Affiliation:
1. Centre for Inflammatory Diseases, Monash University Department of Medicine Monash Medical Centre Clayton Victoria Australia
2. Monash Ramaciotti Centre for Cryo‐Electron Microscopy Monash University Clayton Victoria Australia
3. Department of Nephrology Monash Medical Centre Clayton Victoria Australia
4. Department of Pediatric Nephrology Monash Medical Centre Clayton Victoria Australia
Abstract
AbstractObjectiveThe endothelial surface layer (ESL), a layer of macromolecules on the surface of endothelial cells, can both impede and facilitate leukocyte recruitment. However, its role in monocyte and neutrophil recruitment in glomerular capillaries is unknown.MethodsWe used multiphoton intravital microscopy to examine monocyte and neutrophil behavior in the glomerulus following ESL disruption with hyaluronidase.ResultsConstitutive retention and migration of monocytes and neutrophils within the glomerular microvasculature was unaltered by hyaluronidase. Consistent with this, inhibition of the hyaluronan‐binding molecule CD44 also failed to modulate glomerular trafficking of these immune cells. To investigate the contribution of the ESL during acute inflammation, we induced glomerulonephritis via in situ immune complex deposition. This resulted in increases in glomerular retention of monocytes and neutrophils but did not induce marked reduction in the glomerular ESL. Furthermore, hyaluronidase treatment did not modify the prolonged retention of monocytes and neutrophils in the acutely inflamed glomerular microvasculature.ConclusionsThese observations indicate that, despite evidence that the ESL has the capacity to inhibit leukocyte‐endothelial cell interactions while also containing adhesive ligands for immune cells, neither of these functions modulate trafficking of monocytes and neutrophils in steady‐state or acutely‐inflamed glomeruli.
Funder
National Health and Medical Research Council
Subject
Physiology (medical),Cardiology and Cardiovascular Medicine,Molecular Biology,Physiology