MIP-2 expression
MIP-2 is a powerful chemokine that contributes to recruitment of neutrophils [27]. MIP-2 is undetectable or present at low levels under physiological conditions, and shows transient increases under pathological conditions via TNF-α and/or interleukin-1β (IL-1β)-dependent mechanisms [14]. Thus, it would be plausible that TNF-α-mediated MIP-2 expression may provoke SE-induced neutrophil infiltrations. To confirm this hypothesis, we investigated MIP-2 expression in the PC. Consistent with our previous study [20], some MIP-2-positive astrocytes were observed in the core and periphery of the vasogenic edema lesions, but not in the non-vasogenic edema region (Figure 6B and 6C). Although the number of MIP-2 positive cells per unit area in the PC region of sTNFp55R-infused animals was significantly lower than that of the saline-infused group due to reduction of the area of vasogenic edema, there was no difference in the number of MIP-2 positive cells per unit area of vasogenic edema between sTNFp55R-infused animals and saline-infused animals (Figure 6F). Furthermore, the number of MIP-2-positive cells showed a direct proportion to the unit area of vasogenic edema with a linear coefficient of correlation of 0.682 (p < 0.05, Figure 6G). Therefore, together with reduction in neutrophil infiltration in the PC region of sTNFp55R-infused animals, our findings provide evidence that TNF-α may regulate SE-induced neutrophil infiltration at least in the PC via vasogenic edema formation and not via direct TNF-α-mediated MIP-2 expression in astrocytes.