ArticleInternational journal of molecular sciences2021
Targeting S100A9 Reduces Neutrophil Recruitment, Inflammation and Lung Damage in Abdominal Sepsis.
Article in International journal of molecular sciences, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.
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Who cites it
39 citing papers in PubMed, 58 citations in OpenAlex.
- Calprotectin as a Diagnostic Marker for Lower Respiratory Tract Infection and Sepsis in the Emergency Department.Open forum infectious diseases · 2026Article
- S100A9 deletion ameliorates acute lung injury by attenuating excessive neutrophil activation via activating the NRF2/HO-1 signaling axis.Respiratory research · 2026Article
- Prostaglandins prevent long-lasting pain in a mouse model of chronic postsurgical pain.British journal of anaesthesia · 2026Article
- Tumor-derived neutrophil extracellular trap-associated DNA impairs treatment efficacy in breast cancer via CCDC25-dependent epithelial-mesenchymal transition.The Journal of clinical investigation · 2026Article
- The S100A8/A9-NETosis feedback loop in sepsis: potential mechanisms, immune crosstalk, and therapeutic targeting.Frontiers in immunology · 2026Review
- Neutrophil in sepsis: functional aberration and regulated cell death.Frontiers in immunology · 2026Review
- Identification and validation of key genes related to apoptosis in multiple organ dysfunction syndrome.European journal of medical research · 2025Article
- Development of novel neutralizing single-chain fragment variable antibodies against S100A8.Scientific reports · 2025Article
- Uncovering critical transitions and molecule mechanisms in disease progressions using Gaussian graphical optimal transport.Communications biology · 2025Article
- Neutrophils initiate proinflammatory immune responses in early endometriosis lesion development.JCI insight · 2025Article
- S100A8/S100A9 through PAD4 activation of neutrophil extracellular traps promotes granulomatous lobular mastitis.Frontiers in immunology · 2025Article
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- Renal Vein Thrombosis Secondary to Pyelonephritis: Targeting a Thrombo-Inflammatory Entity.Clinics and practice · 2024Article
- Silenced-C5ar1 improved multiple organ injury in sepsis rats via inhibiting neutrophil extracellular trap.Journal of molecular histology · 2024Article
- Heterogeneity of immune cells and their communications unveiled by transcriptome profiling in acute inflammatory lung injury.Frontiers in immunology · 2024Article
- Identification and Analysis of PANoptosis-Related Genes in Sepsis-Induced Lung Injury by Bioinformatics and Experimental Verification.Journal of inflammation research · 2024Article
- Serum Mrp 8/14 as a Potential Biomarker for Predicting the Occurrence of Acute Respiratory Distress Syndrome Induced by Sepsis: A Retrospective Controlled Study.Journal of inflammation research · 2024Article
- Metformin Mitigates Sepsis-Induced Acute Lung Injury and Inflammation in Young Mice by Suppressing the S100A8/A9-NLRP3-IL-1β Signaling Pathway.Journal of inflammation research · 2024Article
- Manual Therapy Exerts Local Anti-Inflammatory Effects Through Neutrophil Clearance.Journal of immunology research · 2024Article
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
Abstract
S100A9, a pro-inflammatory alarmin, is up-regulated in inflamed tissues. However, the role of S100A9 in regulating neutrophil activation, inflammation and lung damage in sepsis is not known. Herein, we hypothesized that blocking S100A9 function may attenuate neutrophil recruitment in septic lung injury. Male C57BL/6 mice were pretreated with the S100A9 inhibitor ABR-238901 (10 mg/kg), prior to cercal ligation and puncture (CLP). Bronchoalveolar lavage fluid (BALF) and lung tissue were harvested for analysis of neutrophil infiltration as well as edema and CXC chemokine production. Blood was collected for analysis of membrane-activated complex-1 (Mac-1) expression on neutrophils as well as CXC chemokines and IL-6 in plasma. Induction of CLP markedly increased plasma levels of S100A9. ABR-238901 decreased CLP-induced neutrophil infiltration and edema formation in the lung. In addition, inhibition of S100A9 decreased the CLP-induced up-regulation of Mac-1 on neutrophils. Administration of ABR-238901 also inhibited the CLP-induced increase of CXCL-1, CXCL-2 and IL-6 in plasma and lungs. Our results suggest that S100A9 promotes neutrophil activation and pulmonary accumulation in sepsis. Targeting S100A9 function decreased formation of CXC chemokines in circulation and lungs and attenuated sepsis-induced lung damage. These novel findings suggest that S100A9 plays an important pro-inflammatory role in sepsis and could be a useful target to protect against the excessive inflammation and lung damage associated with the disease.
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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.