BACKGROUND: The mechanisms involved in the initiation and maintenance of Crohn's disease are poorly understood. Previous studies have demonstrated an increased number of infiltrating CD4+ T cells within the inflammatory affected bowel wall in Crohn's disease. Novel therapy approaches using anti-CD4 antibodies are thought to be effective in Crohn's disease. AIMS: Interleukin 16 (IL-16) has been characterised as a chemokine with selective chemoattraction for CD4+ inflammatory T cells. In this study, cellular expression of IL-16 in Crohn's disease and ulcerative colitis was investigated. METHODS: Expression of IL-16 was analysed in tissue samples of Crohn's disease, ulcerative colitis, and normal controls by applying reverse transcription-polymerase chain reaction, non-radioactive in situ hybridisation, and immunohistochemistry. 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 number by step sections. RESULTS: An increased number of IL-16+ cells in Crohn's disease in comparison with ulcerative colitis and control probes was demonstrated. IL-16 was expressed by CD4 and CD8 positive T cells. In addition, in active Crohn's disease there was a substantial number of IL-16 positive mast cells. The increased number of CD4+ lymphocytes correlated positively with the increased number 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 significant 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.
BACKGROUND: The mechanisms involved in the initiation and maintenance of Crohn's disease are poorly understood. Previous studies have demonstrated an increased number of infiltrating CD4+ T cells within the inflammatory affected bowel wall in Crohn's disease. Novel therapy approaches using anti-CD4 antibodies are thought to be effective in Crohn's disease. AIMS: Interleukin 16 (IL-16) has been characterised as a chemokine with selective chemoattraction for CD4+ inflammatory T cells. In this study, cellular expression of IL-16 in Crohn's disease and ulcerative colitis was investigated. METHODS: Expression of IL-16 was analysed in tissue samples of Crohn's disease, ulcerative colitis, and normal controls by applying reverse transcription-polymerase chain reaction, non-radioactive in situ hybridisation, and immunohistochemistry. 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 number by step sections. RESULTS: An increased number of IL-16+ cells in Crohn's disease in comparison with ulcerative colitis and control probes was demonstrated. IL-16 was expressed by CD4 and CD8 positive T cells. In addition, in active Crohn's disease there was a substantial number of IL-16 positive mast cells. The increased number of CD4+ lymphocytes correlated positively with the increased number 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 significant 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.
Authors: A Kaser; S Dunzendorfer; F A Offner; T Ryan; A Schwabegger; W W Cruikshank; C J Wiedermann; H Tilg Journal: J Immunol Date: 1999-09-15 Impact factor: 5.422
Authors: G L Chupp; E A Wright; D Wu; M Vallen-Mashikian; W W Cruikshank; D M Center; H Kornfeld; J S Berman Journal: J Immunol Date: 1998-09-15 Impact factor: 5.422
Authors: V Rumsaeng; W W Cruikshank; B Foster; C Prussin; A S Kirshenbaum; T A Davis; H Kornfeld; D M Center; D D Metcalfe Journal: J Immunol Date: 1997-09-15 Impact factor: 5.422
Authors: S Laberge; S Pinsonneault; P Ernst; R Olivenstein; O Ghaffar; D M Center; Q Hamid Journal: Int Arch Allergy Immunol Date: 1999-06 Impact factor: 2.749
Authors: P Parronchi; P Romagnani; F Annunziato; S Sampognaro; A Becchio; L Giannarini; E Maggi; C Pupilli; F Tonelli; S Romagnani Journal: Am J Pathol Date: 1997-03 Impact factor: 4.307
Authors: J K Franz; S A Kolb; K M Hummel; F Lahrtz; M Neidhart; W K Aicher; T Pap; R E Gay; A Fontana; S Gay Journal: Eur J Immunol Date: 1998-09 Impact factor: 5.532
Authors: H Kim; L Dwyer; J H Song; F E Martin-Cano; J Bahney; L Peri; F C Britton; K M Sanders; S D Koh Journal: Neurogastroenterol Motil Date: 2011-08-01 Impact factor: 3.598
Authors: G V Chaitanya; S E Franks; W Cromer; S R Wells; M Bienkowska; M H Jennings; A Ruddell; T Ando; Y Wang; Y Gu; M Sapp; J M Mathis; P A Jordan; A Minagar; J S Alexander Journal: Lymphat Res Biol Date: 2010-09 Impact factor: 2.589