Fig. 2

Cognitive deficits and up-regulation of CXCR5 in a mouse model of sepsis-associated encephalopathy. Adult male C57BL/6 J mice were subjected to sham surgery or CLP. a Escape latency time, b time spent in the target quadrant, and c number of crossings over the target quadrant in the Morris water maze beginning on day 14 after CLP. d Freezing time in the fear conditioning test on day 19 after CLP (n = 16 per group). e, f Western blot and densitometry of hippocampal CXCR5 on days 3, 7 and 14 after CLP (n = 4 per group). GAPDH was used as an internal control. g Double staining of CXCR5 with microglia marker Iba-1 in the hippocampus at 14 days after CLP. Arrows indicate double-stained cells. Magnification, 200 × . Scale bar, 100 μm. h Quantification of immunofluorescent cells co-staining positive for CXCR5 and Iba-1. *p < 0.05 vs. sham. CLP cecal ligation and puncture, CXCR5 C-X-C chemokine receptor type 5, GAPDH glyceraldehyde-3-phosphate dehydrogenase, Iba-1 ionized calcium binding adaptor molecule-1