Abstract
BackgroundProgrammed 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.MethodsWe 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.ResultsThe 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).ConclusionsThese data demonstrate an association between level of PDCD5 and asthma severity and indicate that PDCD5 may play a role in allergic asthma.Electronic supplementary materialThe online version of this article (doi:10.1186/s12890-016-0317-y) contains supplementary material, which is available to authorized users.
Highlights
Programmed cell death 5 (PDCD5) was first identified as an apoptosis-promoting protein and involved in some autoimmune diseases and inflammatory processes
Respiratory function was markedly changed in OVAchallenged mice Compared with controls, OVA-challenged mice showed lower peak inspiratory flow (PIF) and peak expiratory flow (PEF) (2.26 ± 0.02 vs 2.62 ± 0.12 L/s, 4.65 ± 0.04 vs 6.21 ± 0.95 L/s, respectively, p < 0.05) (Fig. 1a)
Airway inflammation and airway remodeling after OVA sensitization The total number of inflammatory cells in bronchoalveolar lavage fluid (BALF) was higher in OVA-challenged mice than controls (33.47 ± 9.07 vs 16.29 ± 4.72 × 104, p < 0.05)
Summary
Programmed cell death 5 (PDCD5) was first identified as an apoptosis-promoting protein and involved in some autoimmune diseases and inflammatory processes. This study aimed to further explore the significance of PDCD5 in mice with induced allergic asthma. Allergic asthma is a chronic inflammatory disorder of the airways; many cells, such as lymphocytes, mast cells, eosinophils, smooth muscle cells, and cellular elements, contribute to its pathophysiological processes. The frequent occurrence of injury and repair initiated by chronic inflammation could lead to structural changes in the airway, collectively termed airway remodeling, which is characterized by epithelial injury, sub-epithelial fibrosis, enhanced deposition of extracellular matrix proteins, goblet cells and mucous gland hypertrophy and increased airway smooth muscle mass [1]. Duncan et al demonstrated a significant correlation of reduced apoptosis in eosinophils present in induced sputum with asthma severity [3].
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