abs: Glial IL-1 in Equine Postoperative Ileus
_{Large Animal Scientific Abstracts}

Postoperative ileus (POI) is a devastating complication of colic surgery, reporting mortality rates as high as 85.7%. POI is incited neurogenically and amplified by inflammation within the intestinal wall. However, the mechanisms linking these phases have not been fully defined. Enteric glial cells (EGC) could be significant in this link as they sense the intestinal environment and coordinate responses. Specifically, Glial IL1 signaling is known to promote POI in rodent models.
We hypothesized that mucosal IL-1β levels and EGC IL-1β sensitivity would be increased in horses that develop POI.
Small intestinal resection site margins were evaluated by IL-1β ELISA and immunofluorescence of submucosal EGC IL-1 receptor. Horses with indications of POI were defined as those who refluxed greater than 2 liters postoperatively.
Mucosal IL-1β trends towards increased levels within the proximal resection site of horses that develop POI compared to those who do not (p=0.1439) in preliminary analyses. In addition, immunofluorescent signal intensity of submucosal EGC IL-1 receptor is increased in horses that developed POI (p=0.0441).
Horses that develop POI may have increased levels of mucosal IL-1β and EGC IL-1β sensitivity. Ongoing studies will increase statistical power, providing insight into the role of EGC IL-1 signaling in equine POI.
Current results are limited by sample size of preserved resection sites.
Cytokines produced by IL-1β-stimulated EGC can alter intestinal barrier function. Our long-term goal is to determine the mechanism through which stimulated EGC may directly and rapidly increase intestinal barrier permeability to propagate inflammation in POI as a potential therapeutic target.