title: Overexpression of programmed cell death 5 in a mouse model of ovalbumin-induced allergic asthma.
abstract: Programmed cell death 5 (PDCD5) was first identified as an apoptosis-promoting protein and involved in some autoimmune diseases and inflammatory processes. Our previous study demonstrated greater expression of serum PDCD5 in asthmatic patients than controls. This study aimed to further explore the significance of PDCD5 in mice with induced allergic asthma.
  
  
  
  We divided 16 female mice into 2 groups: control (n = 8) and allergen (ovalbumin, OVA)-challenged mice (n = 8). The modified ovalbumin inhalation method was used to generate the allergic asthma mouse model, and the impact of OVA was assessed by histology of lung tissue and morphometry. The number of cells in bronchoalveolar lavage fluid (BALF) was detected. Pulmonary function was measured by pressure sensors. PDCD5 and active caspase-3 levels were detected.
  
  
  
  The expression of PDCD5 was higher with OVA challenge than for controls (p < 0.05). PDCD5 level was correlated with number of inflammatory cells in BALF and lung function. Moreover, active caspase-3 level was increased in the OVA-challenged mice (p < 0.001) and correlated with PDCD5 level (p = 0.000).
  
  
  
  These data demonstrate an association between level of PDCD5 and asthma severity and indicate that PDCD5 may play a role in allergic asthma.
authors.affiliation: Department of Respiratory Medicine, Peking University Third Hospital, No. 49 Huayuan North Road, Haidian District, Beijing, 100191, China.
authors.forename: Xiaolin
authors.initials: X
authors.lastname: Diao
authors.affiliation: Department of Respiratory Medicine, Peking University Third Hospital, No. 49 Huayuan North Road, Haidian District, Beijing, 100191, China.
authors.forename: Juan
authors.initials: J
authors.lastname: Wang
authors.affiliation: Department of Respiratory Medicine, Peking University Third Hospital, No. 49 Huayuan North Road, Haidian District, Beijing, 100191, China.
authors.forename: Hong
authors.initials: H
authors.lastname: Zhu
authors.affiliation: Department of Respiratory Medicine, Peking University Third Hospital, No. 49 Huayuan North Road, Haidian District, Beijing, 100191, China. puh3_hb@bjmu.edu.cn.
authors.forename: Bei
authors.initials: B
authors.lastname: He
mesh_terms: D000818:Animals; D051017:Apoptosis Regulatory Proteins / Q000235:genetics / Q000378:metabolism*; D001249:Asthma / Q000139:chemically induced / Q000378:metabolism*; D001992:Bronchoalveolar Lavage Fluid / Q000166:cytology; D053148:Caspase 3 / Q000378:metabolism; D004195:Disease Models, Animal; D005260:Female; D007249:Inflammation / Q000276:immunology; D008168:Lung / Q000473:pathology* / Q000503:physiopathology*; D051379:Mice; D008807:Mice, Inbred BALB C; D009363:Neoplasm Proteins / Q000235:genetics / Q000378:metabolism*; D010047:Ovalbumin
chemical_list: D051017:Apoptosis Regulatory Proteins; D009363:Neoplasm Proteins; C486488:Pdcd5 protein, mouse; D010047:Ovalbumin; C505409:Casp3 protein, mouse; D053148:Caspase 3
keywords: Asthma; Caspase-3; Inflammation; Lung function; Programmed cell death protein 5