ArticleInfection and immunity2000
Transforming growth factor-beta inhibits lipopolysaccharide-stimulated expression of inflammatory cytokines in mouse macrophages through downregulation of activation protein 1 and CD14 receptor expression.
Article in Infection and immunity, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 59 citations in OpenAlex.
- Emerging Roles of Bile Acids and TGR5 in the Central Nervous System: Molecular Functions and Therapeutic Implications.International journal of molecular sciences · 2024Review
- Two murine models of sepsis: immunopathological differences between the sexes-possible role of TGFβ1 in female resistance to endotoxemia.Biological research · 2023Article
- TGF-β uncouples glycolysis and inflammation in macrophages and controls survival during sepsis.Science signaling · 2023Article
- Effect of 1-Carbaldehyde-3,4-dimethoxyxanthone on Prostate and HPV-18 Positive Cervical Cancer Cell Lines and on Human THP-1 Macrophages.Molecules (Basel, Switzerland) · 2021Article
- Periodontal CD14 mRNA expression is downregulated in patients with chronic periodontitis and type 2 diabetes.BMC oral health · 2015Article
- Extracellular Matrix and Growth Factors Improve the Efficacy of Intramuscular Islet Transplantation.PloS one · 2015Article
- Article
- Inducible NOS-induced chloride intracellular channel 4 (CLIC4) nuclear translocation regulates macrophage deactivation.Proceedings of the National Academy of Sciences of the United States of America · 2012Article
- SPARC oppositely regulates inflammation and fibrosis in bleomycin-induced lung damage.The American journal of pathology · 2011Article
- IL-37 is a fundamental inhibitor of innate immunity.Nature immunology · 2010Article
- Inflammation anergy in human intestinal macrophages is due to Smad-induced IkappaBalpha expression and NF-kappaB inactivation.The Journal of biological chemistry · 2010Article
- Complex two-gene modulation of lung disease severity in children with cystic fibrosis.The Journal of clinical investigation · 2008Article
- Latent TGF-beta1 protects against crescentic glomerulonephritis.Journal of the American Society of Nephrology : JASN · 2008Article
- Acute alcohol intake impairs lung inflammation by changing pro- and anti-inflammatory mediator balance.Alcohol (Fayetteville, N.Y.) · 2007Article
- Role of formyl peptide receptor-like 1 (FPRL1/FPR2) in mononuclear phagocyte responses in Alzheimer disease.Immunologic research · 2005Review
- Article
- Nef protein of human immunodeficiency virus and lipopolysaccharide induce expression of CD14 on human monocytes through differential utilization of interleukin-10.Clinical and diagnostic laboratory immunology · 2002Article
- Targeted gene disruption of natural anticoagulant proteins in mice.International journal of hematology · 2002Review
- Lipopolysaccharide induced synthesis of CD14 proteins and its gene expression in hepatocytes during endotoxemia.World journal of gastroenterology · 2002Article
- Syndecan-4 as a molecule involved in defense mechanisms.Glycoconjugate journalArticle
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The septic shock that occurs in gram-negative infections is caused by a cascade of inflammatory cytokines. Several studies showed that transforming growth factor-beta1 (TGF-beta1) inhibits this septic shock through suppression of expression of the lipopolysaccharide (LPS)-induced inflammatory cytokines. In this study, we investigated whether TGF-beta1 inhibition of LPS-induced expression of inflammatory cytokines in the septic shock results from downregulation of LPS-stimulated expression of CD14, an LPS receptor. TGF-beta1 markedly inhibited LPS stimulation of CD14 mRNA and protein levels in mouse macrophages. LPS-stimulated expression of CD14 was dramatically inhibited by addition of antisense, but not sense, c-fos and c-jun oligonucleotides. Since TGF-beta1 pretreatment inhibited LPS-stimulated expression of c-fos and c-jun genes and also the binding of nuclear proteins to the consensus sequence of the binding site for activation protein 1 (AP-1), a heterodimer of c-Fos and c-Jun, in the cells, TGF-beta1 inhibition of CD14 expression may be a consequence of downregulation of AP-1. LPS-stimulated expression of interleukin-1beta and tumor necrosis factor alpha genes in the cells was inhibited by addition of CD14 antisense oligonucleotide. Also, TGF-beta1 inhibited the LPS-stimulated production of both inflammatory cytokines by the macrophages. In addition, TGF-beta1 inhibited expression of the two cytokines in several organs of mice receiving LPS. Thus, our results suggest that TGF-beta1 inhibition of LPS-stimulated inflammatory responses resulted from downregulation of CD14 and also may be a possible mechanism of TGF-beta1 inhibition of LPS-induced septic shock.
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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.