Published online May 7, 2018. doi: 10.3748/wjg.v24.i17.1888
Peer-review started: January 26, 2018
First decision: February 5, 2018
Revised: February 23, 2018
Accepted: March 18, 2018
Article in press: March 18, 2018
Published online: May 7, 2018
Processing time: 100 Days and 19.3 Hours
Activation of guanylate cyclase-C (GC-C) signaling is an emerging therapeutic target for the treatment of gastrointestinal disorders and inflammatory diseases. Loss of GC-C signaling may disrupt intestinal water and ion secretion, resulting in chronic idiopathic constipation or irritable bowel syndrome with constipation (IBS-C). In addition, reduced GC-C signaling may also disrupt intestinal barrier function due to increased paracellular permeability, allowing entry of inflammatory mediators to promote low-grade inflammation and visceral hypersensitivity associated with abdominal pain in IBS-C patients.
Plecanatide and dolcanatide are analogs of human uroguanylin, the endogenous agonist of GC-C receptors, and are targeted at the treatment of functional constipation disorders and inflammatory bowel disease (IBD), respectively; therefore we sought to further characterize the mechanisms of these peptides using in vitro and in vivo models of these diseases.
To discern the role of plecanatide and dolcanatide in the maintenance of mucosal membrane integrity and in the reduction of visceral hypersensitivity in inflammatory and non-inflammatory animal models.
Maintenance of epithelial cell integrity by plecanatide or dolcanatide in response to chemical challenge by lipopolysaccharide (LPS) was assessed using cell lines, as well as tissue harvested from rat intestines. Paracellular permeability was determined by calculating the flux of fluorescein isothiocyanate (FITC)-dextran using immunofluorescence microscopy. Electromyographic recordings were used to assess suppression of visceral hypersensitivity by plecanatide or dolcanatide in rat models of inflammatory and non-inflammatory visceral pain.
Plecanatide or dolcanatide effectively suppressed LPS-induced paracellular permeability. Oral treatment with plecanatide or dolcanatide considerably attenuated visceral hypersensitivity in inflammatory and non-inflammatory models of visceral pain.
The data presented suggest further mechanisms, in addition to their better known secretory effects, whereby plecanatide or dolcanatide treatment, through activation of the GC-C receptor, may protect the epithelial barrier from increased paracellular permeability and provide anti-nociceptive activity, which may ultimately benefit patients with functional constipation disorders and IBD.
Plecanatide is a secretagogue approved in the US for the treatment of adults with chronic idiopathic constipation or IBS-C. Dolcanatide is under evaluation for the treatment of opioid-induced constipation and ulcerative colitis. This study provides preclinical evidence that plecanatide and dolcanatide may act to preserve the integrity of the intestinal epithelium and to provide anti-nociceptive activity, supporting ongoing investigations of these peptides in functional constipation disorders and IBD.