Interleukin 16 is up-regulated in Crohn's disease and participates in TNBS colitis in mice
AC Keates, I Castagliuolo, WW Cruickshank, B Qiu… - Gastroenterology, 2000 - Elsevier
AC Keates, I Castagliuolo, WW Cruickshank, B Qiu, KO Arseneau, W Brazer, CP Kelly
Gastroenterology, 2000•ElsevierBackground & Aims: Interleukin (IL)-16 is a T lymphocyte-derived cytokine that uses CD4 as
its receptor and hence selectively recruits CD4-bearing cells. Infiltrating CD4+ T cells are a
feature of Crohn's disease; however, the role of IL-16 in intestinal inflammation is unknown.
The aim of this study was to determine whether IL-16 production is increased in
inflammatory bowel disease and whether IL-16 participates in trinitrobenzene sulfonic acid
(TNBS)-induced colitis in mice. Methods: IL-16 messenger RNA and protein levels in …
its receptor and hence selectively recruits CD4-bearing cells. Infiltrating CD4+ T cells are a
feature of Crohn's disease; however, the role of IL-16 in intestinal inflammation is unknown.
The aim of this study was to determine whether IL-16 production is increased in
inflammatory bowel disease and whether IL-16 participates in trinitrobenzene sulfonic acid
(TNBS)-induced colitis in mice. Methods: IL-16 messenger RNA and protein levels in …
Background & Aims
Interleukin (IL)-16 is a T lymphocyte-derived cytokine that uses CD4 as its receptor and hence selectively recruits CD4-bearing cells. Infiltrating CD4+ T cells are a feature of Crohn's disease; however, the role of IL-16 in intestinal inflammation is unknown. The aim of this study was to determine whether IL-16 production is increased in inflammatory bowel disease and whether IL-16 participates in trinitrobenzene sulfonic acid (TNBS)-induced colitis in mice.
Methods
IL-16 messenger RNA and protein levels in inflammatory bowel disease tissues were determined by reverse-transcription polymerase chain reaction and enzyme-linked immunosorbent assay. C57BL/6 or BALB/c mice were treated with vehicle, TNBS alone, TNBS + anti-IL-16 monoclonal antibody (mAb), TNBS + control mAb, or were untreated. Colonic injury and inflammation were evaluated after 3 or 10 days.
Results
Colonic IL-16 protein levels were increased in patients with Crohn's disease (P < 0.05) but not ulcerative colitis. Anti-IL-16 mAb treatment significantly reduced TNBS-induced weight loss (P < 0.001), mucosal ulceration (P < 0.05), myeloperoxidase activity (P < 0.001), and TNBS-mediated increases in mucosal levels of IL-1(3 (P < 0.05) and tumor necrosis factor α (P < 0.01).
Conclusions
Anti-IL-16 mAb reduced colonic injury and inflammation induced by TNBS in mice. Colonic mucosal IL-16 levels were elevated in Crohn's disease, suggesting a role for IL-16 in the pathophysiology of inflammatory bowel disease.
Elsevier