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Fig. 5 | Journal of Neuroinflammation

Fig. 5

From: Type I IFN signaling limits hemorrhage-like disease after infection with Japanese encephalitis virus through modulating a prerequisite infection of CD11b+Ly-6C+ monocytes

Fig. 5

IFN-I signal-dependent induction of a “cytokine storm” following JEV inoculation. a and b Highly enhanced expression of inflammatory cytokines and chemokines in the peripheral and CNS tissues of IFN-I signal-incompetent mice. The mRNA levels of inflammatory cytokines and chemokines were determined by real-time qRT-PCR using total RNA extracted from popliteal LNs (pLNs), spleen, mesenteric LNs (mLNs), iliac LN (iLN), liver, spinal cord (SC), and brain at the indicated days after JEV infection (5 × 106 ffu/mouse) via the footpad route. c Serum levels of IL-6 and TNF-a. d Enhanced production of CC chemokines in sera of IFN-I signal-incompetent mice. Serum levels of IL-6 and TNF-α were determined by cytokine ELISA using sera collected from IFN-I signal-competent and -incompetent mice. The levels of CC chemokines including CCL2, CCL3, CCL4, CCL5, and CCL7 in sera were determined by cytokine bead array. Data in the graphs denote the mean ± SEM. Results are representative of one out of at least two individual experiments with four to five mice per group. Statistical significance *p < 0.05; **p < 0.01; ***p < 0.001 was assessed by an unpaired two-tailed Student’s t test

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