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. 2016 Feb 10;30(5):1880–1891. doi: 10.1096/fj.201500047

Figure 2.

Figure 2.

O3 serum primes the microglial proinflammatory response to LPS ex vivo. Young adult male rats were exposed to FA or O3 (1 ppm) for 4 h, and serum was collected 24 h later, during the time microglia had shown activated morphology. Ex vivo serum bioactivity was assessed using cultures treated with 2% rat serum acquired from FA- or O3-exposed rats. A, B) Although O3 serum did not initiate TNFα production, O3 serum enhanced LPS-induced TNFα production in the 3 h supernatant of the HAPI rat microglial cell line (A) and rat primary microglia cultures (B). C) O3 serum caused a slight but insignificant elevation of H2O2 at 3 h after treatment and amplified LPS-induced H2O2 in primary rat microglia cultures. D) O3 serum failed to cause any microglia toxicity alone at 3 h after treatment in HAPI rat microglia cell lines and significantly reduced LPS-induced toxicity, as measured by MTT (n = 3–6). Values are reported as the mean or the mean percentage of control ± sem. *P < 0.05 vs. control; †P < 0.05, O3 serum vs. FA serum.