Pancreas-specific RelA/p65 truncation increases susceptibility of acini to inflammation-associated cell death following cerulein pancreatitis
J. Clin. Invest. Hana Algül, et al. 117:1490 doi:10.1172/JCI29882 [Go to this article.]

Figure 5
Increased infiltration and TNF-α production in the pancreata of rela^Δ/Δ mice. (A) Mononuclear infiltration into the pancreas was visualized by immunohistochemical detection of granulocytes using a Gr-1 antibody. bv, blood vessel; ed, edema. Original magnification, ×100. (B) Pancreatic MPO activity was measured in the pancreata of rela^flox/flox and rela^Δ/Δ mice. (C) Infiltrating cells produced and released TNF-α. Pancreata from cerulein-treated rela^flox/flox and rela^Δ/Δ mice were stained using antibody to TNF-α. Arrowheads indicate TNF-α accumulation; asterisks indicate acinar cells. Original magnification, ×200. (D) TNF-α levels were measured by ELISA in pancreatic cell lysates from rela^flox/flox and rela^Δ/Δ mice following 8 hourly injections of 50 μg/kg cerulein. ND, not detected. Values are mean ± SD for independent animals (n = 4). *P < 0.05 versus rela^flox/flox.