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. 2013 Jan;182(1):180–191. doi: 10.1016/j.ajpath.2012.09.010

Figure 5.

Figure 5

KC progenitor development is independent of gut bacteria. A: Relative expression of monocyte colony-stimulating factor (csf1) (analysis of variance, P = 0.50) and granulocyte-monocyte colony-stimulating factor (csf2) (analysis of variance, P = 0.84) mRNA revealed no significant differences among the mouse groups. Black line represents mean expression, with Hrpt1 used as an internal control [n = 4 in the CL group (white circle), n = 4 in the AVMN group (gray circle), and n = 4 in the GF group (black circle)]. B: KC progenitors in the livers of CL, GF, and AVMN mice (analysis of variance, P = 0.663) revealed no difference among groups. Representative of three independent experiments (n = 3 to 6 in the CL group, n = 3 to 5 in the GF group, and n = 3 to 4 in the AVMN group). C: KC progenitors in systemic circulation (percentage of PBMCs) in CL and GF mice were not significantly different; CD11b+Ly6C+ PBMCs (lined gate) (P = 0.27). Circulating CD11b-Ly6C+ PBMC counts (arrow) were significantly lower in GF mice (n = 6 in the CL group; n = 6 in the GF group). D: KC progenitors in bone marrow (percentage of MDCs) in CL (n = 6) and GF (n = 6) mice were not significantly different (P = 0.37); CD11b+Ly6C+ BMDCs (lined gate). CL, GF, and AVMN mice were used. ***P < 0.01.