Miscellaneous 08

• Published in: British journal of surgery Vol. 89; no. S1; p. 34
• Main Authors: Aherne, N.J., O'Mahony, C., Wu, T., Kirwan, W.O., Kavanagh, E.G., Redmond, H.P.
• Format: Journal Article
• Language: English
• Published: Chichester, UK John Wiley & Sons, Ltd 2002
• ISSN: 0007-1323; 1365-2168
• DOI: 10.1046/j.1365-2168.89.s.1.26_4.x

Background: It has been known for some time that mucosal T‐cells specific to mycobacterial heat shock proteins (hsp) are induced in inflammatory bowel disease (IBD). Hsp‐60 peptide therapy has been shown to induce a T helper 2 cytokine profile characteristic of remission in autoimmune diseases. As human hsp60 is highly homologous with mycobacterial hsp60 and is abundantly expressed following tissue injury, we hypothesized that self‐hsp60 may play a role in regulating acute inflammation in IBD. Methods: Peripheral blood mononuclear cells (PBMC) were harvested with informed consent from 11 patients undergoing surgery for acute IBD and compared to normal controls. Cells were cultured for 5 days with recombinant human hsp60 antigen and proliferation was measured by 3H‐thymidine incorporation. Cultures were restimulated for a further 48 h to amplify a hsp60‐specific T‐cell population, and cytokine production was measured by immunoassay. In addition, mesenteric lymph node cells were harvested from five patients and hsp60‐specific cytokine production was assessed after 3, 5 or 7 days of culture. Results: Control PBMC proliferated well in response to hsp60 (142 per cent of unstimulated) while IBD PBMC proliferated poorly (99 per cent of unstimulated). Production of the anti‐inflammatory cytokine IL‐10, but not TGF‐β, was increased (3.1(2) ng/mL versus 2.6(1) control) while pro‐inflammatory IFN‐γ production was decreased (9.4(2.5) ng mL−1versus 17.9(6.6) control). Mesenteric lymph node IL‐10 production was increased at all time points compared to IFN‐γ production. Conclusion: Our data provides evidence of a self‐antigen‐specific immune response which may act in vivo as an anti‐inflammatory regulatory mechanism in IBD.