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(Reference retrieved automatically from Web of Science through information on FAPESP grant and its corresponding number as mentioned in the publication by the authors.)

Acute kidney injury in a mouse model of meningococcal disease

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Author(s):
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Kolbe, Karin R. [1] ; Sanches, Talita R. [1] ; Fanelli, Camilla [1] ; Garnica, Margoth R. [1] ; de Castro, Leticia Urbano [1] ; Gooch, Karen [2] ; Thomas, Stephen [2] ; Taylor, Stephen [2] ; Gorringe, Andrew [2] ; Noronha, Irene de L. [1] ; Andrade, Lucia [1]
Total Authors: 11
Affiliation:
[1] Univ Sao Paulo, Div Nephrol, Sch Med, Av Dr Arnaldo 455, Room 3310, BR-01246903 Sao Paulo - Brazil
[2] Publ Hlth England, Salisbury, Wilts - England
Total Affiliations: 2
Document type: Journal article
Source: INTERNATIONAL JOURNAL OF IMMUNOPATHOLOGY AND PHARMACOLOGY; v. 35, DEC 20 2021.
Web of Science Citations: 0
Abstract

Introduction Meningococcal disease is associated with high mortality. When acute kidney injury (AKI) occurs in patients with severe meningococcal disease, it is typically attributable to sepsis, although meningococcal disease and lipopolysaccharide release are rarely investigated. Therefore, we evaluated renal tissue in a mouse model of meningococcal disease. Methods Female BALB/c mice were induced to AKI by meningococcal challenge. Markers of renal function were evaluated in infected and control mice. Results In the infected mice, serum concentrations of tumor necrosis factor alpha, interferon gamma, interleukins (IL-1 beta, IL-2, IL-4, IL-5, IL-6, IL-10, and IL-12), and granulocyte-macrophage colony-stimulating factor were elevated, as was renal interstitial infiltration with lymphocytes and neutrophils (p < 0.01 for the latter). Histological analysis showed meningococcal microcolonies in the renal interstitium, without acute tubular necrosis. Infected mice also showed elevated renal expression of toll-like receptor 2, toll-like receptor 4, and Tamm-Horsfall protein. The expression of factors in the intrinsic pathway of apoptosis was equal to or lower than that observed in the control mice. Urinary sodium and potassium were also lower in infected mice, probably due to a tubular defect. Conclusion Our findings corroborate those of other studies of AKI in sepsis. To our knowledge, this is the first time that meningococci have been identified in renal interstitium and that the resulting apoptosis and inflammation have been evaluated. However, additional studies are needed in order to elucidate the mechanisms involved. (AU)

FAPESP's process: 10/19012-0 - Evaluation of hematopoietic stem cell treatment in dogs with chronic renal failure
Grantee:Lucia da Conceição Andrade
Support Opportunities: Research Projects - Thematic Grants