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Purpose@#Asthma is a serious inflammatory disease of the respiratory system in which airway smooth muscle cells (ASMCs) play a key role. This study aimed to investigate the expression of SLC26A2 in human ASMCs (HASMCs) and the regulatory mechanism of SLC26A2 in the proliferation and inflammatory factor production of HASMCs. @*Materials and Methods@#We obtained the asthma-associated differential mRNA SLC26A2 by bioinformatics analysis in childhood acute asthma samples. To investigate its role in airway inflammation and airway remodeling, we treated HASMCs with plateletderived growth factor (PDGF) in an in vitro model and determined SLC26A2 expression in cells using western blotting. Cell proliferation was detected by MTT and EdU assays, and cell contractile phenotype marker proteins were measured. Cell migration and production of inflammatory factors were determined by Transwell and ELISA assays. Additionally, the upstream regulatory miRNA and LncRNA of SLC26A2 were identified by bioinformatics, luciferase reporter gene, and RIP analyses. @*Results@#SLC26A2 was significantly upregulated in bioinformatics analysis of pediatric asthma-related sample. PDGF treatment up-regulated SLC26A2 expression in HASMCs, whereas the knockdown of SLC26A2 inhibited PDGF-stimulated proliferation, migration, and production of inflammatory factors, and enhanced the expression of cell contractile phenotype marker proteins in HASMCs. Luciferase reporter and RIP experiments validated that NEAT1 targeted miR-9-5p to regulate SLC26A2, thereby influencing the biological function of PDGF-induced HASMCs. @*Conclusion@#These findings indicate that NEAT1-mediated miR-9-5p targeting of SLC26A2 inhibits the PDGF-induced proliferation and production of inflammatory factors in HASMCs. These findings highlight potential therapeutic targets for asthma and airway inflammation.
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Purpose@#Asthma is a serious inflammatory disease of the respiratory system in which airway smooth muscle cells (ASMCs) play a key role. This study aimed to investigate the expression of SLC26A2 in human ASMCs (HASMCs) and the regulatory mechanism of SLC26A2 in the proliferation and inflammatory factor production of HASMCs. @*Materials and Methods@#We obtained the asthma-associated differential mRNA SLC26A2 by bioinformatics analysis in childhood acute asthma samples. To investigate its role in airway inflammation and airway remodeling, we treated HASMCs with plateletderived growth factor (PDGF) in an in vitro model and determined SLC26A2 expression in cells using western blotting. Cell proliferation was detected by MTT and EdU assays, and cell contractile phenotype marker proteins were measured. Cell migration and production of inflammatory factors were determined by Transwell and ELISA assays. Additionally, the upstream regulatory miRNA and LncRNA of SLC26A2 were identified by bioinformatics, luciferase reporter gene, and RIP analyses. @*Results@#SLC26A2 was significantly upregulated in bioinformatics analysis of pediatric asthma-related sample. PDGF treatment up-regulated SLC26A2 expression in HASMCs, whereas the knockdown of SLC26A2 inhibited PDGF-stimulated proliferation, migration, and production of inflammatory factors, and enhanced the expression of cell contractile phenotype marker proteins in HASMCs. Luciferase reporter and RIP experiments validated that NEAT1 targeted miR-9-5p to regulate SLC26A2, thereby influencing the biological function of PDGF-induced HASMCs. @*Conclusion@#These findings indicate that NEAT1-mediated miR-9-5p targeting of SLC26A2 inhibits the PDGF-induced proliferation and production of inflammatory factors in HASMCs. These findings highlight potential therapeutic targets for asthma and airway inflammation.
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Objective To analyze the clinical features of nonimmunocompromised patients with allergic bronchopulmonary aspergillosis (ABPA).Methods The clinical data of 11 nonimmunocompromised patients diagnosed as ABPA from June 2010 to December 2015 in Zhejiang Jinhua People's Hospital were retrospectively analyzed.SPSS 18.0 was used for analysis.Results Among 11 patients with ABPA, Five were males and 6 were females, with an average age of (49.3 ±11.0) years.All patients had cough, expectoration and wheezing;cough and tan sputum in 4 cases, bloody sputum in 3 cases, fever in 2 cases and chest pain in 2 cases.In auscultation dry rales were heard in all patients , and limited wet rales were heard in 3 cases.The peripheral blood leukocyte counts were elevated in 5 patients [11.7(10.3-13.5) × 109/L)] and the eosinophils counts were increased in 9 patients [1.79(0.09-7.63) ×109/L].The total IgE was elevated to 3640(1329-9430) IU/mL.Skin prick test was positive ( grade 3 to 5) in 10 cases, Aspergillus fumigatus specific IgE increased to 23.6(1.75-67.30) kU/L in 6 cases, Aspergillus fumigatus specific IgG raised to 83.3(51-126) mg/L in 5 cases.Chest CT showed patchy, punctate exudation in 8 cases, central bronchiectasis in 9 cases, bronchial mucosal plug formation in 4 cases, and atelectasis in 1 case.Mediastinal lymph nodes were found in 2 cases.All 11 patients were treated with glucocorticoid hormone, and 8 patients were also received itraconazole oral solution for treatment.After treatment, the clinical symptoms were improved rapidly.Conclusion Nonimmunocompromised patients with ABPA have no specific clinical manifestations , and often are misdiagnosed as asthma , which is worth the attention of clinicians.
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Objective To study on immunity function in infectious mononucleosis (IM) children infected by Epstein-Barr virus (EBV) and its relationship with clinic and prognosis.Methods Serum immunoglobulin was detected by immunoradiometric nephelometry,expressions of C D3+,CD4+,CD8+,CD19+,CD23+ on T-lymphocytes subset in peripheral blood were measured by flow cytometry in 50 IM (IM group)who was in acute and convalescent period,and compared with 50 healthy controls (control group).Results The levels of IgA,IgG,IgM in IM group with acute period were (0.75 ± 0.65),(7.55 ± 2.05),(1.85 ± 0.55)g/L,in IM group with convalescent period were (0.95 ± 0.55),(8.85 ± 2.25),(1.75 ± 0.65) g/L.In control group,those were (1.25 ± 0.75),(10.65 ± 2.55),(1.80 ± 0.50) g/L.IgA and IgG in IM group with acute period were significantly lower than those in IM group with convalescent period and control group (P ＜0.01),but IgM was no significant difference among them (P ＞0.05).The levels of CD3+,CD4+,CD8+,CD4+/CD8+,CD19+,CD23+ in IM group with acute period were 0.6050 ± 0.0850,0.2080 ± 0.0315,0.6520 ± 0.0520,0.45 ± 0.35,0.0580 ± 0.0205,0.0250 ± 0.0135,in IM group with convalescent period were 0.7220 ± 0.0820,0.3575 ± 0.0375,0.3565 ± 0.0565,1.45 ± 0.45,0.1580 ± 0.0280,0.0625 ± 0.0225.In control group,those were 0.7530 ± 0.0830、0.4850 ± 0.0450、0.3275 ± 0.0575 1.48 ± 0.55、0.1850 ± 0.0560、0.0805 ± 0.0175.CD3+,CD4+,CD4+/CD8+,CD19+,CD23+ in IM group with acute period were significantly lower than those in IM group with convalescent period and control group (P ＜ 0.05),but CD8+ was significantly higher than that in IM group with convalescent period and control group (P ＜0.05).Conclusion The abnormality of immunoglobulin and T-lymphocytes subset in children infected by EBV is obvious.