ArticleCytokine2013
SAA does not induce cytokine production in physiological conditions.
Article in Cytokine, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
37 citing papers in PubMed, 47 citations in OpenAlex.
- Role of serum amyloid A in Mycoplasma pneumoniae pneumonia and related respiratory diseases.Frontiers in pediatrics · 2026Review
- Serum amyloid A: multifaceted roles in inflammation and cellular interactions.Immunologic research · 2025Review
- Serum Amyloid A: A Double-Edged Sword in Health and Disease.International journal of molecular sciences · 2025Review
- Interactions of Serum Amyloid A Proteins with the Blood-Brain Barrier: Implications for Central Nervous System Disease.International journal of molecular sciences · 2024Review
- The Impact of Aerobic Exercise on HDL Quantity and Quality: A Narrative Review.International journal of molecular sciences · 2023Review
- Article
- Association of Serum Interleukin-8 and Serum Amyloid A With Anxiety Symptoms in Patients With Cerebral Small Vessel Disease.Frontiers in neurology · 2022Article
- Role of Serum Amyloid A in Abdominal Aortic Aneurysm and Related Cardiovascular Diseases.Biomolecules · 2021Review
- Effect of High-Density Lipoprotein from Healthy Subjects and Chronic Kidney Disease Patients on the CD14 Expression on Polymorphonuclear Leukocytes.International journal of molecular sciences · 2021Article
- Serum amyloid A is a soluble pattern recognition receptor that drives type 2 immunity.Nature immunology · 2020Article
- Soluble pattern recognition molecules: Guardians and regulators of homeostasis at airway mucosal surfaces.European journal of immunology · 2020Review
- Serum amyloid A is not incorporated into HDL during HDL biogenesis.Journal of lipid research · 2020Article
- High-Density Lipoprotein (HDL) Inhibits Serum Amyloid A (SAA)-Induced Vascular and Renal Dysfunctions in Apolipoprotein E-Deficient Mice.International journal of molecular sciences · 2020Article
- Serum Amyloid A-Mediated Inflammasome Activation of Microglial Cells in Cerebral Ischemia.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2019Article
- Role of serum amyloid A in atherosclerosis.Current opinion in lipidology · 2019Review
- Intestinal Serum amyloid A suppresses systemic neutrophil activation and bactericidal activity in response to microbiota colonization.PLoS pathogens · 2019Article
- Serum amyloid A binds to fibrin(ogen), promoting fibrin amyloid formation.Scientific reports · 2019Article
- High-Density Lipoprotein from Chronic Kidney Disease Patients Modulates Polymorphonuclear Leukocytes.Toxins · 2019Article
- Serum Amyloid A Contributes to Chronic Apical Periodontitis via TLR2 and TLR4.Journal of dental research · 2019Article
- Bacterial Lipoproteins Constitute the TLR2-Stimulating Activity of Serum Amyloid A.Journal of immunology (Baltimore, Md. : 1950) · 2018Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
SAA has been shown to have potential proinflammatory properties in inflammatory diseases such as atherosclerosis. These include induction of tumor necrosis factor α, interleukin-6, and monocyte chemoattractant protein 1 in vitro. However, concern has been raised that these effects might be due to use of recombinant SAA with low level of endotoxin contaminants or its non-native forms. Therefore, physiological relevance has not been fully elucidated. In this study, we investigated the role of SAA in the production of inflammatory cytokines. Stimulation of mouse monocyte J774 cells with lipid-poor recombinant human SAA and purified SAA derived from cardiac surgery patients, but not ApoA-I and ApoA-II, elicited pro-inflammatory cytokines like granulocyte colony stimulating factor (G-CSF). However, HDL-associated SAA failed to stimulate production of these cytokines. Using neutralizing antibodies against toll like receptor (TLR) 2 and 4, we could evaluate that TLR 2 is responsible for G-CSF production by lipid-poor SAA. To confirm these data in vivo, we expressed mouse SAA in SAA deficient C57BL/6 mice using an adenoviral vector. G-CSF was identically expressed in SAA-Adenoviral infected mice as well as in control null-Adenoviral mice at the early time points (4-8h) and could not be detected in plasma 24h after infection when plasma SAA levels were maximally elevated, indicating that adenoviral vector rather than SAA affected G-CSF levels. Taken together, our findings suggest that lipid-poor SAA, but not HDL-associated SAA, stimulates G-CSF production and this stimulation is mediated through TLR 2 in J774 cells. However, its physiological role in vivo remains ambiguous.
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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.