1. Colonic bacterial superantigens evoke an inflammatory response and exaggerate disease in mice recovering from colitis 
Jun Lu, Arthur Wang, Sara Ansari, Robert M Hershberg, Derek M Mckay 
Gastroenterology 
Volume 125, Issue 6, Pages (December 2003)
DOI: /j.gastro

2. Figure 1
(A) Representative photomicrographs showing normal murine colonic structure and the immune cell infiltrate (∗) that occurs in response to ir. (B) SEB treatment (50 μg, +24 h). (C and D) Ki67 staining (i.e., proliferating cells) in the colonic crypt epithelia of (C) control and (D) SEB-treated mice (20 μg, +24 h). Note Ki67+ cells in the lamina propria and submucosa of SEB-treated mice only (arrows). Original magnifications were (A) 200× and (B—D) 320×.
Gastroenterology  , DOI: ( /j.gastro )

3. Figure 2
Colonic tissues show a (A and B) dose- and (C and D) time-dependent increase in (A and C) MPO and (B and D) histologic damage scores after SEB treatment (n = 4; mean ± SEM; ∗P < 0.05 compared with time-matched controls; ∗∗P < 0.05 compared with other groups).
Gastroenterology  , DOI: ( /j.gastro )

4. Figure 3
Immunocytochemical staining for the macrophage-associated F4/80 antigen (arrows). (A) Representative image of control tissue (B) shows increased numbers of F4/80+ cells in colonic tissue for mice treated with SEB (50 μg IR) 48 hours previously. (l, gut lumen; m, muscle; la, lymphoid aggregate; representative images from 3–5 mice/time-point are shown; original magnification 320×). (C) Quantification of F4/80+ colonic macrophages after SEB treatment and in tissues excised from mice 2 weeks post-DSS treatment ± 24 hours SEB challenge (n = 3–5; ∗P < 0.05 compared with time-matched controls; ∗∗P < 0.05 compared with all other groups; 1SEB at 20 μg IR).
Gastroenterology  , DOI: ( /j.gastro )

5. Figure 4
Representative photomicrographs showing CD25+ cells (stained brown, arrows) in colonic sections from (A) control mice and (B) mice recovering from DSS-induced colitis challenged with SEB (20 μg ir., +24 h). (C) Number of CD25+ cells/high-power microscopic field (n = 3–4 mice; mean ± SEM; ∗P < compared with other groups).
Gastroenterology  , DOI: ( /j.gastro )

6. Figure 5
Bar chart showing the increase in tissue MPO that occurs in Balb/c (n = 4), SCID (n = 7), and OVA Tg (n = 6) colon 24 hours after IR SEB (50 μg) treatment. Colonic damage scores on tissues from the same mice are shown in the box (mean ± SEM; ∗P < 0.05 compared with Balb/c control (con); ∗∗P < 0.05 compared with OVA Tg control and SEB-treated Balb/c mice).
Gastroenterology  , DOI: ( /j.gastro )

7. Figure 6
Bar chart showing colonic MPO levels in SEB (50 μg IR) challenged C57bl/6 or IL-10 KO mice, 72 hours post-SAg treatment (n = 3–6, ∗P < 0.05 compared with PBS-treated controls, ∗∗P < 0.05 compared with PBS-treated IL-10 KO and SEB-treated C57bl/6 control mice).
Gastroenterology  , DOI: ( /j.gastro )

8. Figure 7
Intrarectal SEB challenge exaggerates DSS colitis. (A) All DSS-treated mice had a shortened colon on autopsy and SEB (20 μg IR, +24 h) exaggerated this in animals losing greater than 10% of their body weight (n = 9–11). Similarly, colon from DSS-treated mice have (B) increased MPO activity and (C) damage scores at 14 days after DSS treatment and both indices of inflammation are increased by subsequent ir. SEB (n = 4–10; ∗P < 0.05 compared with control (Con); #P < 0.05 compared with appropriate DSS group; †P = 0.09 compared with DSS only).
Gastroenterology  , DOI: ( /j.gastro )

9. Figure 8
Midcolonic segments from mice treated with DSS (4%, 5 days) 14 days previously (i.e., those losing >10% body weight) show diminished responses to prosecretory stimuli that are exaggerated by SEB treatment (20 μg IR, +24 h) (n = 9–11; efs, electrical field stimulation; Δisc, change in short-circuit current; carbachol at 10−4 mol/L; forskolin at 10−5 mol/L; ∗P < 0.05 compared with control; #P < 0.05 compared with DSS only).
Gastroenterology  , DOI: ( /j.gastro )