Gut ischemia/reperfusion induced acute lung injury is an alveolar macrophage dependent event

Luciana Borsoi Moraes1, Abel Hiroshi F Murakami, Belchor Fontes

  • 1Laboratory of Medical Investigation of the 3rd Division of Surgical Clinic, Hospital das Clinicas, University of Sao Paulo School of Medicine, Sao Paulo, Brazil.

Abstract

Insights

Eliminating lung alveolar macrophages (AMs) prevented acute lung injury (ALI) following intestinal ischemia/reperfusion (I/R) in rats. This indicates AMs are crucial mediators of ALI after intestinal I/R.

Area of Science:

  • Physiology
  • Immunology
  • Pathology

Background:

  • Alveolar macrophages (AMs) are implicated in lung acute lung injury (ALI) following lung ischemia/reperfusion (I/R).
  • The role of AMs in ALI after intestinal I/R remains unclear.
  • This study investigates AMs' role in ALI subsequent to intestinal I/R.

Purpose of the Study:

  • To determine if AM elimination impacts ALI development after intestinal I/R in rats.
  • To elucidate the specific contribution of AMs to intestinal I/R-induced ALI.

Main Methods:

  • Male Wistar rats were treated with clodronate-liposomes (CLOD-LIP) to deplete AMs, liposomes (LIP), or no treatment (UNTREAT).
  • Animals underwent intestinal ischemia/reperfusion (I/R), laparotomy (LAP), or served as controls (CTR).
  • Acute lung injury (ALI) was quantified using the Evans blue dye (EBD) method to measure lung vascular permeability.

Main Results:

  • Intestinal I/R significantly increased ALI in LIP and UNTREAT groups compared to sham and control groups.
  • CLOD-LIP treatment significantly reduced ALI in the I/R group compared to LIP and UNTREAT groups.
  • These findings demonstrate that I/R induces ALI, which is preventable by AM depletion.

Conclusions:

  • Alveolar macrophages (AMs) play a critical role in the pathogenesis of ALI following intestinal ischemia/reperfusion (I/R).
  • Depletion of AMs effectively mitigates intestinal I/R-induced ALI.
  • Targeting AMs may represent a therapeutic strategy for preventing ALI in the context of intestinal I/R injury.

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