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Updated: Aug 13, 2026

Quantitative In vitro Assay to Measure Neutrophil Adhesion to Activated Primary Human Microvascular Endothelial Cells under Static Conditions
11:22

Quantitative In vitro Assay to Measure Neutrophil Adhesion to Activated Primary Human Microvascular Endothelial Cells under Static Conditions

Published on: August 23, 2013

Neutrophil adhesion to glomerular mesangial cells: regulation by lipoxygenase-derived eicosanoids

H R Brady1, M D Denton, B M Brenner

  • 1Department of Medicine, Brigham & Women's Hospital, Harvard Medical School, Boston, MA 02115.

Advances in Experimental Medicine and Biology
|January 1, 1991
PubMed

Insights

Leukotrienes increase polymorphonuclear neutrophil (PMN) adhesion to kidney cells, with distinct mechanisms for LTB4 and LTD4. Lipoxins counteract LTD4-induced adhesion, suggesting therapeutic potential for glomerular nephritis (GN).

Area of Science:

  • Immunology
  • Nephrology
  • Cell Biology

Background:

  • Glomerular nephritis (GN) involves inflammation and cell adhesion in the kidney.
  • Leukotrienes and lipoxins are key lipid mediators in inflammatory processes.

Purpose of the Study:

  • To investigate the role of leukotrienes (LTB4, LTD4) and lipoxins in polymorphonuclear neutrophil (PMN) adhesion to glomerular mesangial cells.
  • To elucidate the specific mechanisms and cellular targets involved in leukotriene-mediated adhesion.

Main Methods:

  • Assessing PMN adhesion to mesangial cells under various conditions.
  • Investigating the roles of LTB4 and LTD4 in mediating adhesion.
  • Examining the inhibitory effects of lipoxins on leukotriene-induced adhesion.

Main Results:

  • LTB4 promoted PMN adhesion via PMN-dependent mechanisms (CD11/CD18).
  • LTD4 promoted PMN adhesion via mesangial cell-dependent mechanisms (CD11/CD18-independent).
  • Lipoxins inhibited LTD4-induced adhesion but not LTB4-induced adhesion.

Conclusions:

  • Leukotrienes play a significant role in PMN adhesion to glomerular mesangial cells through distinct pathways.
  • Lipoxins exhibit counterregulatory effects, specifically inhibiting LTD4-mediated adhesion.
  • Understanding these interactions may offer therapeutic targets for glomerular nephritis.

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