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Chang-zheng Wang

Publications and source records attributed to Chang-zheng Wang.

5 recordsLinked to original sources
PubMed2006

[Effects and mechanism of CD4+ CD25+ T cells on the airway inflammation of asthmatic mice].

OBJECTIVE: To investigate the effects and mechanism of CD(4)(+) CD(25)(+) T cells on the airway inflammation of asthmatic mice. METHODS: Sixty mice were divided into 3 groups (20 in each group) including group A [ovalbumin (OVA) sensitized/challenged mice], group B (saline sensitized/challenged mice), group C [CD(25)(+) T cells deleted by anti-CD(25)(+) and OVA sensitized/challenged mice]. Mice of A group were sensitized on days 1 and 13 by OVA and challenged from days 21 to 29 by 2% OVA 10 ml repeatedly to establish a murine model of asthma characterized by airway inflammation. The mice of group B were treated by saline 10 ml. The mice of group C were treated by the same method of group A after deletion of the CD(25)(+) T cells by anti-mouse CD(25)(+) monoclonal antibody (McAb). Lymphocytes were separated from the spleen of the three groups and the number of T cells were calculated by Fluorescence Activated Cell Sorter (FACS). The CD(4)(+) T cells were purified and the expression of interleukin-10 (IL-10), transforming growth factor-beta(1) (TGF-beta(1)) and cytotoxic T lymphocyte-associated antigen-4 (CTLA-4) mRNA were analyzed by the method of reverse transcriptase-polymerase chain reaction (RT-PCR). The airway inflammatory indices were detected by hematoxylin and eosin (HE) staining. RESULTS: In repeatedly OVA-challenged mice (group A), the ratio of CD(4)(+) CD(25)(+) T cells to CD(4)(+) T cells decreased significantly [(3.10 +/- 0.03)%] as compared with group B [(9.60 +/- 0.04)%, P < 0.01]. The expression of IL-10, CTLA-4 mRNA and TGF-beta(1) mRNA of OVA-challenged mice (group A) decreased significantly (0.250 +/- 0.040 vs 0.29 +/- 0.03, 0.28 +/- 0.06 vs 0.480 +/- 0.080, 0.47 +/- 0.05 vs 0.50 +/- 0.03, all P < 0.01). The expression of IL-10, CTLA-4 mRNA and TGF-beta(1) mRNA of the mice treated by anti-CD(25)(+) McAb (group C) decreased as compared with groups A and B (0.080 +/- 0.020, 0.11 +/- 0.04, 0.12 +/- 0.05, P < 0.01). The inflammation in the lungs of mice with depleted CD(4)(+) CD(25)(+) T cells by anti-CD(25)(+) McAb was more marked than that in the OVA-challenged and control group mice. CONCLUSION: The polarization of CD(4)(+) CD(25)(+) T cells in asthmatic mice decreased significantly, which may play an important role in the pathogenesis of asthma.

Animals↗
PubMed2006

[Effects of immunotherapy on the expression of costimulatory molecules on dendritic cells in a mouse model of asthma].

