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Background Acute cellular rejection (ACR) is a common complication of small bowel transplantation (SBTx) and the major cause of graft loss. However, little is known regarding the genetic graft response to ACR in clinical transplants. In this study, we have determined a genetic expression profile of intestinal graft response to ACR after living related (LR) SBTx. Results By identifying the expression profiles of reported markers of rejection we were able to identify 57 genes that had significantly increased (more than twofold) expression in response to ACR. Known markers of rejection identified: MMP-9, MMP-2, VIP, IFNγ, IL-2R, MADCAM-1, HSP-60 , and HSP-70 all had greater than twofold increased expression after ACR diagnosed (week 3 to week 6). The newly identified genes were: IFI27, EPST11, APAF1, LAP3, STK6 , and MDK. Conclusion Newly identified up-regulated genes in response to ACR in small bowel graft are involved in the immune response, cell adhesion, neurogenesis, cell division and proliferation, DNA replication/repair, protein ubiqutin/proteolysis, and apoptosis. TNF α up-regulated early at week 2 biopsy may be an early genetic marker of ACR in SBTx.

The purpose was to determine whether magnification endoscopy (ME) accurately diagnosed rejection in living related small bowel transplants (LRSBTx) during initial morphological adaptation of segmental intestinal grafts. The small bowel recipient was a 44-year-old woman with short gut syndrome following multiple bowel surgeries for familial adenomatous polyposis. ME was enhanced by chromoendoscopy staining. Bowel mucosa was washed with acetic acid and stained with methylene blue for optimal visualization of mucosal villi and to improve the diagnostic yield of biopsies. The recipient underwent surveillance ME with biopsy 16 times through the ileostomy in the first 9 months following transplantation. The recipient developed diarrhea in the postoperative course, which led to the suspicion of rejection. ME findings of patchy villus blunting were consistent with biopsy samples that showed mild acute cellular rejection. Episodes of rejection were treated with high-dose immunosuppressants and steroids. Reversal of rejection was monitored by follow-up ME, which showed increased length of villi and normalization of morphology. Biopsy confirmed these findings. The first endoscopy, at 5 days posttransplant, showed no evidence of intestinal ischemia. LRSBTx involves early morphological adaptation of the recipient small bowel mucosa, characterized by an increased length of villi. ME is a reliable technique to follow adaptation and detect early rejection. The superior imaging of small bowel mucosa created by ME chromoendoscopy enables early diagnosis and delivery of more prompt antirejection therapy to prevent progression of rejection. ME also confirmed that segmental LRSBTx caused minimal ischemic injury to the recipient.