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Therapeutic Effects of DNA Vaccine on Allergen-Induced allergic airway inflammation in Mouse Model

Cellular & Molecular Immunology 2006年第5期3卷 379-384页

作者： Guoping Li Zhigang Liu Nanshan Zhong Bin Liao Ying Xiong Inflammafion ＆ allergic Diseases Research Unit Affiliated Hospital of Luzhou Medical College Luzhou 646000 Sichuan China College of Life Sciences Shenzhen University Shenzhen 518060 China Guangzhou Institute of Respiratory Diseases Guangzhou Medical College Guangzhou 510120 China Department of Respiratory Disease Affiliated Hospital of Luzhou Medical College Luzhou 646000 China

Vaccination with DNA encoding Dermatophagoides pteronyssinus group 2 （Der p 2） allergen previously showed its effects of immunologic protection on Der p 2 allergen-induced allergic airway inflammation in mice. In present study, we investigated whether DNA vaccine encoding Der p 2 could exert therapeutic role on allergen-induced allergic airway inflammation in mouse model and explored the mechanism of DNA vaccination in asthma specific-allergen immunotherapy. After sensitized and challenged by Der p 2, the BALB/c mice were immunized with DNA vaccine. The degrees of cellular infiltration were scored. IgE levels in serum and IL-4/IL-13 levels in BALF were determined by ELISA. The lung tissues were assessed by histological examinations. Expressions of STAT6 and NF-kB in lung were determined by immunohistochemistry staining. Vaccination of mice with DNA vaccine inhibited the development of airway inflammation and the production of mucin induced by allergen, and reduced the level of Der p 2-specific IgE level. Significant reductions of eosinophil infiltration and levels of IL-4 and IL-13 in BALF were observed after vaccination. Further more, DNA vaccination inhibited STAT6 and NF-kB expression in lung tissue in Der p 2-immunized mice. These results indicated that DNA vaccine encoding Der p 2 allergen could be used for therapy of allergen-induced allergic airway inflammation in our mouse model. Cellular ＆ Molecular Immunology.

关键词： DNA vaccine Dermatophagoides pteronyssinus group 2 allergic airway inflammation

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DNA vaccine encoding Der p2 allergen down-regulates STAT6 expression in mouse model of allergen-induced allergic airway inflammation

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Chinese Medical Journal 2006年第3期119卷 185-190页

作者： QIU Jing LI Guo-ping LIU Zhi-gang RAN Pei-xing ZHONG Nan-shan College of Life Sciences Shenzhen University Shenzhen 518060China Affiliated Hospital Luzhou Medical College Guangzhou Institute of Respiratory Diseases Guangzhou MedicalCollege Guangzhou 510120 China

Background Activation of signal transducer and activator of transcription 6 （STAT6） plays a critical role in the late phase of Th2-dependent allergy induction. STAT6 is essential to Th2 cell differentiation, recruitment, and effector function. Our previous study confirmed that DNA vaccination inhibited STAT6 expression of spleen cells induced by allergen. In the present study, we determined whether DNA vaccine encoding Dermatophagoides pteronyssinus group 2 （Der p2 ） could down-regulate the expression and activation of STAT6 in lung tissue from asthmatic mice. Methods After DNA vaccine immunization, BALB/c mice were sensitized by intmperitoneal injection and challenged by intranasal instillation of rDer p2. The levels of the cytokines IL-4 and IL-13 in BAL fluid were measured by enzyme-linked immunosorbent assay. The lung tissue was assessed by immunohistochemical staining with anti-STAT6. The protein expression of STAT6 was determined by Western blot. The activation of STAT6 binding ability was analyzed with electrophoretic mobility shift assay. Results DNA vaccine encoding Der p2 allergen effectively decreased the levels of IL-4 and IL-13 in the asthmatic mice. Histological evidence and Western blot showed that the expression of STAT6 in the DNA treated mice was markedly attenuated. STAT6 binding to specific DNA motif in lung tissue from the gene vaccinated mice was inhibited. Condusion DNA vaccine encoding Der p2 prevents allergic pulmonary inflammation probably by inhibiting the STAT6 signaling pathway in mice with Der p2 allergen-induced allergic airway infammafion.

