1. Volume 118, Issue 6, Pages 1106-1116 (June 2000)
Lipopolysaccharide is radioprotective in the mouse intestine through a prostaglandin- mediated mechanism 
Terrence Riehl, Steven Cohn, Teresa Tessner, Suzanne Schloemann, William F. Stenson 
Gastroenterology 
Volume 118, Issue 6, Pages (June 2000)
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2. Fig. 1
Diagram of a small intestinal crypt showing location of stem cells and proliferative (transit) cells.
Gastroenterology  , DOI: ( /S (00) )
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3. Fig. 2
LPS treatment before radiation increases crypt survival in a PGE2-dependent manner. FVB/N mice received vehicle (control), indomethacin (1.5 mg/kg every 8 hours), NS-398 (1 mg/kg every 8 hours), LPS alone (0.5 mg/kg), LPS plus indomethacin, or LPS plus NS-398 beginning 14 hours before irradiation (14 Gy). Mice were killed 3.5 days after radiation, and the number of surviving crypts per cross section was determined. Data are the mean ± SEM for 9 animals. *P < compared with control; **P < compared with LPS alone.
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4. Fig. 3
LPS pretreatment as little as 2 hours before radiation increases crypt survival. FVB/N mice received LPS (0.5 mg/kg) or vehicle (control) at the indicated time before irradiation (14 Gy). The number of surviving crypts per cross section was determined 3.5 days after radiation. Data are the mean ± SEM for 3 animals. *P < 0.01 compared with control.
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5. Fig. 4
LPS treatment increases PGE2 production in the mouse small intestine. FVB/N mice were treated with vehicle (control), indomethacin (1.5 mg/kg every 8 hours), NS-398 (1 mg/kg every 8 hours), LPS (0.5 mg/kg), LPS plus indomethacin, or LPS plus NS-398. After 14 hours, mice were killed and the PGE2 content of intestine was determined by enzyme immunoassay. Data are the mean ± SEM of 3-15 animals. *P < compared with control; **P < compared with LPS alone.
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6. Fig. 5
Time course for LPS-induced PGE2 synthesis. FVB/N mice received LPS (0.5 mg/kg) at the time indicated before death. Control mice received no LPS. The mice were killed, and the PGE2 content of small intestine determined by enzyme immunoassay. Data are the mean ± SEM for 3 animals. *P < compared with control.
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7. Fig. 6
(A) LPS increases PGE2 synthesis in a dose-dependent manner. FVB/N mice were given the indicated doses of LPS intraperitoneally 14 hours before death. After death, the small intestine was assayed for PGE2 by enzyme immunoassay as described in Materials and Methods. Data are the mean ± SEM for 3 animals. *P < 0.01 compared with control. (B) Body temperature response of FVB/N mice injected with LPS (♦, 0.15 mg/kg; ■, 0.5 mg/kg; ▴, 1.5 mg/kg) or pyrogen-free PBS (●). Data are the mean ± SEM for 3 animals.
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8. Fig. 6
(A) LPS increases PGE2 synthesis in a dose-dependent manner. FVB/N mice were given the indicated doses of LPS intraperitoneally 14 hours before death. After death, the small intestine was assayed for PGE2 by enzyme immunoassay as described in Materials and Methods. Data are the mean ± SEM for 3 animals. *P < 0.01 compared with control. (B) Body temperature response of FVB/N mice injected with LPS (♦, 0.15 mg/kg; ■, 0.5 mg/kg; ▴, 1.5 mg/kg) or pyrogen-free PBS (●). Data are the mean ± SEM for 3 animals.
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9. Fig. 7
Detection of (A) COX-1 and (B) COX-2 in epithelial cells isolated from small intestines of control and LPS-treated mice by Western blotting. LPS (0.5 mg/kg) was given to FVB/N mice 1 hour before death, intestinal tissue was harvested, epithelial cells were isolated, and the expression of COX-1 and COX-2 proteins in the epithelial lysates was determined by Western blotting using anti-mouse antibodies. A mouse macrophage cell line (RAW cells) was used as a negative control. RAW cells stimulated with LPS (LPS-induced mouse macrophage) were used as a positive control.
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10. Fig. 8
Immunohistochemical localization of COX-1 and COX-2 in the proximal jejunum of control and LPS-treated mice. The cellular localization of COX-1 in epithelial cells of crypts and lower regions of the villi was the same in (A) control and (B) LPS-treated mice. (C) Control mice showed COX-2 staining of a few villous epithelial nuclei. (D) One hour after LPS (0.5 mg/kg intraperitoneally) treatment, there was COX-2 staining of villous epithelial cells. Arrows in A, B, and D indicate the crypt-villus junction. Higher power views of the intestines from LPS-treated mice showed staining of villous epithelial cells with sparing of the villus tip. There is no staining of intraepithelial lymphocytes (arrow in E). There is staining of subepithelial fibroblasts (arrows in F) but no staining of crypt epithelial cells. (Original magnification: A, B, and D, 400×; C, 200×; E and F, 1000×).
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11. Fig. 9
COX-2 expression is required for LPS-induced enhancement of crypt survival. Bl6/129 F2 COX-1 knockout mice (COX-1 K.O.), COX-2 knockout mice (COX-2 K.O.), or their wild-type (W.T.) littermates received vehicle or LPS (0.5 mg/kg) 14 hours before 14-Gy irradiation. The number of surviving crypts per cross section was determined 3.5 days after irradiation. Data are the mean ± SEM of 3 animals. **P < compared with wild-type irradiated control; *P < compared with COX-1 knockout irradiated control.
Gastroenterology  , DOI: ( /S (00) )
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