-
Views
-
Cite
Cite
Kerstin Wolk, Ellen Witte, Ute Hoffmann, Wolf-Dietrich Döcke, Stefanie Endesfelder, Khusru Asadullah, Wolfram Sterry, Hans-Dieter Volk, Bianca Maria Wittig, Robert Sabat, Interleukin-22 Induces Lipopolysaccharide Binding Protein in Hepatocytes: a Potential Systemic Role of Interleukin-22 in Crohn’s Disease (B60), The Journal of Immunology, Volume 178, Issue 1_Supplement, April 2007, Pages LB12–LB13, https://doi.org/10.4049/jimmunol.178.Supp.B60
- Share Icon Share
Abstract
Crohn’s disease (CD) is characterized by intestinal infiltration of activated immune cells and distortion of the gut architecture. Here, we demonstrate that IL-22, a cytokine that is mainly produced by activated Th1 and Th17 cells, was present in high quantities in the blood of CD patients in contrast to IFN-[gamma] and IL-17. In a mouse colitis model, IL-22 mRNA expression was elevated predominantly in the inflamed intestine but also in the mesenteric lymph nodes. Simultaneously, IL-22BP showed strong a constitutive expression in the gut and lymph nodes and was decreased in the inflamed intestine. To investigate the possible role of systemic IL-22 in CD, we administered IL-22 to healthy mice and found an up-regulation of LPS binding protein blood levels reaching concentrations known to neutralize LPS. This systemic up-regulation was associated with increased hepatic but not renal or pulmonary LBP mRNA levels. IL-22 also enhanced the secretion of LBP in hepatocytes in vitro. This increase was mainly transcriptionally regulated and synergistic with that of other LBP inducers. Finally, elevated LBP levels were detected in CD patients and the mouse colitis model. These data suggest that systemic IL-22 may contribute to the prevention of systemic inflammation provoked by LPS present in the blood of CD patients through its induction of hepatic LBP.