Possible involvement of neutrophil elastase in impaired mucosal repair in patients with ulcerative colitis

Abstract

HGF produced in the intestinal mucosa may be an important stimulator acting on epithelial cell restitution in patients with IBD. However, NE released in situ may impair mucosal repair through inhibiting epithelial cell proliferation in patients with UC.

Inflammatory gene signature in ulcerative colitis with cDNA macroarray analysis

“…On the contrary, HNE has been proposed as a marker 12 and a therapeutic target for UC. 13,14 Moreover, HNE by cleaving key receptors such as CD14 may be responsible for the impaired apoptotic cell recognition by macrophages, thereby prolonging inflammation. 15 Taken together, augmentation of these inhibitor activities seems intuitively promising as a novel targeting therapy against active UC.…”

Possible involvement of the interleukin-15 and interleukin-15 receptor system in a heightened state of lamina propria B cell activation and differentiation in patients with inflammatory bowel disease

“…35,41 Briefly, 4-µm-thick cryostat sections were fixed in acetone at room temperature for 15 min and incubated with normal goat serum diluted 1 : 40. The sections were incubated with a combination of the anti-human IL-15Rα polyclonal antibody, H-107 (1 : 40 dilution) and the monoclonal antibody (1 : 50 dilution), L-26 (anti-CD20; Dakopatts) or UCHT-1 (anti-CD3; Dakopatts), followed by incubation with the fluorescein isothiocyanate (FITC)-conjugated Fab fraction of goat anti-mouse IgG (Jackson ImmunoResearch Laboratories, West Grove, PA, USA) and lissamine rhodamine-conjugated Fab fraction of goat anti-rabbit IgG (Jackson ImmunoResearch Laboratories).…”

Inhibition of neutrophil elastase prevents the development of murine dextran sulfate sodium-induced colitis

“…[9][10][11] It has also been demonstrated that the plasma NE level is correlated with the clinical activity of UC. 9,12 However, a definitive conclusion cannot be Background.…”