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Ann Thorac Surg 1990;49:927-931
© 1990 The Society of Thoracic Surgeons

Articles

Prostaglandin E2 inhibits in vitro and in vivo lymphocyte responses in allogeneic transplantation

Christopher D. Stonc, MD, Bruce R. Rosengard, MD, Stephen M. Boorstein, BS, Robert C. Robbins, MD, Hani A. Hennein, MD, Richard E. Clark, MD*

Surgery Branch, National Heurt, Lung, and Blood Institute, and Immunology Branch, National Cancer Institute, National Institutes of Health, Bethesda, Maryland USA

* Address reprint requests to Dr Clark, Surgery Branch, NHLBI, NIH, Bldg 10, Room Sharet Bethesda, MD 20897.

Prostaglandin E, (PGE2) has been shown to have a clear role in the suppression of immune responses after burn and trauma injury. This probably results from inhibition of interleukin-2 production. This study examined the effects of PGE2 in vivo on the survival of solid-organ allografts and in vitro on the rat allogeneic mixed lymphocyte response. Administration of 16,16-dimethyl prostaglandin E2 (DMPGE2), a stable analogue of PGE2, significantly prolonged the survival of heterotopic cardiac allografts from ACI to LBN rats: 10.4 ± 1.7 days versus 5.7 ± 1.1 days (mean ± standard error of the mean) (p <- 0.001). In 1 animal, DMPGE2 apparently ied to the induction of long-term tolerance. Mixed lymphocyte cultures using splenocytes from naive LBN and ACI rats to which DMPGE2 was added showed a dose-dependend suppression of the mixed lymphocyte response with concentrations as low as 1 x 10–7 mol/L. Splenocytes harvested from treated animals with functioning but histologically rejecting hearts demonstrated a marked decrease in mixed lymphocyte response to donor (ACI) stimulators compared with naive LBN controls (3,804 ± 603 versus 27,395 ± 2,668 cpm, n = 4), but maintained a normal response to (third-party (Wistar Furth) stimulators. We conclude that DMPGE2 suppressed solid-organ allograft rejection, inhibited the allogeneic mixed lymphocyte response, and induced donor-specific in vitro hyporesponsiveness.




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