administration did not alter severity of chronic colitis. A. Cumulative disease activity index (DAI) score defined as body weight change, hemocult blood, and stool consistency. Score was measured three times per week. B. Histological score of colitis. There are no statistical differences in severity of colitis between the mice that received different PGE 2 treatment doses and timing (n = 13 WT; n = 7 PBS group; n = 8 high dose PGE 2 200 μg group; and n = 6 low dose PGE 2 100 μg group; n = 5 PGE 2 200 μg during DSS treatment; NS: no significance). C. Mucosal 15d-PGJ2 (left panel) and endogenous PGE 2 (right panel) synthesis during acute colitis. Mice received AOM and after 14 days, DSS was given for 7 days. PGE 2 treatment (200 μg/day) significantly up-regulates mucosal 15d-PGJ2 synthesis but not endogenous PGE 2 in TLR4-/- mice at day 7 of DSS colitis (n = 5 each). WT mice received only AOM and DSS. Data are expressed as mean (± SD) (*P < 0.05). D. 15d-PGJ2 (left panel) and endogenous PGE 2 (right panel) synthesis at 14 day recovery from DSS colitis. Mice were examined at the end of the first cycle of AOM-DSS treatment. There is no difference of 15d-PGJ2 synthesis between TLR4-/- mice that received PGE 2 (200 μg/day) during DSS colitis and during the recovery from DSS colitis (n = 5 each, P = 0.441). By contrast, significant increase of endogenous PGE 2 is shown in the mice that received PGE 2 during the recovery phase. This increase of endogenous PGE 2 is not seen in the mice that received PGE 2 during DSS treatment (acute phase). Data are expressed as mean (± SD).