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Updated: Jan 19, 2026
Imaging Neutrophils and Monocytes in Mesenteric Veins by Intravital Microscopy on Anaesthetized Mice in Real Time
Published on: November 16, 2015
Neutrophil and monocyte kinetics play critical roles in mouse peritoneal adhesion formation
Jonathan M Tsai1,2,3, Maia Shoham1, Nathaniel B Fernhoff1
1Institute for Stem Cell Biology and Regenerative Medicine and.
Abstract:
Peritoneal adhesions are pathological fibroses that ensnare organs after abdominal surgery. This dense connective tissue can cause small bowel obstruction, female infertility, and chronic abdominal pain. The pathogenesis of adhesions is a fibrotic response to tissue damage coordinated between mesothelial cells, fibroblasts, and immune cells. We have previously demonstrated that peritoneal adhesions are a consequence of mechanical injury to the mesothelial layer sustained during surgery. Neutrophils are among the first leukocytes involved in the early response to tissue damage. Here, we show that when subjected to mechanical stress, activated mesothelial cells directly recruit neutrophils and monocytes through upregulation of chemokines such as CXCL1 and monocyte chemoattractant protein 1 (MCP-1). We find that neutrophils within the adhesion sites undergo cell death and form neutrophil extracellular traps (NETosis) that contribute to pathogenesis. Conversely, tissue-resident macrophages were profoundly depleted throughout the disease time course. We show that this is distinct from traditional inflammatory kinetics such as after sham surgery or chemically induced peritonitis, and suggest that adhesions result from a primary difference in inflammatory kinetics. We find that transient depletion of circulating neutrophils significantly decreases adhesion burden, and further recruitment of monocytes with thioglycolate or MCP-1 also improves outcomes. Our findings suggest that the combination of neutrophil depletion and monocyte recruitment is sufficient to prevent adhesion formation, thus providing insight for potential clinical interventions.
Insights
Post-surgical peritoneal adhesions involve neutrophil extracellular traps (NETosis) and depleted macrophages. Targeting neutrophils and monocytes may prevent adhesion formation, offering new clinical interventions for abdominal surgery complications.
Area of Science:
- Surgical pathology
- Immunology
- Fibrosis research
Background:
- Peritoneal adhesions are pathological fibroses following abdominal surgery, causing complications like bowel obstruction and infertility.
- Adhesion formation involves mesothelial cells, fibroblasts, and immune cells responding to surgical tissue damage.
- Mechanical injury to the mesothelial layer is a key trigger for peritoneal adhesions.
Purpose of the Study:
- To investigate the role of immune cells and inflammatory kinetics in peritoneal adhesion pathogenesis.
- To identify cellular mechanisms and potential therapeutic targets for preventing post-surgical adhesions.
Main Methods:
- Mechanical stress applied to mesothelial cells in vitro.
- Analysis of chemokine upregulation (CXCL1, MCP-1) and leukocyte recruitment (neutrophils, monocytes).
- Assessment of neutrophil extracellular trap (NETosis) formation and macrophage depletion in adhesion sites.
- Evaluation of the effects of neutrophil depletion and monocyte recruitment on adhesion burden in vivo.
Main Results:
- Activated mesothelial cells recruit neutrophils and monocytes via chemokines like CXCL1 and MCP-1.
- Neutrophils form neutrophil extracellular traps (NETosis), contributing to adhesion pathogenesis.
- Tissue-resident macrophages are depleted, differing from standard inflammatory responses.
- Transient neutrophil depletion and enhanced monocyte recruitment significantly reduce adhesion formation.
Conclusions:
- Peritoneal adhesion pathogenesis is characterized by specific inflammatory kinetics involving NETosis and macrophage depletion.
- Targeting neutrophils and promoting monocyte recruitment presents a promising strategy for preventing post-surgical adhesions.
- These findings offer insights for developing novel clinical interventions against peritoneal adhesions.
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