Literature DB >> 33910203

Characterization of a Rat Model of Myeloperoxidase-Anti-Neutrophil Cytoplasmic Antibody-Associated Crescentic Glomerulonephritis.

Domenico Cerullo1, Daniela Rottoli1, Daniela Corna1, Paola Rizzo1, Mauro Abbate1, Daniela Macconi1, Ariela Benigni1, Giuseppe Remuzzi1, Carlamaria Zoja1.   

Abstract

BACKGROUND/AIM: Necrotizing crescentic glomerulonephritis (GN) associated with anti-neutrophil cytoplasmic antibodies (ANCA) against myeloperoxidase (MPO) is a devastating disease that quickly progresses to kidney failure. Current therapies are broadly immunosuppressive and associated with adverse effects. We wanted to set up a model that could be suitable for testing narrowly targeted therapies.
METHODS: The model was constructed in male Wistar Kyoto rats through injections of human MPO (hMPO) and pertussis toxin, followed by a sub-nephritogenic dose of sheep anti-rat glomerular basement membrane (GBM) serum to boost the disease. Rats were monitored for 35 days. Rats given hMPO alone, saline, or human serum albumin with or without anti-GBM serum were also studied.
RESULTS: Rats receiving hMPO developed circulating anti-hMPO and anti-rat MPO antibodies. Challenging hMPO-immunized rats with the anti-GBM serum led to more glomerular neutrophil infiltration and MPO release, and severe haematuria, heavy proteinuria, and higher blood urea nitrogen than hMPO alone. Pauci-immune GN developed with crescents, affecting 25% of glomeruli. The majority of crescents were fibrocellular. Necrotizing lesions and Bowman capsule ruptures were detected. Cells double positive for claudin-1 (a marker of parietal epithelial cells [PECs]) and neural cell adhesion molecule (NCAM; progenitor PECs) were present in crescents. Double staining for NCAM and Ki-67 established proliferative status of progenitor PECs. Podocyte damage was associated with endothelial and GBM changes by electron microscopy. Monocyte/macrophages and CD4+ and CD8+ T cells accumulated in glomeruli and the surrounding area and in the tubulointerstitium. Lung haemorrhage also manifested.
CONCLUSION: This model reflects histological lesions of human ANCA-associated rapidly progressive GN and may be useful for investigating new therapies.
© 2021 S. Karger AG, Basel.

Entities:  

Keywords:  Anti-myeloperoxidase antibodies; Glomerular crescents; Inflammatory cells; Parietal epithelial cells; Podocytes; Wistar Kyoto rats

Mesh:

Substances:

Year:  2021        PMID: 33910203     DOI: 10.1159/000515421

Source DB:  PubMed          Journal:  Nephron        ISSN: 1660-8151            Impact factor:   2.847


  3 in total

Review 1.  Molecular Mechanisms of Kidney Injury and Repair.

Authors:  Sandra Rayego-Mateos; Laura Marquez-Expósito; Raquel Rodrigues-Diez; Ana B Sanz; Roser Guiteras; Nuria Doladé; Irene Rubio-Soto; Anna Manonelles; Sergi Codina; Alberto Ortiz; Josep M Cruzado; Marta Ruiz-Ortega; Anna Sola
Journal:  Int J Mol Sci       Date:  2022-01-28       Impact factor: 5.923

Review 2.  Emerging Technologies to Study the Glomerular Filtration Barrier.

Authors:  Emma Gong; Laura Perin; Stefano Da Sacco; Sargis Sedrakyan
Journal:  Front Med (Lausanne)       Date:  2021-11-25

3.  Add-On Cyclic Angiotensin-(1-7) with Cyclophosphamide Arrests Progressive Kidney Disease in Rats with ANCA Associated Glomerulonephritis.

Authors:  Domenico Cerullo; Daniela Rottoli; Daniela Corna; Mauro Abbate; Ariela Benigni; Giuseppe Remuzzi; Carlamaria Zoja
Journal:  Cells       Date:  2022-08-05       Impact factor: 7.666

  3 in total

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