| First Author | Keates AC | Year | 2000 |
| Journal | Gastroenterology | Volume | 119 |
| Issue | 4 | Pages | 972-82 |
| PubMed ID | 11040184 | Mgi Jnum | J:65144 |
| Mgi Id | MGI:1891822 | Doi | 10.1053/gast.2000.18164 |
| Citation | Keates AC, et al. (2000) Interleukin 16 is Up-regulated in Crohn's disease and participates in TNBS colitis in mice. Gastroenterology 119(4):972-82 |
| abstractText | 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-1beta (P < 0.05) and tumor necrosis factor alpha (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. |
