 68.03±8.94), and healthy control groups (23, 9 males, aged 30.06±7.50). We determined the IL-35 levels in plasma by enzyme-linked immunosorbent assay. Result: The median and the range of values for IL-35 were 118.55 pg/ml (range 74.43~1767.22 pg/ml) in patients with asthma, 275.86 pg/ml (range 26.11~1766.20 pg/ml) in patients with COPD, and 136.09 pg/ml (range 62.54~697.49 pg/ml) in control subjects. The levels of IL-35 in plasma showed a positive correlation with FEV1% and FVC% in asthmatic patients whose plasma IL-35 values were over 150 pg/ml. A positive correlation was also found between plasma IL-35 and FVC% in COPD patientswhose plasma IL-35 values were over 150 pg/ml. Conclusions: These findings suggest that IL-35 may very probably be involved in the Th2 and Th17 mediated inflammation process of asthma and COPD. Its role in the mechanisms of COPD and asthma in human beings, as well as its therapeutic value in these diseases, need further investigation.

Background: Whether CD8 + IL-17-producing T cells, namely Tc17 cells, play a role in asthma has not been determined. The aim of this study was to evaluate and compare the frequency of peripheral blood Th17 cells and Tc17 cells in asthmatic patients. In addition, the number, ratio and distribution of Th17 cells and Tc17 cells in the lung tissue and splenocytes of asthmatic mice were also investigated. Methods: Th17 and Tc17 cells in the peripheral blood samples of asthmatic patients and in murine spleens were detected by flow cytometric analysis. Th17 and Tc17 cells in murine lung tissues were detected by double immunofluorescence stain. IL-17A levels in murine bronchoalveolar lavage were detected by ELISA. Results: The result of the flow cytometric analysis showed the percentage of Th17 cells among CD3+ T cell populations in patients with asthma was higher than that in healthy controls ( P

It has been of great interest whether mometasone furoate (MF) is better than other inhaled corticosteroids (ICSs) as the controller therapy in patients with moderate or severe asthma who had previously been taking ICSs.The aim of this meta-analysis is to thoroughly compare the efficacy and safety of MF versus other ICSs with equipotent daily doses in those patients.Relative databases were searched. Randomised controlled trials of more than or equal to 4 weeks' treatment duration comparing MF with other ICSs were reviewed.Six trials with 1354 randomised patients met the inclusion criteria. Significant differences favouring MF were found in all indices of pulmonary function. MF was superior compared to other ICSs in decreasing the frequency of rescue medication use and morning difficulty breathing score. There was no significant difference between MF and other ICSs therapy in morning wheezing score, cough score and percentage of patients with no nocturnal awakenings due to asthma. For the treatment-related adverse effects (AEs), treatment-related severe AEs, discontinuations due to AEs and some common symptom of AEs, MF was all similar to other ICSs in their incidence.In adult patients with moderate or severe asthma who had previously been taking ICSs, MF was superior to other ICSs with equipotent daily doses as controller monotherapy in improving pulmonary function and decreasing the frequency of rescue medication use, and was similar to other ICSs in the incidence of AEs. These results demonstrated the priority of MF in asthma therapy.

We sought to determine whether the aryl hydrocarbon receptor (AhR) and interleukin (IL)-22 may be involved in the pathogenesis of the peripheral blood mononuclear cells (PBMCs) in allergic asthmatic patients and whether their expression may be related to the severity of the disease.Blood samples were obtained from each subject with allergic asthma (n =18), controlled asthma (n = 17) and healthy controls (n = 12) respectively. The PBMCs were collected for AhR mRNA detection by real-time quantitative polymerase chain reaction (PCR). The plasma was collected for IL-22 protein detection by enzyme-linked immunosorbent assay (ELISA).The expression of AhR mRNA in PBMCs and IL-22 protein in plasma of patients with allergic asthma were higher than those in controlled asthma cases and healthy controls. The plasma concentrations of IL-22 had negative correlation with the predicted percentage of forced expiratory volume in the first second (FEV1%) and the percentage of FEV1 and forced vital capacity (FEV1/FVC%) and it was positively correlated with the asthma severity score (ASS) of the asthmatics.Our results suggested that both AhR and IL-22 might be involved in the pathogenesis of allergic asthma in human and the level of IL-22 might have some relationship with the severity of the disease.