ArticleCellular and molecular life sciences : CMLS2013
Loss of Siglec-14 reduces the risk of chronic obstructive pulmonary disease exacerbation.
Article in Cellular and molecular life sciences : CMLS, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers, 2 of them syntheses that pooled it.
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
47 citing papers in PubMed, 2 syntheses or guidelines pooled it, 82 citations in OpenAlex.
- An integrative genomics approach identifies KDM4 as a modulator of trained immunity.European journal of immunology · 2022Pooled it
- Genetic variants in PLG, LPA, and SIGLEC 14 as well as smoking contribute to plasma plasminogen levels.Blood · 2014Pooled it
- Protective Role of The SIGLEC14 Null Allele Against Type 2 Diabetes Mellitus: Evidence From an Egyptian Case-Control Study.Molecular biology reports · 2026Article
- Immunological and pathological roles of Siglecs: a molecular review.Frontiers in immunology · 2026Review
- Siglec-14-LGALS3BP glycoimmune axis shapes tumor-associated macrophage polarization and confers poor outcome in colorectal cancer.NPJ precision oncology · 2025Article
- Hypoxia suppressed the Siglec-5 signaling in TAMs via modulating the balance of SHP2/SYK activation in hepatocellular carcinoma.Scientific reports · 2025Article
- Beyond the Toll-Like Receptor 4. Structure-Dependent Lipopolysaccharide Recognition Systems: How far are we?ChemMedChem · 2025Review
- Uncloaking the viral glycocalyx: How do viruses exploit glycoimmune checkpoints?Advances in virus research · 2024Review
- Study on Potential Differentially Expressed Genes in Idiopathic Pulmonary Fibrosis by Bioinformatics and Next-Generation Sequencing Data Analysis.Biomedicines · 2023Article
- Genomic structural variation: A complex but important driver of human evolution.American journal of biological anthropology · 2023Review
- Comparative physiological anthropogeny: exploring molecular underpinnings of distinctly human phenotypes.Physiological reviews · 2023Review
- Discovery, classification, evolution and diversity of Siglecs.Molecular aspects of medicine · 2023Review
- Validation of disease-specific biomarkers for the early detection of bronchopulmonary dysplasia.Pediatric research · 2023Article
- Review
- Article
- Sialic Acid-Siglec Axis in Human Immune Regulation, Involvement in Autoimmunity and Cancer and Potential Therapeutic Treatments.International journal of molecular sciences · 2021Review
- Sialic acid-binding immunoglobulin-like lectin 9 as a potential therapeutic target for chronic obstructive pulmonary disease.Chinese medical journal · 2021Article
- Article
- Integrative Analysis of the Expression of SIGLEC Family Members in Lung Adenocarcinoma via Data Mining.Frontiers in oncology · 2021Article
- Common determinants of severe Covid-19 infection are explicable by SARS-CoV-2 secreted glycoprotein interaction with the CD33-related Siglecs, Siglec-3 and Siglec-5/14.Medical hypotheses · 2020Article
Corrections and comments
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Authors and funding
16 authors at 4 institutions in 3 countries.
Funding
Abstract
Chronic obstructive pulmonary disease (COPD) is a leading cause of mortality worldwide. COPD exacerbation, or episodic worsening of symptoms, often results in hospitalization and increased mortality rates. Airway infections by new bacterial strains, such as nontypeable Haemophilus influenzae (NTHi), are a major cause of COPD exacerbation. NTHi express lipooligosaccharides that contain sialic acids, and may interact with Siglec-14, a sialic acid recognition protein on myeloid cells that serves as an activating signal transduction receptor. A null allele polymorphism in SIGLEC14 may attenuate the inflammatory responses to NTHi by eliminating Siglec-14 expression. We asked if the loss of Siglec-14 attenuates the inflammatory response by myeloid cells against NTHi, and if the SIGLEC14-null polymorphism has any effect on COPD exacerbation. We found that NTHi interacts with Siglec-14 to enhance proinflammatory cytokine production in a tissue culture model. Inhibitors of the Syk tyrosine kinase suppress this response. Loss of Siglec-14, due to SIGLEC14-null allele homozygosity, is associated with a reduced risk of COPD exacerbation in a Japanese patient population. Taken together, Siglec-14 and its downstream signaling pathway facilitate the "infection-inflammation-exacerbation" axis of COPD disease progression, and may represent promising targets for therapeutic intervention.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.