Skip to main content
. Author manuscript; available in PMC: 2012 Dec 17.
Published in final edited form as: Immunity. 2012 Aug 16;37(2):326–338. doi: 10.1016/j.immuni.2012.05.024

Figure 7. Involvement of type I IFN signaling in the development of pancreatitis.

Figure 7

(A, B, C) IFNαβ receptor-intact (Ifnar1+/+) or -deficient (Ifnar1−/−) mice were subjected to induction of FK156/low-dose cerulein pancreatitis as indicated in Figure 2. (A, B) Serum levels of amylase, MCP-1, IL-6, IFN-β, and IP-10 at 6 hours after systemic challenge with FK156 and pathology scores of the pancreatic tissue at 24 hours after systemic challenge with FK156. Results are expressed as means ±SD. *p < 0.01, as compared with Ifnar1+/+ mice. (C) Whole cell extracts were prepared from pancreatic tissue of mice at 5 hours after systemic challenge with FK156 and subjected to immunoblotting to determine expression of phospho-STAT3, STAT3, phospho-STAT1, STAT1, phospho-IκBα, IκBα, andactin. The results shown are representative one of two experiments. (D, E) C57BL6 mice were subjected to induction of FK156-low-dose cerulein pancreatitis; blood and peritoneal lavage fluid were collected 8 hours after the injection. (D) Percentage and number (parentheses) of mice that were positive for bacterial culture in the blood and peritoneal lavage fluids. (E) Bacterial loads in the blood determined by counting colonies in columbia agar, trypticase soy agar, and chocolate agar plates. Results are expressed as means ±SD and summary of three independent experiments.