Change of surfactant protein D and A after renal ischemia reperfusion injury

Autoři: Islam Md Imtiazul aff001;  Redwan Asma aff001;  Ji-Hye Lee aff002;  Nam-Jun Cho aff003;  Samel Park aff003;  Ho-Yeon Song aff001;  Hyo-Wook Gil aff003
Působiště autorů: Department of Microbiology, College of Medicine, Soonchunhyang University, Cheonan, Republic of Korea aff001;  Department of Pathology, Soonchunhyang University Cheonan Hospital, Cheonan, Republic of Korea aff002;  Department of Internal Medicine, Soonchunhyang University Cheonan Hospital, Cheonan, Republic of Korea aff003
Vyšlo v časopise: PLoS ONE 14(12)
Kategorie: Research Article
doi: 10.1371/journal.pone.0227097


Acute kidney injury (AKI) is associated with widespread effects on distant organs, including the lungs. Surfactant protein (SP)-A and SP-D are members of the C-type lectin family, which plays a critical role in host defense and regulation of inflammation in a variety of infections. Serum levels of SP-A and SP-D are markers to reflect lung injury in acute respiratory distress syndrome, idiopathic pulmonary fibrosis, and sarcoidosis. We investigated the change of lung-specific markers, including SP-A and SP-D in an AKI mice model. We studied C57BL/6J mice 4 and 24 hours after an episode of ischemic AKI (23 min of renal pedicle clamping and then reperfusion); numerous derangements were present, including SP-A, SP-D, and lung tight-junction protein. Neutrophil infiltration and apoptosis in the lungs increased in ischemic AKI. Receptor for advanced glycation end products (RAGE) in the lungs, a marker of pneumocyte I, was not changed. Lung tight-junction proteins, particularly claudin-4, claudin-18, and anti-junctional adhesion molecule 1 (JAMA-1), were reduced in 24 hours after AKI. Serum SP-A and SP-D significantly increased in ischemic AKI. SP-A and SP-D in the lungs did not increase in ischemic AKI. The immunohistochemistry showed that the expression of SP-A and SP-D was intact in ischemic AKI. SP-A and SP-D in the kidneys were significantly higher in AKI than in the sham. These patterns of SP-A and SP-D in the kidneys were similar to those of serum. AKI induces apoptosis and inflammation in the lungs. Serum SP-A and SP-D increased in ischemic AKI, but these could have originated from the kidneys. So serum SP-A and SP-D could not reflect lung injury in AKI. Further study is needed to reveal how a change in lung tight-junction protein could influence the prognosis in patients with AKI.

Klíčová slova:

Apoptosis – Cytokines – Inflammation – Kidneys – Neutrophils – Reperfusion – Renal ischemia


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Článek vyšel v časopise


2019 Číslo 12