关键词： DNA vaccine Dermatophagoides pteronyssinus group 2 allergic airway inflammation signal transducer and activator of transcription 6 （STAT6）

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Plasmacytoid dendritic cell deficiency in neonates enhances allergic airway inflammation via reduced production of IFN-α

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Cellular & Molecular Immunology 2020年第5期17卷 519-532页

作者： Min Wu Liuchuang Gao Miao He Hangyu Liu Han Jiang Ketai Shi Runshi Shang Bing Liu Shan Gao Hebin Chen Feili Gong Erwin WGelfand Yafei Huang Junyan Han Department of Immunology School of Basic MedicineTongji Medical CollegeHuazhong University of Science and TechnologyWuhanChina Department of Respiratory Medicine Zhongnan Hospital of Wuhan UniversityWuhanChina Department of Respiratory Diseases Wuhan Central HospitalTongji Medical CollegeHuazhong University of Science and TechnologyWuhanChina Department of Pulmonary Medicine Wuhan Children’s HospitalTongji Medical CollegeHuazhong University of Science and TechnologyWuhanChina Division of Cell Biology Department of PediatricsNational Jewish HealthDenverCOUSA Department of Pathogen Biology School of Basic MedicineTongji Medical CollegeHuazhong University of Science and TechnologyWuhanChina

allergic asthma,a chronic inflammatory airway disease associated with type 2 cytokines,often originates in early life.Immune responses at an early age exhibit a Th2 cell bias,but the precise mechanisms remain elusive.Plasmacytoid dendritic cells(pDCs),which play a regulatory role in allergic asthma,were shown to be deficient in neonatal mice.We report here that this pDC deficiency renders neonatal mice more susceptible to severe allergic airway inflammation than adult mice in an OVA-induced experimental asthma model.Adoptive transfer of pDCs or administration of IFN-αto neonatal mice prevented the development of allergic inflammation in wild type but not in IFNAR1−/−mice.Similarly,adult mice developed more severe allergic inflammation when pDCs were depleted.The protective effects of pDCs were mediated by the pDC-/IFN-α-mediated negative regulation of the secretion of epithelial cell-derived CCL20,GM-CSF,and IL-33,which in turn impaired the recruitment of cDC2 and ILC2 cells to the airway.In asthmatic patients,the percentage of pDCs and the level of IFN-αwere lower in children than in adults.These results indicate that impairment of pDC-epithelial cell crosstalk in neonates is a susceptibility factor for the development of allergeninduced allergic airway inflammation.

关键词： Neonate Plasmacytoid Dendritic Cells allergic airway inflammation IFN-α airway epithelial cells

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Establishment of allergic airway inflammation Model in Late-phase Response of Sprague-Dawley Rats

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Journal of Nanjing Medical University 2002年第4期16卷 163-167页

作者：朱敏敏傅诚章周钦海 Department of Anesthesiology the First Affiliated Hospital of Nanjing Medical University

