Related Experiment Video

Updated: Sep 28, 2026

A Microphysiological System to Study Leukocyte-Endothelial Cell Interaction during Inflammation
12:55

A Microphysiological System to Study Leukocyte-Endothelial Cell Interaction during Inflammation

Published on: December 9, 2021

Adhesion molecule-dependent mechanisms regulate the rate of macrophage clearance during the resolution of peritoneal

Geoffrey John Bellingan1, Ping Xu, Helen Cooksley

  • 1Centre for Respiratory Research, Rayne Institute, University College London, University Street, London WC1E 6JJ, United Kingdom. g.bellingan@ucl.ac.uk

The Journal of Experimental Medicine
|December 4, 2002
PubMed

Insights

Macrophage clearance from inflammation relies on specific adhesion molecules, not just apoptosis. Targeting these interactions, like very late antigen (VLA)-4 and VLA-5, controls macrophage exit into lymphatics for resolving inflammation.

Area of Science:

  • Immunology
  • Cell Biology
  • Physiology

Background:

  • Macrophage clearance is crucial for resolving inflammation.
  • Mechanisms of macrophage emigration from inflammatory sites are poorly understood.
  • Previous work showed macrophages leave via lymphatics, not apoptosis.

Purpose of the Study:

  • To investigate the mechanisms regulating macrophage clearance from inflammatory sites.
  • To test if adhesion interactions between macrophages and lymphatic endothelial cells control clearance rate.
  • To identify specific adhesion molecules involved in macrophage emigration.

Main Methods:

  • In vivo studies in a peritonitis model.
  • Evaluation of macrophage adherence to lymphatic mesothelium.
  • Assessment of the role of specific integrins (VLA-4, VLA-5, alpha(v), beta(2)) and Arg-Gly-Asp (RGD) sequences.
  • In vivo blockade experiments using RGD peptides and blocking antibodies.

Main Results:

  • Macrophages specifically adhere to mesothelium overlying draining lymphatics.
  • Macrophage emigration rate is regulated by the macrophage activation state.
  • Adhesion is Arg-Gly-Asp (RGD) sensitive and involves very late antigen (VLA)-4 and VLA-5 integrins.
  • Macrophage clearance into lymphatics can be blocked by RGD peptides and antibodies against VLA-4 and VLA-5.

Conclusions:

  • Macrophage emigration from inflamed tissues is a controlled process.
  • Specific adhesion molecules regulating macrophage-mesothelial interactions govern this emigration.
  • Targeting these adhesion molecules offers a novel strategy for manipulating inflammatory resolution by controlling lymphatic entry.

More Related Videos

Isolation of Murine Peritoneal Macrophages to Carry Out Gene Expression Analysis Upon Toll-like Receptors Stimulation08:21

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

Published on: April 29, 2015

Quantification of Monocyte Chemotactic Activity In Vivo and Characterization of Blood Monocyte Derived Macrophages09:57

Quantification of Monocyte Chemotactic Activity In Vivo and Characterization of Blood Monocyte Derived Macrophages

Published on: August 12, 2019

Related Concept Videos

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...
Chronic Inflammation: Introduction01:12

Chronic 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...
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...
Inflammation01:38

Inflammation

Overview
Inflammatory Response01:28

Inflammatory Response

An inflammatory response is a localized, nonspecific immune reaction that occurs when a tissue is injured. It is characterized by redness, swelling, heat, and pain, which are commonly called the cardinal signs and symptoms of inflammation. Inflammation can sometimes result in a loss of function.
Inflammation can be triggered by various stimuli, such as impact, abrasion, chemical irritation, infections, and extreme hot or cold temperatures. These can damage cells and connective tissue fibers,...
Adherens Junctions01:24

Adherens Junctions

Strong contact points between adjacent cells anchor them to each other, forming tissues. Such anchoring junctions are of two types –  adherens junctions and desmosomes. Adherens junctions are abundant in tissues such as  epithelium and endothelium, forming a continuous zone of adhesion called the adhesion belt. In other tissues, such as  heart muscle, they appear as clusters, linking the cells to produce coordinated heart muscle contraction.
Adherens Junctions are Dynamic
The endothelial cells...