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. Author manuscript; available in PMC: 2009 Nov 17.
Published in final edited form as: J Immunol. 2008 Oct 1;181(7):5035–5044. doi: 10.4049/jimmunol.181.7.5035

FIGURE 6.

FIGURE 6

ALX/FPRL-1 stimulation rescues the susceptibility of AnxA1-deficient mice to DSS-induced colitis. AnxA1 (−/−) animals demonstrated a more pronounced weight loss following DSS treatment that was restored to that of WT controls with ALX/FPRL-1 stimulation via administration of 15-epi-lipoxin A4 (denoted as L in the figure) (A; *, p-value <0.05, n = 7 mice). Conversely, WT animals did not show a reduction in weight loss due to ALX/FPRL-1 stimulation during DSS treatment. AnxA1 (−/−) mice exhibit an increased DAI over the course of DSS treatment which was restored similar to that of WT controls on days 4–7 with simultaneous ALX/FPRL-1 agonization via 15-epi-lipoxin A4 treatment (B; *, p-value <0.05, n = 7 mice). Treatment of WT animals with 15-epi-lipoxin A4 did not results in a consistent decrease in the DAI during DSS administration. Representative photomicrographs of H&E-stained histologic sections (C) and histologic scoring (D; *, p-value <0.05, n = 7 mice) demonstrate a similar degree of DSS-induced colonic injury in AnxA1-deficient animals treated with 15-epi-lipoxin A4 and WT controls (*, p-value <0.05). 15-epi-lipoxin A4 did not significantly improve the histologic injury induced by DSS in WT BALB/c mice.