A new study entitled “Distinct compartmentalization of SP-A and SP-D in the vasculature and lungs of patients with idiopathic pulmonary fibrosis” suggests the level of the surfactant protein D (SP-D) is a more efficient biomarker of idiopathic pulmonary fibrosis than the surfactant protein A (SP-A). The study was published in the journal BMC Pulmonary Medicine.
Idiopathic pulmonary fibrosis (IPF) belongs to the group of interstitial lung diseases and is characterized by a progressive decline in lung functions due to accumulation of scarred tissue over time. The lung thickening leads to an impaired mobilization of oxygen to the bloodstream and eventually to vital organs such as brain and heart. The term “idiopathic” refers to an unknown cause for the disease. Patients affected with IPF have a poor prognosis, however, disease progression differs from patient to patient. Therefore, individual prognosis markers are required to find the most appropriate treatment. While some have been proposed, including age, forced vital capacity (FVC), diffusing capacity (DLCO), chronological variance in respiratory functions, and desaturation during the 6-min walk test, blood biomarkers represent an easier and effortless measure to IPF patients. Currently, these include surfactant protein A (SP-A), SP-D, Krebs von den Lungen-6 (KL-6), matrix metalloproteinase-7 (MMP-7), and chemokine (C-C motif) ligand 18 (CCL18).
Notably, the surfactant protein A and D levels in the blood represent a good indicator of severity and prognosis of interstitial lung diseases, such as IPF; however, they present distinctive affinities for other components of the pulmonary surfactant complex (present at the alveolar surface of lungs and having an active role in lung innate immunity and structure) and can be present at different concentrations in IPR patients.
In this retrospective study, the authors determined SP-A and SP-D levels, hydrophilicity, and distribution in both IPF patients and healthy individuals. The study included 36 IPF patients and 18 patients with sarcoidosis (SAR), as these patients often exhibit pulmonary fibrosis, and 20 healthy subjects.
The authors found evidence suggesting SP-D is a more efficient biomarker for IPF than SP-A: despite SP-D levels in the blood of IPF patients being lower, when compared to both healthy and SAR subjects (who maintain constant SP-A levels), the authors found that SP-D is preferentially leaking from the lungs’ alveolar space to the bloodstream. Further studies confirmed that while SP-A remains bound to its lipid partner in the alveolar space, SP-D remains free thus indicating its easier relocation to the blood. Accordingly, when the authors performed immunocytochemistry, SP-D was found inside blood vessels in the fibrotic parenchyma, but not SP-A.
Thus, the authors suggest that measuring SP-D levels in the blood is a better indicator of disease severity than SP-A. This measurement should be included along with other specific biomarkers, therefore indicating a more sensitive and reliable profile of IPF.
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