ArticleFunctional & integrative genomics2024
The role of lipoprotein‑associated phospholipase A2 in inflammatory response and macrophage infiltration in sepsis and the regulatory mechanisms.
Article in Functional & integrative genomics, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed.
- Pathological Signal-Responsive Nanoplatforms for Sepsis: Integrating Biomarker Sensing With Spatiotemporal Drug Delivery and Immunomodulation.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Review
- Analyzing the clinical profile and potential biomarkers to differentiate idiopathic angioedema from hereditary or mast cell-mediated angioedema.The World Allergy Organization journal · 2026Article
- Diagnostic accuracy of SeptiCyte® RAPID to discriminate sepsis from non-infectious critical illness in patients meeting sepsis criteria according to sepsis-3 definition at ICU admission.European journal of clinical microbiology & infectious diseases : official publication of the European Society of Clinical Microbiology · 2026Observational
- Likelihood of Blood Culture Positivity Using SeptiCyte RAPID.Journal of clinical medicine · 2026Article
- Single-Cell Profiling Identifies JUNB/SPI1-Driven Inflammatory Programs and Novel Communication Axes in Myeloid Cells of SepsisEndocrine, metabolic & immune disorders drug targets · 2026Article
- Phospholipase A2 and Systemic-Immune Inflammation Index as Early Predictors of Neurotoxicity Induced by Acute Glufosinate Ammonium Poisoning: A Population-Based Case-Control Analysis.Emergency medicine international · 2026Article
- Lipoprotein-associated phospholipase A2 (Lp-PLA2): a key hub linking lipid metabolism and immune inflammation.Frontiers in immunology · 2026Review
- Lp‑PLA2 in the cancer landscape: From molecular mechanisms to therapeutic potential (Review).International journal of oncology · 2025Review
- SPI1 upregulated LILRB2 to enhance the immunosuppressive phenotype of LPS-tolerant macrophages by inhibiting TLR8-mediated MyD88/NF-κB signaling.Biology direct · 2025Article
- ER-resident proteins are key players in cartilage and bone homeostasis.Frontiers in cell and developmental biology · 2025Review
Corrections and comments
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Authors and funding
6 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Lipoproteinassociated phospholipase A2 (Lp-PLA2), encoded by the phospholipase A2 group VII (Pla2g7) gene, has been pertinent to inflammatory responses. This study investigates the correlation between Lp-PLA2 and inflammatory injury in septic mice and explores its regulatory mechanism. Lp-PLA2 was found to be upregulated in the serum of septic mice induced by cecal ligation and puncture and in the culture supernatant of RAW264.7 cells following lipopolysaccharide and adenosine triphosphate treatments. The contents of Lp-PLA2 were positively correlated with increased concentrations of proinflammatory cytokines in patients with sepsis. Both animal and cellular models showed increased concentrations of proinflammatory cytokines. Spi-1 proto-oncogene (Spi1), highly expressed in these models, was found to activate Pla2g7 transcription. Knockdown of Pla2g7 or Spi1 reduced the proinflammatory cytokine production, mitigated organ damage in mice, and suppressed macrophage migration in vitro. Retinoblastoma binding protein 6 (Rbbp6), poorly expressed in both models, was found to reduce Spi1 protein stability through ubiquitination modification. Rbbp6 overexpression similarly suppressed inflammatory activation of RAW264.7 cells, which was counteracted by Pla2g7 or Spi1 upregulation. In summary, this study demonstrates that the Pla2g7 loss and Spi1 upregulation participate in inflammatory responses in sepsis by elevating the Lp-PLA2 levels.
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