Related Experiment Video

Updated: Aug 3, 2026

Isolation of Murine Peritoneal Macrophages to Carry Out Gene Expression Analysis Upon Toll-like Receptors Stimulation
08:21

Isolation of Murine Peritoneal Macrophages to Carry Out Gene Expression Analysis Upon Toll-like Receptors Stimulation

Published on: April 29, 2015

Role of macrophage inflammatory protein 2 in acute lung injury in murine peritonitis

Hironori Tsujimoto1, Satoshi Ono, Hidetaka Mochizuki

  • 1Department of Surgery I, National Defense Medical College, 3-2 Namiki, Tokorozawa, Saitama, 359-8513, Japan.

The Journal of Surgical Research
|February 22, 2002
PubMed
Abstract

Insights

Macrophage inflammatory protein 2 (MIP-2) drives neutrophil recruitment to the lungs during bacterial peritonitis. Neutralizing MIP-2 reduces lung injury and mortality, offering a potential therapeutic strategy.

Area of Science:

  • Immunology
  • Pathophysiology
  • Pulmonary Medicine

Background:

  • Bacterial peritonitis frequently causes acute lung injury, with neutrophils playing a key role.
  • Macrophage inflammatory protein 2 (MIP-2) is a key chemoattractant for neutrophils, similar to human IL-8.
  • This study investigates MIP-2's role in neutrophil recruitment during murine peritonitis.

Purpose of the Study:

  • To elucidate the role of MIP-2 in neutrophil recruitment to the lungs in a murine model of peritonitis.
  • To evaluate the therapeutic potential of targeting MIP-2 in peritonitis-induced lung injury.

Main Methods:

  • Murine model of peritonitis using cecal ligation and puncture (CLP).
  • Measurement of MIP-2 levels and mRNA expression in blood and lung tissue.
  • Assessment of neutrophil CD11b expression and chemotaxis.
  • Evaluation of anti-MIP-2 antibody effects on lung injury and mortality.

Main Results:

  • MIP-2 mRNA expression and neutrophil accumulation were observed in lung tissue post-CLP.
  • Anti-MIP-2 antibody treatment inhibited neutrophil CD11b expression and lung neutrophil chemotaxis.
  • Neutralization of MIP-2 reduced lung edema and decreased peritonitis-related mortality.

Conclusions:

  • MIP-2 is critical for neutrophil recruitment in the lung during peritonitis.
  • Targeting MIP-2 by neutralization represents a promising therapeutic approach for peritonitis-associated lung damage.

More Related Videos

Inducing Acute Lung Injury in Mice by Direct Intratracheal Lipopolysaccharide Instillation11:07

Inducing Acute Lung Injury in Mice by Direct Intratracheal Lipopolysaccharide Instillation

Published on: July 6, 2019

Non-Invasive Endotracheal Administration of Lipopolysaccharide to Induce Acute Lung Injury in Rodents04:10

Non-Invasive Endotracheal Administration of Lipopolysaccharide to Induce Acute Lung Injury in Rodents

Published on: December 5, 2025

Related Concept Videos

Acute Inflammation I: Inflammatory Response01:26

Acute Inflammation I: Inflammatory Response

Acute inflammation is a rapid, short-lived physiological response to tissue injury or infection, designed to eliminate harmful agents and initiate repair. This tightly regulated process typically lasts from minutes to several days and is triggered by factors such as microbial invasion, physical trauma, or chemical injury.Recognition and Mediator ReleaseThe inflammatory response begins when resident immune cells—such as mast cells, macrophages, and dendritic cells—detect damage-associated...
Acute Inflammation II: Cellular Phase01:26

Acute Inflammation II: Cellular Phase

The cellular phase of acute inflammation is a tightly orchestrated sequence of events that recruits leukocytes, primarily neutrophils, to sites of tissue injury or infection. Following the initial vascular changes, this phase ensures effective immune cell migration, activation, and function at the affected site to eliminate pathogens and initiate tissue repair.Leukocyte Recruitment CascadeLeukocyte recruitment happens in four steps: margination, adhesion, transmigration, and chemotaxis. Reduced...