ArticleInnate immunity2021
Regulation of CAMP (cathelicidin antimicrobial peptide) expression in adipocytes by TLR 2 and 4.
Article in Innate immunity, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 18 citations in OpenAlex.
- MEK Inhibitors and Toll-like Receptor Signaling: Implications for Infection and Inflammation.International journal of molecular sciences · 2026Review
- GDF15 (Growth/Differentiation Factor-15) Expression in Human Adipose Tissue and in Adipocyte Cell Lines.Biomedicines · 2026Article
- Cellular gatekeepers of infected wounds: the dual role of adipocytes in coordinating immunity and regeneration.Frontiers in immunology · 2026Review
- Characterization of growth differentiation factor 15 (GDF15) as a neurotropic adipokine permeable to the brain.Scientific reports · 2025Article
- Thyroid-Stimulating Hormone Regulates the Glucose Metabolism in Hepatocytes via Toll-Like Receptor 4/Tollip Pathway.International journal of endocrinology · 2025Article
- Cathelicidin: Insights into Its Impact on Metabolic Syndrome and Chronic Inflammation.Metabolites · 2024Review
- Gut Microbiome and Metabolic and Immune Indices in Males with or without Evidence of Metabolic Dysregulation.Journal of obesity & metabolic syndrome · 2024Article
- Regulation of Cathelicidin Antimicrobial Peptide (CAMP) Gene Expression by TNFα and cfDNA in Adipocytes.International journal of molecular sciences · 2023Article
- Circulating Levels of Cathelicidin Antimicrobial Peptide (CAMP) Are Affected by Oral Lipid Ingestion.Nutrients · 2023Article
- Wound infiltrating adipocytes are not myofibroblasts.Nature communications · 2023Article
- The sequencing of the key genes and end products in the TLR4 signaling pathway from the kidney ofOpen life sciences · 2023Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Recent data argue for a pro-inflammatory role of CAMP (cathelicidin antimicrobial peptide) in adipocytes and adipose tissue (AT) and for regulatory circuits involving TLRs. In order to investigate regulatory effects of TLR2 and TLR4, 3T3-L1 adipocytes were stimulated with TLR2 agonistic lipopeptide MALP-2 and with TLR4 agonist LPS in presence or absence of signal transduction inhibitors. CAMP gene expression was analysed by quantitative real-time PCR in adipocytes and in murine AT compartments and cellular subfractions. CAMP expression was higher in gonadal than in subcutaneous AT and there was a gender-specific effect with higher levels in males. Adipocytes had higher CAMP expression than the stroma-vascular cell (SVC) fraction. MALP-2 up-regulated CAMP expression significantly, mediated by STAT3 and PI3K and potentially (non-significant trend) by NF-κB and MAPK, but not by raf-activated MEK-1/-2. Moreover, LPS proved to act as a potent inducer of CAMP via NF-κB, PI3K and STAT3, whereas specific inhibition of MAPK and MEK-1/-2 had no effect. In conclusion, activation of TLR2 and TLR4 by classical ligands up-regulates adipocyte CAMP expression involving classical signal transduction elements. These might represent future drug targets for pharmacological modulation of CAMP expression in adipocytes, especially in the context of metabolic and infectious diseases.
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