Related Experiment Video
Updated: Jul 14, 2026
11:44
Long Term Intravital Multiphoton Microscopy Imaging of Immune Cells in Healthy and Diseased Liver Using CXCR6.Gfp Reporter Mice
Published on: March 24, 2015
CXCL10/SLC11A1 Axis Exacerbates Septic Liver Injury by Regulating Neutrophil Extracellular Traps Formation to Drive
Haiping Lin1, Shicong Zheng1, Pei Song2
1Department of General Surgery, Jinhua Central Hospital, Teaching Hospital of Mathematical Medicine College, Zhejiang Normal University, Zhejiang, China.
Advanced Science (Weinheim, Baden-Wurttemberg, Germany)
|July 13, 2026
Summary
Sepsis causes liver injury by activating neutrophils to release neutrophil extracellular traps (NETs) via the CXCL10-SLC11A1 axis. Targeting this pathway may treat sepsis-induced liver damage.
Area of Science:
- Immunology
- Hepatology
- Molecular Biology
Background:
- Intra-abdominal infection often leads to sepsis, a condition where the liver is frequently injured early.
- Neutrophil infiltration and activation are key features of sepsis-associated liver injury.
Purpose of the Study:
- To investigate the molecular mechanisms underlying sepsis-induced liver injury.
- To identify novel therapeutic targets for sepsis-associated liver damage.
Main Methods:
- Utilized a cecal ligation and puncture (CLP) mouse model with bulk and single-cell RNA sequencing.
- Performed conditional knockout of solute carrier family 11 member 1 (SLC11A1) in neutrophils.
- Analyzed hepatocyte secretion of C-X-C motif chemokine ligand 10 (CXCL10) and its effects on neutrophil extracellular traps (NETs) formation.
Main Results:
- Sepsis induced significant neutrophil infiltration in the liver, with upregulated SLC11A1 expression.
- Knockout of Slc11a1 in neutrophils attenuated liver injury and improved survival.
- A CXCL10-SLC11A1-NETs axis was identified, promoting pro-inflammatory macrophage polarization and exacerbating liver damage.
- Elevated CXCL10 levels in patients correlated with liver injury markers.
Conclusions:
- The study identified a novel CXCL10-SLC11A1-NETs signaling axis contributing to sepsis-induced liver injury.
- Targeting this axis, particularly CXCL10, presents a potential therapeutic strategy for sepsis-associated liver damage.
Related Concept Videos
01:12Chronic Inflammation: Introduction
Chronic inflammation is a prolonged, dysregulated immune response that persists for weeks to years when the inciting stimulus is difficult to eradicate or when self‑antigens drive ongoing reactivity. Morphologically, it is defined by mononuclear cell infiltration, progressive tissue destruction, and concurrent attempts at healing via angiogenesis and fibrosis. Compared with acute inflammation, edema is less prominent while cellular infiltration predominates; triggers include persistent...
01:24Cirrhosis II: Pathophysiology
Cirrhosis is a progressive chronic liver injury caused by prolonged inflammation, excessive fibrotic remodeling, and impaired regeneration. Over time, repeated hepatic insults disrupt the liver’s architecture and function, leading to reduced blood flow, impaired bile drainage, and diminished metabolic capacity.Pathophysiology of cirrhosisCirrhosis arises from three main responses to chronic liver damage: inflammation, immune activation, and hepatocyte death. These processes lead to structural...
01:25Inflammatory Bowel Disease III: Crohn's Disease
Crohn’s disease is a chronic, relapsing form of inflammatory bowel disease characterized by segmental, transmural inflammation that can affect any part of the gastrointestinal tract. Its pathogenesis arises from a combination of genetic susceptibility, environmental exposures, epithelial barrier dysfunction, and immune dysregulation. Together, these factors lead to an exaggerated immune response against components of the gut microbiome.Genetic and Environmental InfluencesMultiple genetic...