IL-22BP Modulates Injury in Acute Pancreatitis but Delays Tissue Recovery in Chronic Pancreatitis.

ABSTRACT:

Background & aims

In acute pancreatitis, interleukin (IL)-22 signaling is increased, whereas overall expression of the cytokine paradoxically drops, suggesting an additional level of control. Here, we investigate the regulation of IL-22 signaling by its soluble neutralizing receptor interleukin-22 binding protein (IL-22BP) in the context of both acute and chronic pancreatitis.

Methods

Cerulein was used to induce acute and chronic pancreatitis in both wild-type mice and IL-22BP knockout mice. Histology, multiplex immunofluorescence and flow cytometry were performed to compare differences in tissue injury, recovery, fibrosis, and inflammation at various times of recovery.

Results

Loss of IL-22BP resulted in increased canonical IL-22 signaling and the expression of the a

SUBMITTER: Sun L 

PROVIDER: S-EPMC12173607 | biostudies-literature | 2025

REPOSITORIES: biostudies-literature