Decreased Serum Levels of Surfactant Protein D (SP-D) Prior Transplant Is Associated with the Development of Bronchiolitis Obliterans (BO) and Idiopathic Pneumonia Syndrome (IPS) Following Allogeneic Hematopoietic Stem Cell Transplantation.

Non-infectious pulmonary complications which occur beyond 3 months of allogeneic hematopoietic stem cell transplantation (allo-HSCT) have become recognized as a critical problem. Above all, bronchiolitis obliterans (BO) and idiopathic pneumonia syndrome (IPS) are difficult to be cured and cause high mortality. Therefore, early identification of patients with higher risk for BO/IPS may lead to improving outcome of allo-HSCT.

Surfactant protein D (SP-D) is one of collectins mainly synthesized by alveolar type II cells. The best known function is to prevent the collapse of alveoli by decreasing surface tension at alveolar air-lipid interface, and SP-D plays an important roles as a mediator in innate immunity in the lung. In clinical practice, high serum SP-D level is used as a marker lung diseases. Recently, low production of SP-D in the alveoli has been considered as an important pathgenesis of adult respiratory distress.

We analyzed serum SP-D levels before allo-HSCT of 42 patients who received allo-HSCT in our institution between November 2001 and February 2006 and survived more than 90 days after transplant. In all patients, 5 patients had BO and 3 had IPS at a median interval of 303 and 117 days of transplantation (range; 100–452 and 95–153 days). As a result of univariate analysis, BO/IPS patients had lower serum SP-D levels prior allo-HSCT and extensive type of cGVHD except lung compared with no BO/IPS patients (p=0.06 and 0.07). KL-6 had also mildly associated with BO/IPS. On the other hand, we couldn’t find the association in sex, age, donor source, conditioning regimen, disease status, aGVHD, and FEV1.0/FVC and SP-A prior HSCT. We could not clarify the precise mechanism of the association between Decreased serum levels of SP-D and the development of BO and IPS following allo-HSCT. However, we speculate that low production of SP-D in the alveoli, which causes innate immune compromise, might contribute to extreme pulmonary alloreaction.