Proinflammatory cytokines trigger MUC gene expression and mucin release in the intestinal cancer cell line LS180

Abstract

Our data demonstrate differential cytokine effects on mucin synthesis, secretion and composition. These alterations may contribute to the defective mucus layer in colitis.

Pathophysiological Investigation of the Gastric Surface Mucous Gel Layer of Patients with Helicobacter pylori Infection by Using Immunoassays for Trefoil Factor Family 2 and Gastric Gland Mucous Cell-Type Mucin in Gastric Juice

“…Treatment of cultured chondrocytes with tumor necrosis factor (TNF)-α or interleukin (IL)-1β was reported to increase TFF3 expression [34]. On the other hand, the expression of MUC6 (a core protein of GMC-type mucin) and the secretion of mucins were reported to be stimulated by TNF-α and IL-6 in the human colonic carcinoma-derived cell line LS180 [35]. The levels of TNF-α, IL-6, and IL-1β levels were reported to be elevated in the gastric mucosa in H. pylori-associated gastritis [36], and thus cytokine-mediated mechanisms may be involved in the upregulation of the expression of TFF2 and GMC-type mucin in the gastric mucosa in H. pylori-associated gastritis.…”

A sticky end for gastrointestinal helminths; the role of the mucus barrier

“…For example, a study conducted by Marillier and colleagues demonstrated goblet cell hyperplasia is observed independent of the IL‐13/IL‐4 signalling apparatus,62 and Muc2 and Muc3 transcripts were augmented even in the absence of IL‐4 during T. spiralis infection 50. Furthermore, inflammatory cytokines have been implicated to have a role in goblet cell function during parasitic infection, including IL‐1, TNF and IL‐22,63, 64, 65 and it is yet to be defined if microbial factors, the inflammasome and adrenergic and cholinergic receptors can influence the secretion of mucins and other goblet cell‐associated products during parasitic invasion.…”

Cathelicidins in inflammation and tissue repair: Potential therapeutic applications for gastrointestinal disorders

“…This is linked to the depletion of goblet cells and downregulation of mucin production which could be influenced by immunological or bacterial factors during inflammation. In vitro study has revealed that pro-inflammatory cytokines IL-1, IL-6 or tumor necrosis factor (TNF)-α can cause an increased synthesis of MUC2 and other secretory mucins whereas incubation of individual cytokine additionally results in decreased and altered glycosylation in human goblet cell-like cells [27] . The elevated number of bacteria detected within the colonic mucus layer of UC patients poses another threat to the intestinal mucosa.…”