脾肠联合移植对大鼠小肠移植免疫耐受的影响

目的　探讨脾肠联合移植对小肠移植免疫耐受的诱导作用。方法　选用SD大鼠为供体、Wistar大鼠为受体 ,进行异位全小肠和脾脏联合移植。实验分 3组 ,每组 6只。A组 :小肠移植非免疫干预组 ;B组 :受体脾切除 ,脾肠联合移植组 ;C组 :小肠移植环孢霉素A(CsA)治疗组。术后 3、5、7、10d取移植小肠回肠段 0 .5～ 1.0cm进行病理学检查 ,用病理图像分析系统测量黏膜厚度 ,绒毛高度和隐窝深度。采用TdT介导的脱氧核苷酸原位末端标记法 (TUNEL)检测 3、5、7d移植小肠黏膜细胞凋亡 ,评价移植小肠急性排斥反应损伤程度。结果　A、B两组均有不同程度的急性排斥反应损伤 ,但A组高于B组 ,移植后 3、5、7d分别属于轻、中、重度排斥 ,10d黏膜基本完全脱落。B组移植后 3、5d符合轻度排斥 ,7d中度以下排斥 4只 ,重度排斥 2只 ,10d中度排斥 2只 ,重度 4只 ,但仍可见黏膜层。C组移植后 10d 1只出现轻度排斥其余未见明显损伤。黏膜厚度、绒毛高度和隐窝深度B组明显高于A组 ,黏膜上皮细胞凋亡数目较A组低。结论　受体脾切除 ,脾肠联合移植可减轻移植小肠急性排斥反应损伤 ,诱导一定程度的小肠移植免疫耐受     

移植物浸润T淋巴细胞肿瘤坏死因子相关凋亡诱导配体及受体DR4和DR5表达与大鼠小肠移植急性排斥反应的相关性

目的 探讨浸润T淋巴细胞七的DR4、DR5表达同小肠移植急性排斥反应的关系.方法 将2种近交系大鼠(SD、Wistar)54只按随机配对法分为A、B、C3组.A组大鼠为对照组(18只)行虚拟手术;B组(18只)大鼠行同系小肠移植;C组(18只)大鼠行不同品系小肠移植.各组大鼠于术后5 d取移植肠样本分别做HE染色和免疫荧光双标记染色.采用免疫荧光染色、激光共聚焦技术测定各组标本浸润T淋巴细胞肿瘤坏死因相关凋亡诱导配体及DR4、DR5的表达情况.结果 A组大鼠小肠黏膜正常,B组大鼠小肠表现为免疫耐受,C组大鼠表现为急性排斥反应.C组大鼠高T淋巴细胞表达肿瘤坏死因子相关凋亡诱导配体与A、B组大鼠比较差异有统计学意义(P < 0.01);A、B组大鼠浸润T淋巴细胞DR4、DR5均呈高表达,C组大鼠呈低表达,C组大鼠与A、B组比较差异有统计学意义(P < 0.01);A、B组大鼠比较差异无统计学意义(P > 0.05).结论 急性排斥反应的发生可能与浸润T淋巴细胞DR的低表达有关.减少浸润淋巴细胞DR表达的下调,或者上调DR将有助于控制急性排斥反应,诱导免疫耐受.     

