1. Adrenal cortical activation in murine colitis
Denis Franchimont, Gerd Bouma, Jerome Galon, Gernot W. Wolkersdörfer, Andrea Haidan, George P. Chrousos, Stefan R. Bornstein 
Gastroenterology 
Volume 119, Issue 6, Pages (December 2000)
DOI: /gast
Copyright © 2000 American Gastroenterological Association Terms and Conditions

2. Fig. 1
TNBS induces colitis in SJL/J but not in C57Bl/6 mice. Weight curves (data are expressed as mean ± SD) and colon specimens after intrarectal administration of TNBS in (A) resistant C57Bl/6 mice and (B) susceptible SJL/J mice (n = 5). □, Placebo-treated mice; ●, TNBS-injected mice. TNBS-induced colitis in SJL/J mice leads to statistically significant, ongoing weight loss (P < 0.05 compared with controls), whereas C57Bl/6 mice quickly recover from the TNBS enema. One representative of 5 experiments is shown.
Gastroenterology  , DOI: ( /gast )
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3. Fig. 2
Increased corticosterone secretion during colitis. (A) Plasma corticosterone levels in TNBS colitis–susceptible SJL/J (□) and resistant C57Bl/6 (▴) mice at different time points. Data on the x-axis represent different time points (in days) after the induction of colitis. A rapid and strong increase in corticosterone levels is observed in SJL/J mice developing colitis (P < ). In the resistant strain, a small, stress-related increase in plasma corticosterone is seen (P < 0.01). The magnitude of the increase in plasma corticosterone in SJL/J mice is significantly higher than in C57Bl/6 mice (P < ). (B) Plasma ACTH levels in susceptible SJL/J (□) and resistant C57Bl/6 (▴) mice. Data are means ± SEM. The experiment is representative of 3 different independent experiments (n = 5). *P < 0.01; **P <
Gastroenterology  , DOI: ( /gast )
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4. Fig. 3
Morphologic change of adrenals during colitis. Light microscopy of toluidine blue–stained adrenal slides from (A) placebo-treated and (B) TNBS colitis SJL/J mice. The adrenal glands from the mice with colitis showed dramatic signs of stimulation with hyperplasia of the adrenocortical cells and a marked hypervascularization (arrows) of the cortex.
Gastroenterology  , DOI: ( /gast )
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5. Fig. 4
Ultrastructural changes of the adrenocortical cells. Electron microscopy of adrenocortical cells from (A) placebo-treated and (B) TNBS colitis SJL/J mice. Adrenocortical steroidogenic cells from colitis mice showed signs of marked stimulation with increased mitochondria (Mit), decreased liposomes (Lip), dilated smooth endoplasmic reticulum, and frequent formation of filopodia. Nuc, nucleus; Lym, lymphocyte; E, erythrocyte. Bar = 2 μm.
Gastroenterology  , DOI: ( /gast )
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6. Fig. 5
Interaction of intra-adrenal lymphocytes (Lym) with adrenocortical cells during colitis. Lymphocytes were found in direct contact with adrenocortical cells in SJL/J mice with colitis; the adrenocortical cells extended filopodia to the cell membrane of the lymphocytes. Bar = 0.5 μm. B is a higher-magnification of the insert in A. Mit, mitochondrium; TZ, thrombocyte; E, erythrocyte; Ser, smooth endoplasmic reticulum; Rer, rough endoplasmic reticulum. Bar = 0.2 μm.
Gastroenterology  , DOI: ( /gast )
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7. Fig. 6
Increased intra-adrenal and plasma IL-6 may stimulate adrenocortical cells in mice with colitis. (A) Increased intra-adrenal IL-6 and IL-1β expression in colitis. Adrenals from both control, susceptible SJL/J, and resistant C57BL/6 mice were removed and sonicated in lysis buffer. RNAs were then extracted, and cytokine expression was evaluated by RNase protection. TNF-α, IL-1β, and IL-6 expression in placebo-treated SJL/J and C57BL/6 mice (lanes 1 and 3) and in TNBS-treated SJL/J and C57BL/6 mice (lanes 2 and 4). (B) Increased plasma IL-6 during colitis. Plasma IL-6 level in control and TNBS-treated SJL/J mice (lanes 1 and 2) and in control and TNBS-treated C57BL/6 mice (lanes 3 and 4). Results are representative of 3 different independent experiments (n = 5). (C) Cytokine receptor expression in the adrenal glands. Control lane without adrenal RNAs (lane 1). IL-1RI/RII, IL-6Rα, gp130, and TNF-αRp75/p55 expression in normal adrenal glands (lane 2). (D) IL-6Rα and gp130 were equally expressed in the adrenal glands of placebo-treated (lane 1) and TNBS-treated (lane 2) SJL/J mice. (E) Direct IL-6 stimulation of corticosterone secretion by adrenocortical cells. Corticosterone production by adrenocortical Y-1 cells untreated (lane 1) or treated either with ACTH (lane 2) or with increasing doses of IL-6 (lanes 3–5). These data are from 1 experiment representative of 3 different independent experiments.
Gastroenterology  , DOI: ( /gast )
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8. Fig. 7
Effect of anti–IL-6 treatment on plasma corticosterone levels and adrenal morphology. Light microscopy of toluidine blue–stained adrenal slides from (A) placebo-treated and (B) anti–IL-6–treated (same magnification) SJL/J mice with TNBS colitis. The signs of stimulation with hyperplasia of the adrenocortical cells and hypervascularization of the cortex were markedly reduced by a single injection of 1 mg of monoclonal antibody to IL-6. (C) Anti–IL-6 treatment led to a 22% reduction in plasma corticosterone levels. *P < 0.05; n = 10.
Gastroenterology  , DOI: ( /gast )
Copyright © 2000 American Gastroenterological Association Terms and Conditions