Distribution and expression levels of somatostatin and somatostatin receptors in the ileum of normal and acutely Schistosoma mansoni‐infected SSTR2 knockout/lacZ knockin mice

• Published in: Neurogastroenterology and motility 2008-07, Vol.20 (7), p.798-807
• Main Authors: Van Op Den Bosch, J., Lantermann, K., Torfs, P., Van Marck, E., Van Nassauw, L., Timmermans, J.‐p.
• Format: Article
• Language: English
• Subjects: Animals; Female; Ileum - cytology; Ileum - metabolism; Ileum - microbiology; intestinal inflammation; Male; mast cell; Mice; Mice, Knockout; Receptors, Somatostatin - genetics; Receptors, Somatostatin - metabolism; Schistosoma; Schistosoma mansoni - metabolism; Schistosomiasis mansoni; somatostatin; Somatostatin - genetics; Somatostatin - metabolism; somatostatin receptor; SSTR2 knockout mouse
• ISSN: 1350-1925; 1365-2982
• DOI: 10.1111/j.1365-2982.2008.01088.x

We recently described the widespread expression of somatostatin (SOM) receptors (SSTRs) in the non‐inflamed and inflamed murine ileum. Surprisingly, no significant changes were observed in the SSTR2 expression during intestinal inflammation. These data, combined with several recent independent lines of investigation, raised some question about the long presumed central role of SSTR2 in the SOM‐mediated effects in the physiological and pathological activity of the gastrointestinal (GI) tract. To further unravel the role of SSTR2 in GI physiology, we studied the expression of SOM and SSTRs in the normal and inflamed SSTR2 knockout/lacZ knockin (SSTR2−/−) ileum. The SSTR2−/− ileum was characterized by a widespread distribution of multiple SSTR subtypes in non‐inflamed and inflamed conditions. Moreover, the absence of SSTR2 did not induce any compensatory effect in the distribution pattern or expression level of any of the other SSTR subtypes. In contrast, the amount of SOM mRNA was significantly lower in SSTR2−/− ileum than that in wild type animals. Quantitative analysis revealed a decreased number of SOM‐expressing neurons in both enteric plexuses of the knockout animals, implying a possible link between the number of SOM‐expressing enteric neurons and the expression of SSTR2 in the enteric nervous system. In conclusion, these data show that a reconsideration of the role of SSTR2 in the GI somatostatinergic effects is in order and further corroborate recent data on the role of other SSTR subtypes in the inflammatory effects of SOM during intestinal inflammation.