ArticleMediators of inflammation2014
Uteroglobin, a possible ligand of the lipoxin receptor inhibits serum amyloid A-driven inflammation.
Article in Mediators of inflammation, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 13 citations in OpenAlex.
- From respiratory infections to environmental exposures: CC16 is a key modulator of airway homeostasis.Frontiers in medicine · 2026Review
- Secretoglobin 3A2 peptides have therapeutic potential for allergic airway inflammation.Life sciences · 2024Article
- Circulating CC16 and Asthma: A Population-based, Multicohort Study from Early Childhood through Adult Life.American journal of respiratory and critical care medicine · 2023Article
- Article
- CC16 Binding to αAmerican journal of respiratory and critical care medicine · 2021Article
- Club Cell Protein 16 Attenuates CD16Journal of immunology research · 2021Article
- Club Cell Secretory Protein Deficiency Leads to Altered Lung Function.American journal of respiratory and critical care medicine · 2019Article
- Club cell protein 16 (Cc16) deficiency increases inflamm-aging in the lungs of mice.Physiological reports · 2018Article
- Eosinophilic and Noneosinophilic Asthma.American journal of respiratory and critical care medicine · 2018Review
- The Formyl Peptide Receptors: Diversity of Ligands and Mechanism for Recognition.Molecules (Basel, Switzerland) · 2017Review
- Club Cell Protein 16 (CC16) Augmentation: A Potential Disease-modifying Approach for Chronic Obstructive Pulmonary Disease (COPD).Expert opinion on therapeutic targets · 2016Review
- Serum Proteome Profiles in Stricturing Crohn's Disease: A Pilot Study.Inflammatory bowel diseases · 2015Article
- Serum amyloid A as a marker of persistent inflammation and an indicator of cardiovascular and renal involvement in patients with rheumatoid arthritis.Mediators of inflammation · 2014Article
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Authors and funding
6 authors at 6 institutions in 2 countries.
Funding
Abstract
Serum amyloid A (SAA) production is increased by inflamed arthritic synovial tissue, where it acts as a cytokine/chemoattractant for inflammatory and immune cells and as an inducer of matrix degrading enzymes. SAA has been shown to bind lipoxin A4 receptor, a member of the formyl-peptide related 2 G-protein coupled receptor family (ALX) and elicit proinflammatory activities in human primary fibroblast-like synoviocytes (FLS). We report on the identification of uteroglobin, a small globular protein with potent anti-inflammatory activities, as a possible ligand of ALX. Uteroglobin-specific association with ALX was demonstrated by an enzyme immunoassay experiment employing a cell line engineered to express the human ALX receptor. Uteroglobin's interaction with ALX resulted in the inhibition of SAA responses, such as attenuation of phospholipase A2 activation and cellular chemotaxis. In FLS, uteroglobin showed an antagonism against SAA-induced interleukin-8 release and decreased cell migration. These novel roles described for uteroglobin via ALX may help elucidate genetic and clinical observations indicating that a polymorphism in the uteroglobin promoter is linked to disease outcome, specifically prediction of bone erosion in patients with rheumatoid arthritis or severity of IgA glomerulonephritis and sarcoidosis.
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Registered trials
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