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COX-2 dependent inflammation increases spinal Fos expression during rodent postoperative ileus

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COX-2 dependent inflammation increases spinal Fos expression during rodent postoperative ileus

Auteurs : C. Kreiss [États-Unis] ; L A Birder [États-Unis] ; S. Kiss [États-Unis] ; M M Vanbibber [États-Unis] ; A J Bauer [États-Unis]

Source :

Gut [ 0017-5749 ] ; 2003-04.

RBID : ISTEX:FBA9BF72D884D52B4764A1E0D56D38D5E80B7DAE

English descriptors

Abstract

Background and aims: Cyclooxygenase 2 (COX-2) and prostaglandins (PGs) participate in the pathogenesis of inflammatory postoperative ileus. We sought to determine whether the emerging neuronal modulator COX-2 plays a significant role in primary afferent activation during postoperative ileus using spinal Fos expression as a marker. Methods: Rats, and COX-2+/+ and COX-2−/− mice underwent simple intestinal manipulation. The effect of intestinal manipulation on Fos immunoreactivity (IR) in the L5-S1 spinal cord, in situ circumference, and postoperative leucocytic infiltrate of the intestinal muscularis was measured. Postoperative PGE2 production was measured in peritoneal lavage fluid. The dependence of these parameters on COX-2 was studied in pharmacological (DFU, Merck- Frosst, selective COX-2 inhibitor) and genetic (COX-2−/− mice) models. Results: Postoperative Fos IR increased 3.7-fold in rats and 2.2-fold in mice. Both muscularis leucocytic infiltrate and the circumference of the muscularis increased significantly in rats and COX-2+/+ mice postoperatively, indicating dilating ileus. Surgical manipulation markedly increased PGE2 levels in the peritoneal cavity. DFU pretreatment and the genetic absence of COX-2−/− prevented dilating ileus, and leucocytic infiltrate was diminished by 40% with DFU and by 54% in COX-2−/− mice. DFU reversed postsurgical intra- abdominal PGE2 levels to normal. Fos IR after intestinal manipulation was attenuated by approximately 50% in DFU treated rats and in COX-2−/− mice. Conclusions: Postoperatively, small bowel manipulation causes a significant and prolonged increase in spinal Fos expression, suggesting prolonged primary afferent activation. COX-2 plays a key role in this response. This activation of primary afferents may subsequently initiate inhibitory motor reflexes to the gut, contributing to postoperative ileus.

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https://api.istex.fr/document/FBA9BF72D884D52B4764A1E0D56D38D5E80B7DAE/fulltext/pdf

