Surfactant protein D in serum from patients with allergic bronchopulmonary aspergillosis

Study of Role of Surfactant Protein-D, Malondialdehyde, Protein Carbonyl and its Correlation with Airflow Obstruction (FEV1% Predicted) in Patients with Smoker Chronic Obstructive Pulmonary Disease (COPD)

“…It causes lung tissue [19]. Serum SP-D has been identified as potential biomarker for some pulmonary disease, such as respiratory syncytial virus bronchiolitis [20], idiopathic interstitial fibrosis [21], acute respiratory distress syndrome [22] and allergic broncho pulmonary aspergillosis [23]. In our study, we found significantly increased levels of SP-D in patients with smoker COPD and in patients with non-smoker COPD as compared to healthy controls.…”

Innate Immunity toAspergillusSpecies

“…However, the administration of exogenous surfactant protein D to wild-type mice provides protection in a corticosteroid-induced model of invasive aspergillosis (97). Patients with allergic bronchopulmonary aspergillosis have higher serum concentrations of surfactant protein D, and in a mouse model of pulmonary hypersensitivity to Aspergillus species, there was a parallel marked induction in the expression of surfactant protein D (but not surfactant protein A) in the lungs that was mediated by interleukin-4 (IL-4) and IL-13 (68,69,85). Finally, the administration of exogenous surfactant proteins A and D to mice with pulmonary hypersensitivity to Aspergillus results in an attenuated obstructive defect, airway pathology, Th2 cytokines, and lung histamine release (55,96).…”

Serum surfactant protein D is steroid sensitive and associated with exacerbations of COPD

“…Mice that lack SP-D develop chronic inflammation and emphysema that can be prevented by administration of truncated recombinant human SP-D [8]. Since SP-D is synthesised predominantly within the respiratory tract, it has been evaluated as a potential biomarker in small numbers of individuals with community-acquired pneumonia [9], drug-induced lung disease [10,11], interstitial fibrosis [12] and allergic bronchopulmonary aspergillosis in cystic fibrosis [13]. Levels are reduced in bronchoalveolar lavage fluid from individuals with COPD [14], and there was a weak inverse relationship between serum SP-D level and forced expiratory volume in 1 s (FEV1) in 23 individuals with advanced COPD [15].…”