Increased mortality and spatial memory deficits in TNF-α-deficient mice in ceftriaxone-treated experimental pneumococcal meningitis

Neurobiology of Disease

Alexander Siemer¹  Roland Nau¹  Tobias Böttcher¹  Michael Hahn²  Joachim Gerber²  Stephanie Bunkowski² 

[1] Department of Medical Statistics, Georg-August-University, Göttingen 37075, Germany;Department of Neurology, Georg-August-University, Göttingen 37075, Germany;

关键词: TNF-α;    Meningitis;    Water maze;    Neurogenesis;    S. pneumoniae;   

DOI  :  

来源: DOAJ

【 摘 要 】

Tumor necrosis factor-α (TNF-α) is critically involved in inflammation and may participate in hippocampal injury in bacterial meningitis. In a mouse model of ceftriaxone-treated pneumococcal meningitis, spatial memory and motor performance of TNF-α-deficient (n = 57) and control mice (n = 55) were investigated. After infection, therapy was initiated with ceftriaxone (100 mg/kg twice daily for 5 days). Sixty-three percent TNF-α-deficient mice and 40% control animals died within 6 days (Fisher's exact test: P = 0.02). TNF-α-deficient mice surviving pneumococcal meningitis took substantially longer to reach the hidden platform than controls, and the distance of swim tracks was longer (P = 0.02). The swim speed in both groups was similar (P = 0.59). The proliferation of dentate granule cells was lower in TNF-α-deficient than in wild-type mice (P = 0.03). In pneumococcal meningitis, TNF-α deficiency caused increased mortality and stronger deficits in spatial memory possibly due to impaired neurogenesis.

【 授权许可】

Unknown