Abstract
BackgroundPostoperative ileus is characterized by a transient impairment of the gastrointestinal motility after abdominal surgery. The intestinal inflammation, triggered by handling of the intestine, is the main factor responsible for the prolonged dysmotility of the gastrointestinal tract. Secondary lymphoid organs of the intestine were identified as essential components in the dissemination of inflammation to the entire gastrointestinal tract also called field effect. The involvement of the spleen, however, remains unclear.AimIn this study, we investigated whether the spleen responds to manipulation of the intestine and participates in the intestinal inflammation underlying postoperative ileus.MethodsMice underwent Laparotomy (L) or Laparotomy followed by Intestinal Manipulation (IM). Twenty-four hours later, intestinal and colonic inflammation was assessed by QPCR and measurement of the intestinal transit was performed. Analysis of homeostatic chemokines in the spleen was performed by QPCR and splenic cell populations analysed by Flow Cytometry. Blockade of the egress of cells from the spleen was performed by administration of the Sphingosine-1-phosphate receptor 1 (S1P1) agonist CYM-5442 10 h after L/IM.ResultsA significant decrease in splenic weight and cellularity was observed in IM mice 24 h post-surgery, a phenomenon associated with a decreased splenic expression level of the homeostatic chemokine CCL19. Splenic denervation restored the expression of CCL19 and partially prevented the reduction of splenocytes in IM mice. Treatment with CYM-5442 prevented the egress of splenocytes but did not ameliorate the intestinal inflammation underlying postoperative ileus.ConclusionsIntestinal manipulation results in two distinct phenomena: local intestinal inflammation and a decrease in splenic cellularity. The splenic response relies on an alteration of cell trafficking in the spleen and is partially regulated by the splenic nerve. The spleen however does not participate in the intestinal inflammation during POI.
Highlights
The vast majority of patients undergoing open abdominal surgery will develop postoperative ileus (POI)
A significant decrease in splenic weight and cellularity was observed in Intestinal Manipulation (IM) mice 24 h post-surgery, a phenomenon associated with a decreased splenic expression level of the homeostatic chemokine CCL19
Splenic denervation restored the expression of CCL19 and partially prevented the reduction of splenocytes in IM mice
Summary
The vast majority of patients undergoing open abdominal surgery will develop postoperative ileus (POI). POI is characterized by a transient impairment of the gastrointestinal tract leading to pain and discomfort for the patient as well as increased hospitalization costs [1,2,3]. Infiltrating leucocytes and activated resident macrophages secrete iNOS, Cox-2 and prostaglandins which are largely involved in the impairment of the gastrointestinal motility [6]. In POI, the paralysis of the gastrointestinal tract is not restricted to manipulated parts. Both the stomach and the colon are affected [7], a mechanism partially explained by the activation of neural inhibitory pathways by the local inflammation occurring in the small intestine [8]. Postoperative ileus is characterized by a transient impairment of the gastrointestinal motility after abdominal surgery.
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