Interleukin 16 expression and phenotype of interleukin 16 producing cells in Crohn's disease

Background-The mechanisms involved in the initiation and maintenance of Cro hn's disease are poorly understood. Previous studies have demonstrated an i ncreased number of infiltrating CD4+ T cells within the inflammatory affect ed bowel wall in Crohn's disease. Novel therapy approaches using anti-CD4 a ntibodies are thought to be effective in Crohn's disease. Aims-Interleukin 16 (IL-16) has been characterised as a chemokine with sele ctive chemoattraction for CD4+ inflammatory T cells. In this study, cellula r expression of IL-16 in Crohn's disease and ulcerative colitis was investi gated. Methods-Expression of IL-16 was analysed in tissue samples of Crohn's disea se, ulcerative colitis, and normal controls by applying reverse transcripti on-polymerase chain reaction, non-radioactive in situ hybridisation, and im munohistochemistry. Double staining methods were used to characterise cells expressing IL-16. The amount of infiltrating CD4+ cells was determined by immunohistochemistry and correlated with the corresponding IL-16+ cell numb er by step sections. Results-An increased number of IL-16+ cells in Crohn's disease in compariso n with ulcerative colitis and control probes was demonstrated. IL-16 was ex pressed by CD4 and CD8 positive T cells. In addition, in active Crohn's dis ease there was a substantial number of IL-16 positive mast cells. The incre ased number of CD4+ lymphocytes correlated positively with the increased nu mber of IL- 16 positive cells in Crohn's disease. Conclusion-Our results demonstrate that increased expression of IL-16 in T cells and mast cells in active Crohn's disease is associated with increased numbers of CD4+ lymphocytes. Local expression of IL-16 seems to play a sig nificant role in the initiation and persistence of the inflammatory process in Crohn's disease, presumably by IL-16 mediated recruitment of CD4+ cells , mostly lymphocytes, into the bowel wall.