Please use this identifier to cite or link to this item: https://repository.monashhealth.org/monashhealthjspui/handle/1/50446
Title: Removal of the endothelial surface layer via hyaluronidase does not modulate monocyte and neutrophil interactions with the glomerular endothelium.
Authors: Tan Z.;Hall P.;Costin A.;Crawford S.A.;Ramm G.;Wong C.H.Y.;Kitching A.R. ;Hickey M.J.
Monash Health Department(s): Centre for Inflammatory Diseases at Monash Health
Paediatric - Nephrology
Nephrology
Institution: (Tan, Hall, Wong, Kitching, Hickey) Centre for Inflammatory Diseases, Monash University Department of Medicine, Monash Medical Centre, Clayton, VIC, Australia
(Costin, Crawford, Ramm) Monash Ramaciotti Centre for Cryo-Electron Microscopy, Monash University, Clayton, VIC, Australia
(Kitching) Department of Nephrology, Monash Medical Centre, Clayton, VIC, Australia
(Kitching) Department of Pediatric Nephrology, Monash Medical Centre, Clayton, VIC, Australia
Issue Date: 24-Oct-2023
Copyright year: 2023
Publisher: John Wiley and Sons Inc
Place of publication: United Kingdom
Publication information: Microcirculation. 30(7) (no pagination), 2023. Article Number: e12823. Date of Publication: October 2023.
Journal: Microcirculation
Abstract: Objective: The 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. Method(s): We used multiphoton intravital microscopy to examine monocyte and neutrophil behavior in the glomerulus following ESL disruption with hyaluronidase. Result(s): Constitutive 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. Conclusion(s): These 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.Copyright © 2023 The Authors. Microcirculation published by John Wiley & Sons Ltd.
DOI: http://monash.idm.oclc.org/login?url=https://dx.doi.org/10.1111/micc.12823
PubMed URL: 37494581 [https://www.ncbi.nlm.nih.gov/pubmed/?term=37494581]
URI: https://repository.monashhealth.org/monashhealthjspui/handle/1/50446
Type: Article
Subjects: endothelium
glomerulonephritis
glomerulus
glomerulus capillary
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