title: Breast regression protein-39 (BRP-39) promotes dendritic cell maturation in vitro and enhances Th2 inflammation in murine model of asthma.
abstract: OBJECTIVE
  To determine the roles of breast regression protein-39 (BRP-39) in regulating dendritic cell maturation and in pathology of acute asthma.
  
  
  METHODS
  Mouse bone marrow-derived dendritic cells (BMDCs) were prepared, and infected with adenovirus over-expressing BRP-39. Ovalbumin (OVA)-induced murine model of acute asthma was made in female BALB/c mice by sensitizing and challenging with chicken OVA and Imject Alum. The transfected BMDCs were adoptively transferred into OVA-treated mice via intravenous injection. Airway hyperresponsiveness (AHR), inflammation and pulmonary histopathology were characterized.
  
  
  RESULTS
  The expression of BRP-39 mRNA and protein was significantly increased in lung tissues of OVA-treated mice. The BMDCs infected with adenovirus BRP-39 exhibited greater maturation and higher activity in vitro. Adoptive transfer of the cells into OVA-treated mice significantly augmented OVA-induced AHR and eosinophilic inflammation. Meanwhile, BRP-39 further enhanced the production of OVA-induced Th2 cytokines IL-4, IL-5 and IL-13, but significantly attenuated OVA-induced IFN-γ production in bronchoalveolar lavage fluid.
  
  
  CONCLUSIONS
  In OVA-induced murine model of acute asthma, BRP-39 is over-expressed in lung tissue and augments Th2 inflammatory response and AHR. BRP-39 promotes dendritic cell maturation in vitro. Therefore, BRP-39 may be a potential therapeutic target of asthma.
authors.affiliation: Department of Respiratory Medicine, the Second Affiliated Hospital, School of Medicine, Zhejiang University, Hangzhou 310009, China.
authors.forename: Qian
authors.initials: Q
authors.lastname: Xu
authors.forename: Shou-jie
authors.initials: SJ
authors.lastname: Chai
authors.forename: Ying-ying
authors.initials: YY
authors.lastname: Qian
authors.forename: Min
authors.initials: M
authors.lastname: Zhang
authors.forename: Kai
authors.initials: K
authors.lastname: Wang
mesh_terms: D000256:Adenoviridae; D019264:Adoptive Transfer; D000818:Animals; D001249:Asthma / Q000276:immunology* / Q000378:metabolism / Q000628:therapy*; D001992:Bronchoalveolar Lavage Fluid / Q000276:immunology; D000071451:Chitinase-3-Like Protein 1; D016207:Cytokines / Q000276:immunology; D003713:Dendritic Cells / Q000276:immunology / Q000637:transplantation*; D004195:Disease Models, Animal; D005260:Female; D005822:Genetic Vectors; D006023:Glycoproteins / Q000096:biosynthesis* / Q000235:genetics; D008168:Lung / Q000276:immunology; D051379:Mice; D008807:Mice, Inbred BALB C; D010047:Ovalbumin / Q000276:immunology; D018418:Th2 Cells / Q000276:immunology*
chemical_list: C509289:Chil1 protein, mouse; D000071451:Chitinase-3-Like Protein 1; D016207:Cytokines; D006023:Glycoproteins; D010047:Ovalbumin