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. 2022 Jun 11;23(12):6540. doi: 10.3390/ijms23126540

Figure 2.

Figure 2

E.-coli-K1-induced neutrophil recruitment requires TNF-α, microglia-derived pro-inflammatory cytokine. (a) Real-time quantitative PCR analysis of TNF-α and IL-1β mRNA levels in uninfected mouse brains and those infected with E. coli K1 for 4, 12, 24, and 48 h (n = 6 mice per group). (b) ELISA analysis of TNF-α and IL-1β protein levels in E.-coli-K1-infected brain 4, 12, 24, and 48 h post-infection (n = 6 mice per group). (c) Neutrophil counts in the brains of wild-type (WT) mice and TNF-α-deficient mice infected with E. coli K1 for 24 h (n = 6 mice per group). (d–g) Mice were pretreated with PLX3397 or vehicle (negative control) for 2 weeks and then infected with E. coli K1 for 24 h. Thereafter, the microglia count ((d), n = 4 mice per group), TNF-α protein levels ((e), n = 6 mice per group), neutrophil counts ((f), n = 4 mice per group), and bacterial loads ((g), n = 6 mice per group) in the mouse brain were analyzed. (h) Primary microglia and astrocytes were stimulated with E. coli K1 for 0.5, 1, 2 h, and the production of TNF-α was assessed using ELISA. Data are presented as mean ± SD, n = 3 independent experiments. p values were determined using Student’s t-test (a,h) or Mann–Whitney U test (c–g). * p < 0.05; ** p < 0.01; *** p < 0.001.