OBJECTIVE: To establish a mouse model of ovalbium in (OVA) specific immunotherapy, and to explore the effects of specific immunotherapy on the expression of CD(80) and CD(86) on spleen-derived dendritic cells (DC) in a mouse asthmatic model. METHODS: A hundred and twenty BALB/c mice were randomly divided into three groups, with 40 mice each. The asthma model (group A) was established by intraperitoneal injection of 10 microg OVA and 1% OVA aerosol challenges. Consecutive subcutaneous injection of 1 mg OVA in the dorsal aspect of the foot was then given to establish the model of OVA specific immunotherapy (group B), while PBS (0.01 mol/L) was given in group C to serve as the control. The pathological changes of lung tissues were studied by HE stain. The serum OVA-specific IgE level, and IL-2 and IL-4 production in the splenic T cells were determined by enzyme-linked immunosorbent assay (ELISA). The expression of CD(80) and CD(86) on DC, which were isolated from the spleen, were detected by fluorescein-activated cell sorter. (3)H-thymidine ((3)H-TdR) incorporation assay was used to determine the response of splenic T and the secretion of interleukin-4 (IL-4) and IL-5 was assayed with the use of ELISA after coculture of T cells with DC. RESULTS: (1) The infiltration of eosinophils and lymphocytes within epithelium and lamina propria was present in group B, but was milder than that in group A. The absorbance at 490 nm (A(490)) of serum specific IgE in group A 712 +/- 129, was more than that in group C (20 +/- 13, P < 0.05), but there was no significant difference between group B (124 +/- 59, P > 0.05) and C. The production of IL-2 by splenic T cells in group B (8 +/- 3) pg/ml was less than that in group A [(22 +/- 8) pg/ml, P < 0.05], but there was no significant difference between group B and group C [(6 +/- 4) pg/ml, P > 0.05]. The production of IL-4 by splenic T cells in group B (8.4 +/- 4.3) pg/ml was less than that of group A [(32.4 +/- 12.1) pg/ml, P < 0.05], but there was no significant difference between group B and group C [(5.1 +/- 1.1) pg/ml, P > 0.05]. (2) The expression of CD(86) on splenic DC cells from group B (58.23%) was significantly lower than that from group A (77.59%) and group C (77.84%), while the expressions of CD(80) in group A (96.98%) and group B (95.63%) were higher than that in group C (77.37%). (3) When untreated T cells were cocultured with DC from the individual groups and stimulated by OVA, the secretion of IL-4 from T cells in group B [(10.8 +/- 2.3) pg/ml] was significantly lower than that in group A [(17.3 +/- 4.7) pg/ml, P < 0.05], but there was no significant difference when compared to group C [(5.7 +/- 2.7) pg/ml, P > 0.05], and the secretion of IL-5 from T cells in group B [(18.8 +/- 3.8) pg/ml] was significantly lower than that in group A [(35.7 +/- 7.9) pg/ml, P < 0.05], but there was no significant difference when compared to group C [(11.0 +/- 2.2) pg/ml, P > 0.05]. When untreated T cells were cocultured with DC from the individual groups and stimulated by OVA, the stimulating index of T cells in group B (3.8 +/- 0.7) was significantly lower than that in group A (11.5 +/- 3.2, P < 0.05), but there was no significant difference when compared to group C (5.8 +/- 1.5, P > 0.05). CONCLUSIONS: A mouse model of asthma-specific immunotherapy was successfully established. Downregulation of CD(86) on the surface of DC might be the underlying mechanisms by which specific immunotherapy promotes Th1 to Th2 polarization and induces T cell anergy.

Animals↗
PubMed2005

[Exploration of mechanisms underlying T-cell anergy induced by immunotherapy in allergic murine asthma model].

AIM: To explore the mechanisms underlying the T cell anergy induced by immunotherapy for the treatment of allergic asthma. METHODS: Murine model of allergic asthma was established through the OVA sensitization and challenge. Three injections of 1 mg OVA were used as immunotherapy. Pathological examination of lung tissues, cell count and differential count of bronchoalveolar lavage fluid (BALF), determination of serum OVA-specific IgE, and measurement of IL-2 and IL-4 production and proliferation of the splenic T cells to OVA were preformed to analyze the effect of immunotherapy on asthma. The expression of CTLA-4 on splenic T cells was detected by FACS. RESULTS: Asthma-specific immunotherapy could alleviate lung inflammation, decrease eosinophil infiltration in BALF (P<0.01) and serum OVA-specific IgE, inhibit the production of IL-2 and IL-4 and the proliferation of splenic T cells to OVA (P<0.01), and up-regulate the expression of CTLA-4 on splenic T cells. CONCLUSION: The up-regulation of CTLA-4 expression on T cells may be involved in the T cell anergy induced by asthma-specific immunotherapy.

Animals↗
PubMed2004

[The mechanism and implication of costimulatory molecules in dendritic cells in the development of asthma].

OBJECTIVE: To exploring the role of costimulatory molecules in the development of asthma and its mechanisms. METHODS: Murine asthma model was established with ovalbumin (OVA) sensitization and challenge, and the model was confirmed by histological analysis of lung tissues, cell numbers and differentiations of bronchoalveolar lavage, serum OVA-specific IgE level and interleukin (IL)-4 and IL-5 production by splenic T cells. The purity of spleen-derived dendritic cells was assayed with fluorescein-actived cell sorter (FACS) by analyzing CD(11c) molecule. FACS was also used to measure the expression of CD(80) and CD(86) on spleen-derived dendritic cell (DC) from OVA-sensitized and challenged mice. Finally, the production of IL-4 and IL-5 in naive T cells after stimulation with spleen-derived DC from OVA-sensitized and challenged mice were determined with ELISA. RESULTS: Histological analysis of lung tissues, components of broncho-alveolar fluid, the level of serum OVA-specific IgE, and the production of IL-4 and IL-5 were all consistent with the characteristic of a murine asthma model. The expression of CD(80) on spleen-derived DC from OVA-sensitized and challenged mice was increased significantly compared with that from PBS-treated mice, while there was no difference in CD(86) expression. On the other hand, DC from OVA-sensitized and challenged mice stimulated the production of IL-4 and IL-5 by naïve T cells. CONCLUSION: Our results suggest that DC, via upregulation of CD(80), might play a pivotal role in the maintenance and amplification of allergic immune response, namely the Th2 immune response.

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