Comparative Study of KL-6, Surfactant Protein-A, Surfactant Protein-D, and Monocyte Chemoattractant Protein-1 as Serum Markers for Interstitial Lung Diseases

2002 ◽  
Vol 165 (3) ◽  
pp. 378-381 ◽  
Author(s):  
HIROSHI OHNISHI ◽  
AKIHITO YOKOYAMA ◽  
KEIICHI KONDO ◽  
HIRONOBU HAMADA ◽  
MASAHIRO ABE ◽  
...  
Author(s):  
Ferhan Kerget ◽  
Buğra Kerget ◽  
Sibel İba Yılmaz ◽  
Ömer Karaşahin ◽  
Ahmet Kızıltunç ◽  
...  

Objective: To date, over 7 million people have been infected in the COVID-19 pandemic caused by the novel coronavirus SARS-CoV-2 which emerged in Wuhan, China in December 2019. This study examined the relationships between serum monocyte chemoattractant protein-1 (MCP-1) and surfactant protein-A (SP-A) levels and the clinical course and prognosis of COVID-19. Method: The study included a total of 108 subjects. Those in the patient group (n=88) were diagnosed with COVID-19 using real-time PCR analysis of nasopharyngeal swab samples and treated in the Atatürk University Pulmonary Diseases and the City Hospital Infectious Diseases department between March 24 and April 15. The control group (n=20) included asymptomatic healthcare workers whose real-time PCR results during routine COVID-19 screening in our hospital were negative. Results: The COVID-19 patient group had significantly higher MCP-1 and SP-A levels compared to the control group (p=0.001, p=0.001). Patients who developed macrophage activation syndrome had significantly higher MCP-1 and SP-A levels than those who did not both at admission (p=0.001, p=0.001) and on day 5 of treatment (p=0.05, p=0.04). Similarly, MCP-1 and SP-A levels were significantly higher in patients who developed acute respiratory distress syndrome compared to those who did not at both time points (p=0.001 for all). Both parameters were significantly higher in nonsurviving COVID-19 patients compared to survivors (p=0.001 for both). Conclusion: MCP-1 and SP-A are on opposing sides of the inflammatory balance, and SP-A may be a pneumoprotein of importance in the presentation, course, prognosis, and possibly the treatment of COVID-19 in the future.


2010 ◽  
Vol 16 (3) ◽  
pp. 143-150 ◽  
Author(s):  
Barbara A. Seaton ◽  
Erika C. Crouch ◽  
Francis X. McCormack ◽  
James F. Head ◽  
Kevan L. Hartshorn ◽  
...  

Host defense roles for the lung collectins, surfactant protein A (SP-A) and surfactant protein D (SP-D), were first suspected in the 1980s when molecular characterization revealed their sequence homology to the acute phase reactant of serum, mannose-binding lectin. Surfactant protein A and SP-D have since been shown to play diverse and important roles in innate immunity and pulmonary homeostasis. Their location in surfactant ideally positions them to interact with air-space pathogens. Despite extensive structural similarity, the two proteins show many functional differences and considerable divergence in their interactions with microbial surface components, surfactant lipids, and other ligands. Recent crystallographic studies have provided many new insights relating to these observed differences. Although both proteins can participate in calcium-dependent interactions with sugars and other polyols, they display significant differences in the spatial orientation, charge, and hydrophobicity of their binding surfaces. Surfactant protein D appears particularly adapted to interactions with complex carbohydrates and anionic phospholipids, such as phosphatidylinositol. By contrast, SP-A shows features consistent with its preference for lipid ligands, including lipid A and the major surfactant lipid, dipalmitoylphosphatidylcholine. Current research suggests that structural biology approaches will help to elucidate the molecular basis of pulmonary collectin—ligand recognition and facilitate development of new therapeutics based upon SP-A and SP-D.


Genomics ◽  
1993 ◽  
Vol 17 (2) ◽  
pp. 294-298 ◽  
Author(s):  
Konrad Kölble ◽  
Jinhua Lu ◽  
Sara E. Mole ◽  
Stefan Kaluz ◽  
Kenneth B.M. Reid

1992 ◽  
Vol 286 (1) ◽  
pp. 5-8 ◽  
Author(s):  
J F Van Iwaarden ◽  
H Shimizu ◽  
P H M Van Golde ◽  
D R Voelker ◽  
L M G Van Golde

Rat surfactant protein D (SP-D) was shown to enhance the production of oxygen radicals by rat alveolar macrophages. This enhancement, which was determined by a lucigenin-dependent chemiluminescence assay, was maximal after 18 min at an SP-D concentration of 0.2 micrograms/ml. Surfactant lipids did not influence the stimulation of alveolar macrophages by SP-D, whereas the oxygen-radical production of these cells induced by surfactant protein A was inhibited by the lipids in a concentration-dependent manner.


2020 ◽  
Author(s):  
Jiyang Ling ◽  
Chunsheng Li ◽  
Yun Zhang ◽  
Xiaoli Yuan ◽  
Bo Liu ◽  
...  

Abstract Background: This work examines the protective effect and mechanisms of early extracorporeal membrane oxygenation with cardiopulmonary resuscitation (CPR) on ventricular-fibrillation-induced post-resuscitation lung injury in a swine cardiac-arrest model. Methods: Sixteen male swine were randomised to conventional CPR (CCPR; n=8; CCPR alone) and extracorporeal CPR (ECPR; n=8; extracorporeal membrane oxygenation with CCPR), with restoration of spontaneous circulation for 6 h as an endpoint. Serological specimens were collected at baseline and restoration of spontaneous circulation for 1, 2, 4, and 6 h; lung tissue specimens were obtained postmortem. Between-group comparisons of recovery success rate, extravascular lung water , pulmonary vascular permeability index, electron microscopic features, and serum and tissue biomarkers (surfactant protein A, surfactant protein D, Clara cell protein 16, superoxide dismutase, malondialdehyde, myeloperoxidase) were undertaken. Results: The CCPR group had non-significantly lower 6-h survival rate ( p> 0.05). Serum levels of surfactant protein A, surfactant protein D, Clara cell protein 16, and malondialdehyde were significantly higher ( p< 0.05), whereas serum superoxide dismutase was significantly lower, in the CCPR than in the ECPR group ( p <0.01). Compared with the ECPR group, tissue surfactant protein A, surfactant protein D, and superoxide dismutase significantly decreased compared to the baseline, whereas malondialdehyde and myeloperoxidase significantly increased ( p< 0.01) in the CCPR group. Extravascular lung water and pulmonary vascular permeability index were significantly higher in the CCPR after 6 h compared to the baseline values and the ECPR group ( p< 0.01). Conclusions: Electron microscopy revealed mostly vacuolated intracellular alveolar type II lamellar bodies and fuzzy lamellar structure and widening and blurring of the blood–gas barrier in the CCPR group in contrast to that in the ECPR group. ECPR was found to have protective pulmonary effects, possibly related to the regulation of alveolar surface-active proteins and mitigated oxidative stress response post-resuscitation.


2014 ◽  
Vol 61 (1.2) ◽  
pp. 1-6 ◽  
Author(s):  
Hisatsugu Goto ◽  
Atsushi Mitsuhashi ◽  
Yasuhiko Nishioka

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