ArticleKidney diseases (Basel, Switzerland)2018
TREM-1 Contributes to Inflammation in IgA Nephropathy.
Article in Kidney diseases (Basel, Switzerland), 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 10 citations in OpenAlex.
- Mechanistic Insights and Therapeutic Advances of Anti-Inflammatory Biologics in Immune-Mediated Glomerulonephritis: A Narrative Review.Journal of inflammation research · 2026Review
- Predictive Value of Urinary KIM-1, TIMP-2 and sTREM-1 for Contrast-Induced Acute Kidney Injury in Elderly Patients After Percutaneous Coronary Intervention.International journal of general medicine · 2025Article
- Effects ofFrontiers in pharmacology · 2024Article
- Article
- Molecular insight in intrarenal inflammation affecting four main types of cells in nephrons in IgA nephropathy.Frontiers in medicine · 2023Review
- Extracellular CIRP induces acute kidney injury via endothelial TREM-1.Frontiers in physiology · 2022Article
- The ratio of urinary TREM-1/TREM-2 mRNA expression in chronic kidney disease and renal fibrosis.Annals of medicine · 2021Article
- Monozygotic Twins Discordant for Immunoglobulin A Nephropathy Display Differences in DNA Methylation and Gene Expression.Kidney diseases (Basel, Switzerland) · 2021Article
- TREM-1 promoted apoptosis and inhibited autophagy in LPS-treated HK-2 cells through the NF-κB pathway.International journal of medical sciences · 2021Article
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Authors and funding
6 authors at 2 institutions in 1 country.
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No grant is acknowledged in the PubMed record.
Abstract
backgroundCirculating IgA1-containing immune complexes (cIgA1) were shown to play important roles in IgA nephropathy (IgAN). They could induce the release of multiple inflammatory factors, including MCP-1 and IL-6, and elevated urinary inflammatory factors were also reported in patients with IgAN, which suggested that inflammation is a major contributor to kidney injury in IgAN. After the previous identification of the upregulated release of soluble triggering receptor expressed on myeloid cells-1 (sTREM-1) by mesangial cells under cIgA1 challenge using cytokine array, in the present study, we further explored the role of TREM-1, an amplifier of inflammation, in cIgA1-induced kidney injury.
methodsIn total, 35 patients with IgAN and 17 healthy controls were enrolled. The cIgA1 was isolated from plasma and used to treat cultured mesangial cells. The mRNA expression of TREM-1 as well as levels of sTREM-1, MCP-1, and IL-6 in the mesangial cell supernatant and urine samples were detected.
resultsWe found that cIgA1 from patients with IgAN could significantly upregulate the expression of TREM-1 in mesangial cells compared to healthy controls. The levels of ΔsTREM-1 were positively correlated with MCP-1 levels in the mesangial supernatant. Similarly, higher urinary levels of sTREM-1 were also observed in patients with IgAN compared to healthy controls. Moreover, IgAN patients with detectable urinary sTREM-1 presented with severe clinical and pathological manifestations, including higher IgA and lower eGFR levels, compared to patients whose urinary sTREM-1 levels were below the limit of quantification.
conclusionOur present study suggested that TREM-1 in cIgA1 induced inflammatory kidney injury in IgAN.
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