移植物浸润T淋巴细胞肿瘤坏死因子相关凋亡诱导配体及受体DR4和DR5表达与大鼠小肠移植急性排斥反应的相关性

目的 探讨浸润T淋巴细胞七的DR4、DR5表达同小肠移植急性排斥反应的关系.方法 将2种近交系大鼠(SD、Wistar)54只按随机配对法分为A、B、C3组.A组大鼠为对照组(18只)行虚拟手术;B组(18只)大鼠行同系小肠移植;C组(18只)大鼠行不同品系小肠移植.各组大鼠于术后5 d取移植肠样本分别做HE染色和免疫荧光双标记染色.采用免疫荧光染色、激光共聚焦技术测定各组标本浸润T淋巴细胞肿瘤坏死因相关凋亡诱导配体及DR4、DR5的表达情况.结果 A组大鼠小肠黏膜正常,B组大鼠小肠表现为免疫耐受,C组大鼠表现为急性排斥反应.C组大鼠高T淋巴细胞表达肿瘤坏死因子相关凋亡诱导配体与A、B组大鼠比较差异有统计学意义(P < 0.01);A、B组大鼠浸润T淋巴细胞DR4、DR5均呈高表达,C组大鼠呈低表达,C组大鼠与A、B组比较差异有统计学意义(P < 0.01);A、B组大鼠比较差异无统计学意义(P > 0.05).结论 急性排斥反应的发生可能与浸润T淋巴细胞DR的低表达有关.减少浸润淋巴细胞DR表达的下调,或者上调DR将有助于控制急性排斥反应,诱导免疫耐受.     

移植物浸润T淋巴细胞肿瘤坏死因子相关凋亡诱导配体及受体DR4和DR5表达与大鼠小肠移植急性排斥反应的相关性

目的 探讨浸润T淋巴细胞七的DR4、DR5表达同小肠移植急性排斥反应的关系.方法 将2种近交系大鼠(SD、Wistar)54只按随机配对法分为A、B、C3组.A组大鼠为对照组(18只)行虚拟手术;B组(18只)大鼠行同系小肠移植;C组(18只)大鼠行不同品系小肠移植.各组大鼠于术后5 d取移植肠样本分别做HE染色和免疫荧光双标记染色.采用免疫荧光染色、激光共聚焦技术测定各组标本浸润T淋巴细胞肿瘤坏死因相关凋亡诱导配体及DR4、DR5的表达情况.结果 A组大鼠小肠黏膜正常,B组大鼠小肠表现为免疫耐受,C组大鼠表现为急性排斥反应.C组大鼠高T淋巴细胞表达肿瘤坏死因子相关凋亡诱导配体与A、B组大鼠比较差异有统计学意义(P < 0.01);A、B组大鼠浸润T淋巴细胞DR4、DR5均呈高表达,C组大鼠呈低表达,C组大鼠与A、B组比较差异有统计学意义(P < 0.01);A、B组大鼠比较差异无统计学意义(P > 0.05).结论 急性排斥反应的发生可能与浸润T淋巴细胞DR的低表达有关.减少浸润淋巴细胞DR表达的下调,或者上调DR将有助于控制急性排斥反应,诱导免疫耐受.     

大鼠移植肠管长度、部位与排斥反应的关系

目的　探讨移植肠管的长度、部位与排斥反应之间的关系。方法　行同种异系原位小肠移植 (SD→Wistar) ,分别移植 3 0 %近端小肠 (A组 )、60 %近端小肠 (B组 )、全小肠 (C组 )、3 0 %远端小肠 (D组 )。观察术后生存时间 ;定期 (1、3、5、7、9d)采血测定血清白细胞介素 2 (IL 2 )、白细胞介素 8(IL 8)水平 ;开腹行麦芽糖吸收实验 ;取移植肠管 ,苏木素 伊红 (HE)染色后光镜检查。结果　A、B组的生存时间 (12 .0 0± 1.67)d、(11.17± 1.94)d与C组 (9.17± 1.17)d及D组 (8.3 3±1.0 3 )d相比差异有统计学意义 (P <0 .0 5 )。麦芽糖吸收实验、血清及病理学结果显示 :A、B组分别于术后 5、7、9d发生轻、中、重度排斥反应 ,C、D组分别于术后 3、5、7d发生轻、中、重度排斥反应。结论　大鼠小肠移植排斥反应强弱与移植肠管的长度无直接关系 ;排斥反应发生的时间与移植肠管的部位有一定关系。     

