Objective To study the effect of dendritic cells(DC) stimulated with C5b-9 on allogenic lymphocytes. Methods DC was stimulated with C5b-9.CD4+ T and CD8+ T cells were isolated by magnetic-activated cell sorting (MACS),and were cocultivated with DC.The maturation markers and cytokine secretion of T cells were analyzed by flow cytometry and ELISA.Results The high pure CD4+ T and CD8+ T cells were separated successfully.After cocultivated with DC,the muturation markers CD25 and CD69 of CD4+ T were up-regulated by 26.31% and 52.73%,and IL-2 and IFN-? of CD4+ T cells were promoted from 126.3 ng?L-1 and 156.7 ng?L-1 to 409.2 ng?L-1 and 471.5 ng?L-1;the levels of IL-10 before and after coculture were 104.3 ng?L-1 and 107.1 ng?L-1.However these markers and cytokine secretion of CD8+ T were not influenced.Conclusion C5b-9 can adjust the function of DC and regulate the immuological response of T cells.

Objective To investigate the alteration of aquaporin 1(AQP1) expression in lung tissues in hemorrhage-lipopolysaccharide(LPS) two-hits rats and the effects of panaxadiols(PDS)and dexamthasone(Dex) on it.Methods The rat model of acute lung injury was built with hemorrhage-LPS two hits.The experiment was divided into control group(S),two-hits model group(HL),DEX group(HLD),and PDS group(HLP).The pathological changes of lung tissue were examined by HE staining.The expression of AQP1 was analyzed by RT-PCR,Western blotting and immunohistochemical staining.Results ① Significant inflammatory changes in pulmonary interstitial of rats in HL group were observed.However,in HLD group and HLP group,the pulmonary pathologic changes were much slighter.② AQP1 mRNA and protein expressions in lung tissues in HL group were significantly decreased compared with others groups(P

Objective To explore the application value of lung volumes from 64 multi-slice CT (MSCT) images in patients with chronic obstructive pulmonary disease (COPD) and study the correlation between lung volumes measured by MSCT and pulmonary function test (PFT) results. Methods 24 patients clinically diagnosed with COPD (COPD group) and 22 healthy people (control group) were selected and underwent both chest MSCT scans and PFT within one week. The total lung was scanned at full inspiration and full expiration with MSCT,respectively. The total lung volumes were measured by CT Pulmo software (Siemens,Forchheim,Germany). The quantitative total lung volumes from MSCT images were compared with PFT and SPSS13.0 was applied to assess the correlation. Results Compared with control group,the full inspiration volume (Vin) (P

Objective:To study methods of diagnosis and treatment for severe acute respirtory syndrome,outbreak of the illness.Methods:45 cases with SARS were analyzed, and the cases were admitted.Results:Patients were infected by close quarters contacting each other. All patients manifest high fever ,and accompanied by dyspnea, cough ,weakness and muscular soreness. Chest X ray, shadow of lungs were change to severity during the period of tall cusp.6 cases died with sevierity ARDS. Using general antibiotic was of no effect for the illness. Continual positive airway pressure(CPAP)and glucocorticoid was required that can control depravation of the disease when toxicosis symptom of patients was severity and shadow of lungs diffuse more and more. Conclusion: Infectivity of the illness is evidence and spread by airway. Using general antibiotic was of no effect for the illness.Continual positive airway pressure(CPAP)and glucocorticoid are effective for control of the disease.

To determine the impact of IL-23 knockdown by RNA interference on the development and severity of ovalbumin (OVA)-induced asthmatic inflammation, and the potential mechanisms in mice, the IL-23-specific RNAi-expressing pSRZsi-IL-23p19 plasmid was constructed and inhaled into OVA-sensitized mice before each challenge, as compared with that of control mice treated with alum or budesonide. Inhalation of the pSRZsi-IL-23p19, significantly reduced the levels of OVA-challenge induced IL-23 in the lung tissues by nearly 75%, determined by RT-PCR. In addition, knockdown of IL-23 expression dramatically reduced the numbers of eosinophils and neutrophils in BALF and mitigated inflammation in the lungs of asthmatic mice. Furthermore, knockdown of IL-23 expression significantly decreased the levels of serum IgE, IL-23, IL-17, and IL-4, but not IFNgamma, and its anti-inflammatory effects were similar to or better than that of treatment with budesonide in asthmatic mice. Our data support the notion that IL-23 and associated Th17 responses contribute to the pathogenic process of bronchial asthma. Knockdown of IL-23 by RNAi effectively inhibits asthmatic inflammation, which is associated with mitigating the production of IL-17 and IL-4 in asthmatic mice.
Animals ; Asthma/chemically induced/genetics/metabolism/*prevention & control ; Bronchoalveolar Lavage Fluid/cytology ; Enzyme-Linked Immunosorbent Assay ; Eosinophils ; Female ; Inflammation/metabolism ; Interleukin-23/*genetics ; Leukocyte Count ; Mice ; Mice, Inbred BALB C ; Neutrophils ; Ovalbumin/pharmacology ; Plasmids/genetics ; *RNA Interference ; RNA, Small Interfering/*genetics ; Reverse Transcriptase Polymerase Chain Reaction ; Th17 Cells/immunology