Background and aim. The aetiology of ulcerative colitis is still controversial, however recent studies have emphasised the possible role of infectious agents or ingested substances and their breakdown products, which might activate immune-mediated mechanisms eventually leading to tissue damage. Aim of this investigation was to ascertain the occurrence and the potential role of Epstein-Barr virus infection in large bowel mucosa of ulcerative colitis patients. Patients and methods. Twenty-three biopsies and six total colectomies from 17 patients were analysed for the expression of Epstein-Barr virus proteins and RNAs. Polymerase chain reaction experiments were also carried out to detect Epstein-Barr virus DNA. For comparison, ten biopsies from patients with Crohns disease, ten biopsies from patients with different types of colitis, seven biopsies and five surgical margins of normal colonic mucosa from the small and large bowels were studied (controls). Results. Six biopsies and four colectomies from seven ulcerative colitis patients showed scattered lymphocytes expressing nuclear EBER I-2 and harbouring polymerase chain reaction-amplifiable Epstein-Barr virus-DNA. In some cases, linear viral DNA (typical of lytic Epstein-Barr virus infection) was also found. Epithelial cells were invariably negative in all cases. All control tissues from non-ulcerative colitis patients were also invariably non-reactive. Conclusion. Evidence of Epstein-Barr virus infection in the mucosal inflammatory cells of ulcerative colitis patients suggests a possible role of this virus in the chronicity of ulcerative colitis.

Evidence of Epstein-Barr virus infection in ulcerative colitis / Bertalot, G; Villanacci, V; Gramegna, M; Orvieto, E; Negrini, R; Saleri, A; Terraroli, C; Ravelli, R; Cestari, R; Viale, G. - In: DIGESTIVE AND LIVER DISEASE. - ISSN 1590-8658. - 33:7(2001), pp. 551-558. [10.1016/S1590-8658(01)80106-7]

Evidence of Epstein-Barr virus infection in ulcerative colitis

Bertalot G;
2001-01-01

Abstract

Background and aim. The aetiology of ulcerative colitis is still controversial, however recent studies have emphasised the possible role of infectious agents or ingested substances and their breakdown products, which might activate immune-mediated mechanisms eventually leading to tissue damage. Aim of this investigation was to ascertain the occurrence and the potential role of Epstein-Barr virus infection in large bowel mucosa of ulcerative colitis patients. Patients and methods. Twenty-three biopsies and six total colectomies from 17 patients were analysed for the expression of Epstein-Barr virus proteins and RNAs. Polymerase chain reaction experiments were also carried out to detect Epstein-Barr virus DNA. For comparison, ten biopsies from patients with Crohns disease, ten biopsies from patients with different types of colitis, seven biopsies and five surgical margins of normal colonic mucosa from the small and large bowels were studied (controls). Results. Six biopsies and four colectomies from seven ulcerative colitis patients showed scattered lymphocytes expressing nuclear EBER I-2 and harbouring polymerase chain reaction-amplifiable Epstein-Barr virus-DNA. In some cases, linear viral DNA (typical of lytic Epstein-Barr virus infection) was also found. Epithelial cells were invariably negative in all cases. All control tissues from non-ulcerative colitis patients were also invariably non-reactive. Conclusion. Evidence of Epstein-Barr virus infection in the mucosal inflammatory cells of ulcerative colitis patients suggests a possible role of this virus in the chronicity of ulcerative colitis.
2001
7
Bertalot, G; Villanacci, V; Gramegna, M; Orvieto, E; Negrini, R; Saleri, A; Terraroli, C; Ravelli, R; Cestari, R; Viale, G
Evidence of Epstein-Barr virus infection in ulcerative colitis / Bertalot, G; Villanacci, V; Gramegna, M; Orvieto, E; Negrini, R; Saleri, A; Terraroli, C; Ravelli, R; Cestari, R; Viale, G. - In: DIGESTIVE AND LIVER DISEASE. - ISSN 1590-8658. - 33:7(2001), pp. 551-558. [10.1016/S1590-8658(01)80106-7]
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Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/11572/361203
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