Objective To establish allergic airway inflammation model in late-phase airway reaction of Sprague-Dawley (SD) rats. Methods Thirty-six SD rats were randomly divided into three groups-, control group (Group Ⅰ) ,single challenge group (Group Ⅱ ),consecutive challenge group (Group Ⅲ). The rats in Group Ⅱ and Group Ⅲ were sensitized twice by injection of ovalbumin (OA) together with aluminum hydroxide and Bordetella pertussis as adjuvants, followed by challenge with aerosolized OA for 20 min once in Group Ⅱ or one time on each day for one week in, Group Ⅲ. The rats in Group Ⅰ received 0. 9% saline by injection and inhalation. Results Compared with group Ⅰ , there were positive symptoms observed in the group Ⅱ and group Ⅲ; the amount of total leucocytes and eosinophil percentage in brochoalveolar lavage fluid (BALF) significantly increased (Pallergic inflammation changes in Group Ⅱ: Disrupted epithelium damaged subepithelial structure and eosinophil infiltration in the airway wall. As for the Group Ⅲ, there were allergen- induced characteristic features of chronic allergic airways inflammation: hypertrophy and hyperplasia of bronchial smooth muscle, goblet cell hyperplasia, basement membrane thickening, eosinophil in filtration, edema. Conclusion The model of allergic airway inflammation in late-phase response of SD rats was successfully established by OA sensitization (twice) and consecutive challenge.

关键词： allergic airway inflammation late-phase airway reaction rat model

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1,25(OH)2D3 supplementation inhibits the development of neonatal allergic airway inflammation via the suppression of ILC2 function

1,25(OH)2D3 supplementation inhibits the development of neon...

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第十二届全国免疫学学术大会

作者： He Miao Wu Min Gao Liuchuang Han Junyan Department of Immunology TongJi Medical CollegeHuazhong University of Science & Technology

Background:allergic asthma is clinically characterized by reversible airway obstruction and airway hyperresponsiveness(AHR),which is associated with many inflammatory cells and commonly begins in early life.Group 2 innate lymphoid cells(ILC2 s) produce type 2 cytokines IL-5 and IL-13.It has been recently shown that ILC2 s contribute to not only the allergic inflammation but also the initiation of the adaptive Th2 response.There is growing evidence that vitamin D is a potent immunomodulator.However,the role of vitamin D in childhood allergic asthma remains unclear.Objective:To investigate the effect of 1,25(OH) D,the biologically activated form of vitamin D on AHR and airway inflammation in a neonatal allergic asthma model.Methods:Neonatal BALB/c mice(airway eosinophilia,goblet cell hyperplasia and the levels of cytokines in the bronchoalveolar lavage fluid(BALF) were analyzed 24 hours after the final OVA challenge.Results:We observed that administration of 1,25(OH) D significantly impaired airway eosinophilia and improved lung functions when given either during OVA sensitization or challenge phase.This was accompanied with reduced level of IL-5 and increased level of IL-10 in the BALF(pallergic airway inflammation via suppressing the accumulation and function of airway ILC2 in neonates.The underlying mechanisms still need further investigation.

关键词： 1,25（OH）2D3 ILC2 allergic airway inflammation

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RhoA and Cdc42 in T cells:Are they targetable for T cell-mediated inflammatory diseases?

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Precision Clinical Medicine 2021年第1期4卷 56-61页

作者： Fukun Guo Division of Experimental Hematology and Cancer Biology Children’s Hospital Medical CenterCincinnatiOH 45229USA

Many inflammatory diseases are not curable,necessitating a better understanding of their pathobiology that may help identify novel biological targets.RhoA and Cdc42 of Rho family small GTPases regulate a variety of cellular functions such as actin cytoskeletal organization,cell adhesion,migration,proliferation,and survival.Recent characterization of mouse models of conditional gene knockout of RhoA and Cdc42 has revealed their physiological and cell type-specific roles in a number of cell types.In T lymphocytes,which play an important role in the pathogenesis of most,if not all,of the inflammatory diseases,we and others have investigated the effects of T cell-specific knockout of RhoA and Cdc42 on T cell development in the thymus,peripheral T cell homeostasis,activation,and differentiation to effector and regulatory T cells,and on T cell-mediated allergic airway inflammation and colitis.Here we highlight the phenotypes resulting from RhoA and Cdc42 deletion in T cells and discuss whether pharmacological targeting of RhoA and Cdc42 is feasible in treating asthma that is driven by allergic airway inflammation and colitis.

关键词： RhoA Cdc42 T cells allergic airway inflammation colitis

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