ArticleExperimental and therapeutic medicine2020
Mechanism of IL-8-induced acute lung injury through pulmonary surfactant proteins A and B.
Article in Experimental and therapeutic medicine, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It has been retracted, and should not be counted. Cited by 15 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
15 citing papers in PubMed, 25 citations in OpenAlex.
- Surfactant protein A deficiency aggravates silica-induced pulmonary fibrosis by promoting intrinsic apoptosis of alveolar type II epithelial cells.Respiratory research · 2026Article
- Protective Effect of Low 2-O, 3-O Desulfated Heparin (ODSH) Against LPS-Induced Acute Lung Injury in Mice.Biomolecules · 2025Article
- The value of surfactant protein a in evaluating the severity and prognosis in community-acquired pneumonia patients.BMC pulmonary medicine · 2024Article
- Unraveling the enigma: The emerging significance of pulmonary surfactant proteins in predicting, diagnosing, and managing COVID-19.Immunity, inflammation and disease · 2024Review
- Clinical and Microbiological Features of Fulminant Haemolysis Caused byMicroorganisms · 2023Review
- Acute lung injury caused by sepsis: how does it happen?Frontiers in medicine · 2023Review
- Club cell protein (CC)16 as potential lung injury marker in a porcine 72 h polytrauma model.European journal of trauma and emergency surgery : official publication of the European Trauma Society · 2022Article
- Massive intravascular hemolysis is an important factor in Clostridium perfringens-induced bacteremia.Internal and emergency medicine · 2022Article
- Use of transcutaneous electrical acupoint stimulation in pulmonary surgery for patients with tuberculosis.Journal of clinical tuberculosis and other mycobacterial diseases · 2022Article
- Paraquat Induces Lung InjuryFrontiers in pharmacology · 2022Article
- Pathogenic Characterization ofFrontiers in microbiology · 2021Article
- Methane Inhalation Protects Against Lung Ischemia-Reperfusion Injury in Rats by Regulating Pulmonary SurfactantFrontiers in physiology · 2021Article
- Emodin protects against intestinal and lung injury induced by acute intestinal injury by modulating SP-A and TLR4/NF-κB pathway.Bioscience reports · 2020Article
- Recent progress on surfactant protein A: cellular function in lung and kidney disease development.American journal of physiology. Cell physiology · 2020Review
- Lipid-Protein and Protein-Protein Interactions in the Pulmonary Surfactant System and Their Role in Lung Homeostasis.International journal of molecular sciences · 2020Review
Corrections and comments
- Retraction · 2025-04-28Author Unresponsive · Concerns/Issues about Data · Investigation by Journal/Publisher · Investigation by Third Party · Unreliable Data · · See also: https://pubpeer.com/publications/1942D51EDD6ECB0E7FF5C13FF5D81C
- Retracted
Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
This study explored how interleukin-8 (IL-8) causes acute lung injury (ALI) through pulmonary surfactant protein A (SP-A) and surfactant protein B (SP-B). Serum was collected from 53 ALI patients and further 56 healthy subjects who underwent physical examination. The IL-8, SP-A, and SP-B levels were determined using enzyme-linked immunosorbent assay (ELISA). An ALI model was constructed using lipopolysaccharide (LSP)-induced normal A549 cells. siRNA was employed to interfere with the expression of IL-8, SP-A and SP-B. Western blot analysis was carried out to determine the protein levels, and MTT assay to determine the cell activity. In addition, co-immunoprecipitation (Co-IP) assay was used to verify the interaction between IL-8, SP-A and SP-B. ALI patients showed high expression of serum IL-8, and low expression of SP-A and SP-B, and IL-8 was negatively correlated with SP-A and SP-B, respectively. LSP-induced normal A549 cells showed increased expression of IL-8 and decreased expression of SP-A and SP-B. Silencing IL-8 led to increased expression levels of SP-A, SP-B and Bcl2, decreased expression levels of caspase-9, caspase-3, Bax, TNF-α, IL-17 and IL-1β, reduced cell apoptosis rate, and enhanced cell viability. Silencing SP-A and SP-B resulted in increased expression of IL-8, caspase-9, caspase-3, Bax, TNF-α, IL-17 and IL-1β, and decreased expression of Bcl2. Co-IP assay revealed that IL-8 could interact with SP-A and SP-B, respectively. IL-8 induces apoptosis by inhibiting SP-A and SP-B, and intensifies cellular inflammatory reaction, leading eventually to ALI.
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Registered trials
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