The Effectiveness of the Serum Surfactant Protein D (Sp-D) Level to Indicate Lung Injury in Pulmonary Embolism

Katı, Celal; Alaçam, Hasan; Duran, Latif; Güzel, Aygül; Akdemir, Hızır Ufuk; Şişman, Bülent; Şahin, Canan Batur; Yılmaz, Yücel; Altıntaş, Nejat; Murat, Naci; Okuyucu, Ali

doi:10.7754/clin.lab.2013.131009

Cited by 11 publications

(10 citation statements)

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“…These correlations suggest that the association of SP-D with all-cause mortality may be rather complex. Some recent studies have demonstrated that SP-D levels correlate with alveolar leakage in heart failure ( 433 ), and with the presence of submassive pulmonary embolism ( 434 ), supporting the hypothesis that variation in circulatory SP-D results from disease-mediated lung damage in some types of CVD.…”

Section: Sp-d In Non-respiratory Diseasesmentioning

confidence: 79%

“…Genetic SP-D variation, altered local protein expression, and serum variation have been reported in extrapulmonary diseases involving autoimmune disorders [including rheumatoid disease ( 213 , 423 – 426 ) and diabetes ( 229 , 427 )] and in diseases involving specific organs [including the intestines ( 230 , 428 ), skin ( 20 ), brain ( 41 ), and large arteries ( 214 , 429 )]. In some cases, the association between circulatory SP-D and extrapulmonary disease may be partly explained by the coexistence of respiratory disease or the pulmonary effects of disease ( 430 – 434 ). The antimicrobial or anti-inflammatory effects of SP-D at extrapulmonary sites have been demonstrated using animal models or cell culture, including disease models of the eye ( 258 , 261 , 435 ), pancreas ( 436 ), kidney/urinary tract ( 437 , 438 ), gastric mucosa ( 439 – 441 ), intestine ( 442 ), gestational tissue ( 27 , 331 , 443 ), and large arteries ( 48 ).…”

Section: Sp-d In Non-respiratory Diseasesmentioning

confidence: 99%

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Surfactant Protein D in Respiratory and Non-Respiratory Diseases

2018

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Surfactant protein D (SP-D) is a multimeric collectin that is involved in innate immune defense and expressed in pulmonary, as well as non-pulmonary, epithelia. SP-D exerts antimicrobial effects and dampens inflammation through direct microbial interactions and modulation of host cell responses via a series of cellular receptors. However, low protein concentrations, genetic variation, biochemical modification, and proteolytic breakdown can induce decomposition of multimeric SP-D into low-molecular weight forms, which may induce pro-inflammatory SP-D signaling. Multimeric SP-D can decompose into trimeric SP-D, and this process, and total SP-D levels, are partly determined by variation within the SP-D gene, SFTPD. SP-D has been implicated in the development of respiratory diseases including respiratory distress syndrome, bronchopulmonary dysplasia, allergic asthma, and chronic obstructive pulmonary disease. Disease-induced breakdown or modifications of SP-D facilitate its systemic leakage from the lung, and circulatory SP-D is a promising biomarker for lung injury. Moreover, studies in preclinical animal models have demonstrated that local pulmonary treatment with recombinant SP-D is beneficial in these diseases. In recent years, SP-D has been shown to exert antimicrobial and anti-inflammatory effects in various non-pulmonary organs and to have effects on lipid metabolism and pro-inflammatory effects in vessel walls, which enhance the risk of atherosclerosis. A common SFTPD polymorphism is associated with atherosclerosis and diabetes, and SP-D has been associated with metabolic disorders because of its effects in the endothelium and adipocytes and its obesity-dampening properties. This review summarizes and discusses the reported genetic associations of SP-D with disease and the clinical utility of circulating SP-D for respiratory disease prognosis. Moreover, basic research on the mechanistic links between SP-D and respiratory, cardiovascular, and metabolic diseases is summarized. Perspectives on the development of SP-D therapy are addressed.

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Section: Sp-d In Non-respiratory Diseasesmentioning

confidence: 79%

Section: Sp-d In Non-respiratory Diseasesmentioning

confidence: 99%

Surfactant Protein D in Respiratory and Non-Respiratory Diseases

2018

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“…In addition to lung spillover as primary contributor, it is possible that SP-D can be secreted from the arterial wall and affect the total serum concentration. Recent studies by Kati et al and Gargiulo et al have shown that circulatory SP-D levels correlate with the presence of pulmonary embolism (40) and with alveolar leakage in heart failure (41), thereby supporting the hypothesis that circulatory SP-D variation is partly a consequence of CVD-mediated lung damage. Based on recent clinical studies pinpointing SP-D as a systemic biomarker of CVD morbidity and mortality (42, 43), it is suggested that SP-D has an important function in the cardiovascular system as a regulator of inflammation, which might have implications for atherosclerosis and CVD.…”

Section: Sp-d Sites Of Expression and Functionmentioning

confidence: 85%

The Dual Role of Surfactant Protein-D in Vascular Inflammation and Development of Cardiovascular Disease

2019

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Cardiovascular disease (CVD) is responsible for 31% of all global deaths. Atherosclerosis is the major cause of cardiovascular disease and is a chronic inflammatory disorder in the arteries. Atherosclerosis is characterized by the accumulation of cholesterol, extracellular matrix, and immune cells in the vascular wall. Recently, the collectin surfactant protein-D (SP-D), an important regulator of the pulmonary immune response, was found to be expressed in the vasculature. Several in vitro studies have examined the role of SP-D in the vascular inflammation leading to atherosclerosis. These studies show that SP-D plays a dual role in the development of atherosclerosis. In general, SP-D shows anti-inflammatory properties, and dampens local inflammation in the vessel, as well as systemic inflammation. However, SP-D can also exert a pro-inflammatory role, as it stimulates C-C chemokine receptor 2 inflammatory blood monocytes to secrete tumor necrosis-factor α and increases secretion of interferon-γ from natural killer cells. In vivo studies examining the role of SP-D in the development of atherosclerosis agree that SP-D plays a proatherogenic role, with SP-D knockout mice having smaller atherosclerotic plaque areas, which might be caused by a decreased systemic inflammation. Clinical studies examining the association between SP-D and cardiovascular disease have reported a positive association between circulatory SP-D level, carotid intima-media thickness, and coronary artery calcification. Other studies have found that circulatory SP-D is correlated with increased risk of both total and cardiovascular disease mortality. Both in vitro, in vivo, and clinical studies examining the relationship between SP-D and CVDs will be discussed in this review.

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“…[46] Serum levels of SP-A and SP-D are significantly elevated in patients with IPF, bacterial pneumonia, and tuberculosis, compared to the healthy controls. Kati et al [47] suggested that serum SP-D levels were significantly higher in patients with IPF and submassive pulmonary embolism than in controls and SP-D may have a diagnostic role in sub-massive pulmonary embolism.…”

Section: Discussionmentioning

confidence: 99%