DOI: 10.1136/gut.52.4.527

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<author><name sortKey="Kiss, S" sort="Kiss, S" uniqKey="Kiss S" first="S" last="Kiss">S. Kiss</name>
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<profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Afferent</term>
<term>Birder</term>
<term>Bowel</term>
<term>COX-2</term>
<term>COX-2, cyclooxygenase 2</term>
<term>Circumference</term>
<term>Control mice</term>
<term>Control rats</term>
<term>Cord</term>
<term>Cyclooxygenase</term>
<term>DCM, dorsal commissure</term>
<term>Dorsal</term>
<term>Dorsal commissure</term>
<term>Fos expression</term>
<term>Gastroenterology</term>
<term>Gastrointestinal transit</term>
<term>IR, immunoreactivity</term>
<term>Ileus</term>
<term>Important role</term>
<term>Inducible nitric oxide synthase</term>
<term>Inflammation</term>
<term>Inflammation increases</term>
<term>Inhibitory motor</term>
<term>Intestinal</term>
<term>Intestinal manipulation</term>
<term>Intestinal motility</term>
<term>Intestinal muscularis</term>
<term>Intestine</term>
<term>Jejunal</term>
<term>KO, knockout</term>
<term>Kalff</term>
<term>Kreiss</term>
<term>LDH, lateral dorsal horn</term>
<term>Lamina</term>
<term>Laparotomy</term>
<term>Lateral dorsal horn</term>
<term>Lateral laminae</term>
<term>Leucocyte</term>
<term>Leucocytic</term>
<term>MDH, medial dorsal horn</term>
<term>MPO, myeloperoxidase</term>
<term>Manipulation</term>
<term>Medial dorsal horn</term>
<term>Motility</term>
<term>Muscularis</term>
<term>Muscularis leucocytic</term>
<term>Neuron</term>
<term>Neurones</term>
<term>PG, prostaglandin</term>
<term>Pathway</term>
<term>Peritoneal</term>
<term>Pge2</term>
<term>Pharmacological</term>
<term>Pharmacological blockade</term>
<term>Physiol</term>
<term>Positive cells</term>
<term>Postoperative</term>
<term>Postoperative ileus</term>
<term>Postoperative leucocytic</term>
<term>Postoperatively</term>
<term>Postsurgical</term>
<term>Present study</term>
<term>Primary afferents</term>
<term>Prostaglandin</term>
<term>Rat</term>
<term>Regional distribution</term>
<term>SPN, sacral parasympathetic nucleus</term>
<term>Selective inhibition</term>
<term>Selective inhibitor</term>
<term>Significant increase</term>
<term>Small bowel</term>
<term>Small intestine</term>
<term>Spinal</term>
<term>Spinal cord</term>
<term>Spinal cord segments</term>
<term>Spinal neurons</term>
<term>Surgical</term>
<term>Surgical manipulation</term>
<term>Synthase</term>
<term>Time point</term>
<term>Vehicle control</term>
<term>Visceral afferents</term>
<term>iNOS, inducible nitric oxide synthase</term>
<term>postoperative ileus</term>
</keywords>
<keywords scheme="Teeft" xml:lang="en"><term>Afferent</term>
<term>Birder</term>
<term>Bowel</term>
<term>Circumference</term>
<term>Control mice</term>
<term>Control rats</term>
<term>Cord</term>
<term>Cyclooxygenase</term>
<term>Dorsal</term>
<term>Dorsal commissure</term>
<term>Gastroenterology</term>
<term>Gastrointestinal transit</term>
<term>Ileus</term>
<term>Important role</term>
<term>Inducible nitric oxide synthase</term>
<term>Inflammation</term>
<term>Inflammation increases</term>
<term>Inhibitory motor</term>
<term>Intestinal</term>
<term>Intestinal manipulation</term>
<term>Intestinal motility</term>
<term>Intestinal muscularis</term>
<term>Intestine</term>
<term>Jejunal</term>
<term>Kalff</term>
<term>Kreiss</term>
<term>Lamina</term>
<term>Laparotomy</term>
<term>Lateral dorsal horn</term>
<term>Lateral laminae</term>
<term>Leucocyte</term>
<term>Leucocytic</term>
<term>Manipulation</term>
<term>Medial dorsal horn</term>
<term>Motility</term>
<term>Muscularis</term>
<term>Muscularis leucocytic</term>
<term>Neuron</term>
<term>Neurones</term>
<term>Pathway</term>
<term>Peritoneal</term>
<term>Pge2</term>
<term>Pharmacological</term>
<term>Pharmacological blockade</term>
<term>Physiol</term>
<term>Positive cells</term>
<term>Postoperative</term>
<term>Postoperative ileus</term>
<term>Postoperative leucocytic</term>
<term>Postoperatively</term>
<term>Postsurgical</term>
<term>Present study</term>
<term>Primary afferents</term>
<term>Prostaglandin</term>
<term>Rat</term>
<term>Regional distribution</term>
<term>Selective inhibition</term>
<term>Selective inhibitor</term>
<term>Significant increase</term>
<term>Small bowel</term>
<term>Small intestine</term>
<term>Spinal</term>
<term>Spinal cord</term>
<term>Spinal cord segments</term>
<term>Spinal neurons</term>
<term>Surgical</term>
<term>Surgical manipulation</term>
<term>Synthase</term>
<term>Time point</term>
<term>Vehicle control</term>
<term>Visceral afferents</term>
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<front><div type="abstract" xml:lang="en">Background and aims: Cyclooxygenase 2 (COX-2) and prostaglandins (PGs) participate in the pathogenesis of inflammatory postoperative ileus. We sought to determine whether the emerging neuronal modulator COX-2 plays a significant role in primary afferent activation during postoperative ileus using spinal Fos expression as a marker. Methods: Rats, and COX-2+/+ and COX-2−/− mice underwent simple intestinal manipulation. The effect of intestinal manipulation on Fos immunoreactivity (IR) in the L5-S1 spinal cord, in situ circumference, and postoperative leucocytic infiltrate of the intestinal muscularis was measured. Postoperative PGE2 production was measured in peritoneal lavage fluid. The dependence of these parameters on COX-2 was studied in pharmacological (DFU, Merck- Frosst, selective COX-2 inhibitor) and genetic (COX-2−/− mice) models. Results: Postoperative Fos IR increased 3.7-fold in rats and 2.2-fold in mice. Both muscularis leucocytic infiltrate and the circumference of the muscularis increased significantly in rats and COX-2+/+ mice postoperatively, indicating dilating ileus. Surgical manipulation markedly increased PGE2 levels in the peritoneal cavity. DFU pretreatment and the genetic absence of COX-2−/− prevented dilating ileus, and leucocytic infiltrate was diminished by 40% with DFU and by 54% in COX-2−/− mice. DFU reversed postsurgical intra- abdominal PGE2 levels to normal. Fos IR after intestinal manipulation was attenuated by approximately 50% in DFU treated rats and in COX-2−/− mice. Conclusions: Postoperatively, small bowel manipulation causes a significant and prolonged increase in spinal Fos expression, suggesting prolonged primary afferent activation. COX-2 plays a key role in this response. This activation of primary afferents may subsequently initiate inhibitory motor reflexes to the gut, contributing to postoperative ileus.</div>
</front>
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COX-2 dependent inflammation increases spinal Fos expression during rodent postoperative ileus

COX-2 dependent inflammation increases spinal Fos expression during rodent postoperative ileus

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