Publications by authors named "Marcus Manocha"

Mucosal inflammation in conditions ranging from infective acute enteritis or colitis to inflammatory bowel disease is accompanied by alteration in serotonin (5-hydroxytryptamine [5-HT]) content in the gut. Recently, we have identified an important role of 5-HT in the pathogenesis of experimental colitis. 5-HT type 7 (5-HT7) receptor is one of the most recently identified members of the 5-HT receptor family, and dendritic cells express this receptor.

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The gastrointestinal (GI) tract is the largest producer of serotonin (5-hydroxytryptamine (5-HT)) in the body, and as such it is intimately connected with GI function and physiology. 5-HT produced by enterochromaffin (EC) cells is an important enteric mucosal signaling molecule and has been implicated in a number of GI diseases, including inflammatory bowel disease and functional disorders such as irritable bowel syndrome. This review will focus on what is known of basic 5-HT physiology and also on the emerging evidence for its novel role in activation of immune response and inflammation in the gut.

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Inflammatory bowel disease (IBD) encompasses a range of intestinal pathologies, the most common of which are ulcerative colitis (UC) and Crohn's Disease (CD). Both UC and CD, when present in the colon, generate a similar symptom profile which can include diarrhea, rectal bleeding, abdominal pain, and weight loss.(1) Although the pathogenesis of IBD remains unknown, it is described as a multifactorial disease that involves both genetic and environmental components.

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PTMs, such as glycosylation and phosphorylation of apolipoprotein B100 (apoB), are known to be involved with modulating the metabolism of apoB-containing lipoproteins. Current evidence suggests that intracellular and extracellular PTM of apoB are associated with various disorders such diabetes, dyslipidemia and atherosclerosis. The ability to identify and characterize the specific PTM of apoB correlating to specific pathologies may improve our understanding of the underlying molecular mechanisms regulating apoB metabolism.

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