Interstitial cell of Cajal loss correlates with the degree of inflammation in the human appendix and reverses after inflammation

Discrepancies between c‐Kit positive and Ano1 positive ICC‐SMP in the W/Wv and wild‐type mouse colon; relationships with motor patterns and calcium transients

“…After ablation of the myenteric plexus in mouse colon with the detergent benzalkonium chloride, no c‐Kit positive cells could be identified, but ICC were present as judged by electron microscopy . In a study on appendicitis, loss of c‐Kit was shown, but no loss of ultrastructurally defined ICC based on electron microscopy was observed . In addition, in the Ws/Ws rat jejunum, ICC‐DMP were identified by electron microscopy without the presence of c‐Kit positivity, using rabbit anti c‐Kit polyclonal C‐19 from Santa Cruz.…”

Recent advances in intestinal smooth muscle research: from muscle strips and single cells, via ICC networks to whole organ physiology and assessment of human gut motor dysfunction

“…It has been known that ICC are sensitive to inflammation (36), confirmed by a recent study on the human appendix (37). Gastroparesis (38) and chronic constipation (39) are associated with loss of ICC although the exact pathophysiological mechanisms need further study which is made complicated by the fact that ICC are rarely lost in isolation, often the enteric nervous system is also compromised.…”

Cellular and Molecular Mechanisms of Phenotypic Switch in Gastrointestinal Smooth Muscle

“…Dysmotility occurs in overt bowel inflammatory and infective conditions as well as in functional GI disorders whose multifactorial pathogenesis is likely to be ascribed to impaired intestinal barrier function, low grade inflammation and altered neural control (Vanheel et al, 2013;Chey et al, 2015). All these pathological conditions may directly affect the overall regulatory mechanisms of motility, including the innate contractile properties of the smooth muscle cells, the innervation of the smooth muscle layers by intrinsic and extrinsic neural sources (Lin et al, 2005), or alterations of the ICC (Villanacci et al, 2008;Bettolli et al, 2012;Yang et al, 2015). It is in fact well known that inflammation has a profound impact on the neuromuscular apparatus of the GI tract either at the site of inflammation or at distance from the original site.…”

“…Dysmotility can also occur after resolution of acute gastroenteritis (Mearin, 2011), following persistent low-grade inflammation due to dysbiosis, to alterations of mucosal barrier, or to immune dysregulation (Beatty et al, 2014). All these pathological conditions may directly affect the overall regulatory mechanisms of motility, including the innate contractile properties of the smooth muscle cells, the innervation of the smooth muscle layers by intrinsic and extrinsic neural sources (Lin et al, 2005), or alterations of the ICC (Villanacci et al, 2008;Bettolli et al, 2012;Yang et al, 2015). Changes of gut motility can also derive from alterations of the various non-muscle cells recognized within the muscle layers, for example, glial cells, pericytes, endothelial cells, fibroblasts, and other un-specialized cells (Gabella, 2012).…”