Azithromycin with IVIG or methylprednisolone was better treatment for children with RMPP than azithromycin alone. IVIG treatment may be beneficial, especially when the efficacy of corticosteroids is insecure, thus could be considered as an alternative of primary therapeutic approaches.

The present study aimed to investigate the effect of epigallocatechin gallate (EGCG) on airway inflammation in mice with bronchial asthma, and the regulatory mechanism of transforming growth factor (TGF)-β1 signaling pathway, so as to provide theoretical basis for research and development of a novel drug for clinical treatment. Mouse models of bronchial asthma were established and injected with dexamethasone and EGCG via the caudal vein. 7 days later, bronchoalveolar tissue was collected for hematoxylin and eosin staining. Determination of airway resistance (AWR) and lung function in mice was detected. Serum was separated for cytometric bead array to detect the changes in inflammatory factors. Bronchoalveolar lavage fluid was collected for eosinophil and neutrophil counts. Fresh blood was obtained for flow cytometry to determine the percentages of Th17 and Treg cells. Bronchovesicular tissue was utilized for western blot assay and reverse transcription-quantitative polymerase chain reaction to determine the proteins and transcription factors in the TGF-β1 pathway. EGCG 20 mg/kg significantly reduced asthmatic symptoms, lung inflammatory cell infiltration, and the inflammatory factor levels of interleukin (IL)-2, IL-6 and tumor necrosis factor (TNF)-α. In addition, it increased the levels of inflammatory factors, including IL-10, diminished the percentage of Th17 cells, increased the percentage of Treg cells, and decreased the expression of TGF-β1 and phosphorylated (p)-Smad2/3 expression. Following the inhibition of the TGF-β1 receptor, the anti-inflammatory effect of EGCG disappeared, and the expression of TGF-β1 and p-Smad2/3 increased. EGCG attenuated airway inflammation in asthmatic mice, decreased the percentage of Th17 cells and increased the percentage of Treg cells. The anti-inflammatory effect of EGCG is achieved via the TGF-β1 signaling pathway.

Vitamin D receptors (VDRs) are associated with the occurrence and development of asthma. The aim of the present study was to analyze the secondary structure and B-cell and T-cell epitopes of VDR using online prediction software and aid in the future development of a highly efficient epitope-based vaccine against asthma. Blood samples were collected from peripheral blood of asthmatic children. Reverse transcription quantitative-polymerase chain reaction (RT-qPCR) was performed to detect the expression of VDR in the peripheral blood. Mouse models of asthma were established. Hematoxylin and eosin staining was performed to observe the pathological alterations of the lungs of mice. Immunohistochemistry, western blot analysis and RT-qPCR were performed to detect the expression of VDR in the lungs of asthmatic mice. Online prediction software immune epitope database and analysis resource, SYFPEITHI and linear epitope prediction based on propensity scale and support vector machines were used to predict the B-cell and T-cell epitopes and the RasMol and 3DLigandSite were used to analyze the tertiary structure of VDR. RT-qPCR demonstrated that VDR expression in the peripheral blood of asthmatic children was decreased. Immunohistochemistry, western blotting and RT-qPCR demonstrated that VDR expression also decreased in the lungs of mouse models of asthma. VDR B-cell epitopes were identified at 37–45, 88–94, 123–131, 231–239, 286–294 and 342–350 positions of the amino acid sequence and VDR T-cell epitopes were identified at 125–130, 231–239 and 265–272 positions. A total of six B-cell epitopes and three T-cell epitopes for VDR were predicted by bioinformatics, which when validated, may in the future aid in immunological diagnosis and development of a targeted drug therapy for clinical asthma.

Background Matrix Gla (γ-carboxyglutamate) protein (MGP) is considered a strong inhibitor of ectopic calcification, and it has been associated with OA severity, although not conclusively. We utilized male Dunkin-Hartley (DH) guinea pigs to investigate the expression of MGP throughout aging and disease pathogenesis in a spontaneous model. Method Twenty-five male DH guinea pigs were obtained and nurtured to several timepoints, and then randomly and equally divided by age into five subgroups (1-, 3-, 6-, 9-, and 12-months, with the 1-month group as the reference group). DH guinea pigs in each group were euthanized at the designated month-age and the left or right medial tibial plateaus cartilages were randomly excised. OA severity was described by modified Mankin Score (MMS) at microscopy (Safranin O/Fast Green stain). Proteomic evaluation using isobaric tags for relative and absolute quantification (iTRAQ) was performed to validate the age-related changes in the MGP profiles, and immunohistochemistry (IHC) methods were applied for semi-quantitative determination of MGP expression in articular cartilage. Results The histopathologic findings validated the increasing severity of cartilage degeneration with age in the DH guinea pigs. The MMS showed significant, stepwise (every adjacent comparison P < 0.05) disease progression with month-age. The iTRAQ indicated that MGP levels increased significantly with advancing age (P < 0.05), as supported by the IHC result (P < 0.05). Conclusion Increased expression of MGP in male DH guinea pigs was present throughout aging and disease progression and may be link to increased OA severity. Further studies are needed to investigate and confirm the association between MGP levels and OA severity.