Surfactant protein B: From biochemistry to its potential role as diagnostic and prognostic marker in heart failure

Proteomic diversity of high‐density lipoprotein explains its association with clinical outcome in patients with heart failure

“…Levels of surfactant proteins in plasma, especially SFTPB, are suitable biomarkers to assess lung health and alveolar capillary membrane function, because when damaged, surfactant proteins move into the blood . It is thus logical for SFTPB to be higher in a worse HF disease state (reflecting increased congestion), which has moreover been shown in HF before . Whether the HDL‐bound portion of SFTPB compared to SFTPB levels in plasma is a better predictor of HF outcome is difficult to say since it is not entirely clear what portion of the total amount of SFTPB binds to HDL, but in a previous study investigating the HDL proteome in end‐stage renal disease (ESRD) patients, HDL‐bound SFTPB was associated with ESRD, while its plasma counterpart was comparable between ESRD patients and chronic kidney disease stage 4 patients .…”

“…22 -24 It is thus logical for SFTPB to be higher in a worse HF disease state (reflecting increased congestion), which has moreover been shown in HF before. 25 Whether the HDL-bound portion of SFTPB compared to SFTPB levels in plasma is a better predictor of HF outcome is difficult to say since it is not entirely clear what portion of the total amount of SFTPB binds to HDL, but in a previous study investigating the HDL proteome in end-stage renal disease (ESRD) patients, HDL-bound SFTPB was associated with ESRD, while its plasma counterpart was comparable between ESRD patients and chronic kidney disease stage 4 patients. 26 It is thus possible for the SFTPB HDL-bound portion to be different from its plasma counterpart, which could possibly also be the case in different HF disease states.…”

Surfactant Protein B Suppresses Lung Cancer Progression by Inhibiting Secretory Phospholipase A2 Activity and Arachidonic Acid Production

“…Indeed, the importance of SP-B treatment in alleviation of RDS has been demonstrated by many studies [68][69][70]. Unfortunately, the precise 3D structure and mechanism of surfactant function of SP-B had not been discovered [71]. Therefore, unveiling a biological method for functional treatment of alveoli with SP-B might be promising for further study.…”

Surfactant proteins changes after acute hemodynamic improvement in patients with advanced chronic heart failure treated with Levosimendan

“…The reduction of the immature form of SP-B likely indicates a reduction of the hemodynamic stress on the alveolar capillary membrane. Indeed an acute hemodynamic and/or respiratory stress on the alveolar capillary membrane increases SP-B plasma level (Agostoni et al, 2011a;Agostoni et al, 2011b;Banfi and Agostoni, 2016). The immature form of SP-B is most unlikely found in the blood stream.…”

“…In particular, alveolar-capillary membrane abnormalities, which include increase in interstitial fluids, reduction in the number of the alveolarcapillary units, interstitial fibrosis, local thrombosis and an increase in cellularity, have a role in HF syndrome and significantly influence its clinical course (Guazzi et al, 2002). Alveolar capillary membrane dysfunction is most frequently analyzed in terms of functional abnormalities using carbon monoxide or nitric oxide as markers of lung diffusion (Graham et al, 2017;Zavorsky et al, 2017), but recently several surfactant proteins (SPs), both in the blood and alveolar fluid, have been proposed as biological indicators of alveolar capillary membrane damage including SP type A, B and D. (Banfi and Agostoni, 2016;Gargiulo et al, 2014;Swenson et al, 2002;Whitsett and Weaver, 2002). Specifically SP-A has been suggested as a predictor of lung damage produced by smoking and high altitude (Kobayashi et al, 2008;Swenson et al, 2002), SP-D as a predictor of cardiovascular morbidity and mortality over classical risk factors as well as a prognostic marker of chronic kidney and lung disease, while SP-B, both in its immature and mature forms, has been proposed as a biomarker of an alveolar capillary barrier damage in HF (De Pasquale et al, 2004;De Pasquale et al, 2003;Magri et al, 2009).…”