Figure 5
Figure 5. Hematopoietic deficiency of p16INK4a exacerbates hepatic alternative macrophage activation of S mansoni–infected mice. Hepatic mRNA expression from mice transplanted with either p16+/+ or p16−/− BM which were not infected (naive) or infected with S mansoni, 9 weeks postinfection. mRNA expression of the macrophage markers F4/80 (A), CD68 (B), and CD14 (C); AAMφ markers Ym1/2 (D), Fizz1 (E), and Mgl2 (F) was quantified by QPCR and expressed as fold increase compared with their respective naive controls. Data were obtained from n = 10 naive and n = 14 infected mice per genotype. Hepatic granulomas were isolated by laser-capture microdissection and mRNA expression of the AAMφ markers Ym1/2 (G), Fizz1 (H), and Mgl2 (I) was quantified by QPCR. Statistically significant differences are indicated (t test; **P < .01 and *P < .05).

Hematopoietic deficiency of p16INK4a exacerbates hepatic alternative macrophage activation of S mansoni–infected mice. Hepatic mRNA expression from mice transplanted with either p16+/+ or p16−/− BM which were not infected (naive) or infected with S mansoni, 9 weeks postinfection. mRNA expression of the macrophage markers F4/80 (A), CD68 (B), and CD14 (C); AAMφ markers Ym1/2 (D), Fizz1 (E), and Mgl2 (F) was quantified by QPCR and expressed as fold increase compared with their respective naive controls. Data were obtained from n = 10 naive and n = 14 infected mice per genotype. Hepatic granulomas were isolated by laser-capture microdissection and mRNA expression of the AAMφ markers Ym1/2 (G), Fizz1 (H), and Mgl2 (I) was quantified by QPCR. Statistically significant differences are indicated (t test; **P < .01 and *P < .05).

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