Epstein-Barr virus (EBV) infection and expression of the interleukin-12 family member EBV-induced gene 3 (EBI3) in chronic inflammatory bowel disease.

Herpesviruses have been suggested as possible etiological agents of ulcerative colitis and Crohn's disease. Recently, increased numbers of Epstein-Barr virus (EBV)-infected cells have been detected in ulcerative colitis as compared to Crohn's disease. Interestingly, expression levels of the EBV-induced gene 3 (EBI3), a molecule belonging to the interleukin (IL)-12 family, have also been reported to be elevated in ulcerative colitis as compared to Crohn's disease. To test the hypothesis that these observations might be interrelated, ileocolic resection specimens were examined from 16 patients with ulcerative colitis and from 20 patients with Crohn's disease. The presence of EBV-infected cells and of EBI3-expressing cells was determined quantitatively by in situ hybridisation and immunohistochemistry, respectively. Larger number of EBV-infected cells were seen in areas of active inflammation of ulcerative colitis and Crohn's disease as compared to areas of inactive inflammation. However, there was no statistically significant difference between ulcerative colitis and Crohn's disease. Numbers of EBI3-expressing cells were increased in areas of active inflammation of ulcerative colitis and Crohn's disease but again there was no statistically significant difference between the two diseases. Double labelling experiments showed that EBI3 expression occurred only in a small minority of EBV-infected cells in ulcerative colitis and Crohn's disease. These results suggest that increased numbers of EBV-infected cells in areas of active inflammatory bowel disease (IBD) are secondary to influx or local proliferation of inflammatory cells and do not contribute significantly to local production of EBI3. Assessment of the possible role of EBI3 of the pathogenesis of ulcerative colitis or Crohn's disease requires information regarding the expression of other IL-12 family members. Copyright 2004 Wiley-Liss, Inc.