Related Experiment Video
Updated: Jul 17, 2026
Normothermic Cardiac Arrest and Cardiopulmonary Resuscitation: A Mouse Model of Ischemia-Reperfusion Injury
Published on: August 30, 2011
Acute kidney injury in a mouse model of meningococcal disease
Karin R Kolbe1, Talita R Sanches1, Camilla Fanelli1
1Division of Nephrology, 28133University of São Paulo School of Medicine, São Paulo, Brazil.
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-1β, 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.
Insights
Severe meningococcal disease can cause acute kidney injury (AKI). This study found meningococci in renal tissue, leading to inflammation and tubular defects, but not acute tubular necrosis in a mouse model.
Area of Science:
- Nephrology
- Infectious Diseases
- Immunology
Background:
- Meningococcal disease carries a high mortality rate.
- Acute kidney injury (AKI) in severe meningococcal disease is often attributed to sepsis.
- The direct role of meningococcal infection and lipopolysaccharide in AKI requires further investigation.
Purpose of the Study:
- To evaluate renal tissue in a mouse model of meningococcal disease.
- To investigate the mechanisms of AKI in meningococcal infections.
Main Methods:
- Female BALB/c mice were challenged with meningococci to induce AKI.
- Renal function markers, inflammatory cytokine levels, and renal tissue histology were analyzed.
- Expression of toll-like receptors and apoptosis-related factors was assessed.
Main Results:
- Elevated serum levels of multiple pro-inflammatory cytokines (TNF-α, IFN-γ, ILs, GM-CSF) were observed in infected mice.
- Histological analysis revealed meningococcal microcolonies in the renal interstitium with significant infiltration of lymphocytes and neutrophils.
- Infected mice showed increased renal expression of TLR2, TLR4, and Tamm-Horsfall protein, with no evidence of acute tubular necrosis but a probable tubular defect affecting sodium and potassium excretion.
Conclusions:
- This study provides the first evidence of meningococci within the renal interstitium and evaluates the associated inflammation and apoptosis.
- Findings support the link between meningococcal infection and AKI, highlighting inflammatory responses and tubular dysfunction.
- Further research is necessary to fully elucidate the complex mechanisms underlying AKI in meningococcal disease.