细胞凋亡在大鼠胰腺移植急性排斥反应中的作用

目的探讨细胞凋亡和相关因子Fas、FasL、bcl-2和bax在大鼠胰腺移植急性排斥反应中的作用,评价十二指肠黏膜活检在胰腺移植中诊断排斥反应的价值。方法选SD和Wistar大鼠行全胰十二指肠移植,实验分同基因胰腺移植组和异基因胰腺移植组。于移植术后第3、5及7d分批处死受体,取移植胰腺和十二指肠标本用HE染色和原位末端脱氧核糖核苷酸转移酶标记技术(TUNEL)检测移植物。免疫组化法检测移植后胰腺和十二指肠Fas、FasL、bcl-2和bax的表达。结果异基因胰腺移植组胰腺和十二指肠病理评分相同者占61.1%(11/18);评分不同者占38.9%(7/18),其中胰腺评分较高者6例,十二指肠黏膜评分较高者仅1例。异基因胰腺移植组胰腺和十二指肠病理学评分和细胞凋亡指数均明显高于同基因胰腺移植组(P<0.05,P<0.01)。胰腺和十二指肠细胞凋亡指数与急性排斥反应的病理学评分成正相关(r=0.965,P<0.01;r=0.942,P<0.01)。随着术后时间延长,排斥反应分级上升,细胞凋亡增加,FasL表达升高,在异基因移植组bcl-2表达下降,而Fas和bax表达无明显变化。结论细胞凋亡与移植胰腺急性排斥反应的严重程度呈正相关,细胞凋亡指数可作为判断移植物损伤程度的指标。FasL和bcl-2与胰腺移植急性排斥及组织损伤密切相关。十二指肠黏膜活检有助于判断有无胰腺急性排斥反应发生。     

白细胞介素-12 p35沉默的树突状细胞联合CD40L单克隆抗体对大鼠小肠移植免疫耐受的诱导作用

目的研究供体骨髓来源的白细胞介素12 p35(IL-12p35)基因沉默的树突状细胞(IL-12 p35 silenced DC)联合大鼠CD40L单克隆抗体(CD40L mAb)对大鼠小肠移植免疫耐受的诱导。方法实验动物随机分为3组,每组8对,分别于手术前7天进行不同预处理后进行小肠移植。A组:受体注射生理盐水;B组:受体注射供体IL-12 p35 silenced DC,C组:受体静脉注射供体IL-12 p35 silenced DC,同时腹腔注射CD40L mAb。观察受体存活时间,移植小肠采用病理学检察及细胞凋亡检测,受体血清检测IL-2、干扰素(INF)-γ水平。结果C组受体动物存活时间为(23.3±6.0)d,显著长于A、B两组[(6.5±1.5)d,(15.1±4.9)d];C组移植小肠炎性细胞浸润、黏膜结构破坏程度和肠黏膜细胞的凋亡数目明显低于A、B组[(9.5±5.6)比(23.8±6.2)、(18.7±6.3),(P<0.01)];C组受体大鼠血清IL-2浓度为(185.8±18.2)ng/L,显著低于A、B两组[(294.1±15.6)ng/L、(225.8±14.5)ng/L,(P<0.01、P<0.05)];C组受体大鼠血清INF-γ浓度为(75.6±8.6)ng/L,显著低于A、B两组[(110.5±12.4)ng/L、(89.1±9.2)ng/L,(P<0.01、P<0.05)]。结论术前输注供体来源的IL-12 p35 silenced DC联合CD40L mAb,可在一定程度上抑制小肠移植的排斥反应,诱导受体产生免疫耐受。     

TGF-β1修饰的未成熟树突状细胞对大鼠移植小肠细胞凋亡的影响

目的 探讨经TGF-β1修饰的未成熟树突状细胞(imDC)预处理大鼠小肠移植受体后移植肠细胞凋亡的变化及意义.方法 选用近交系F344/N和BN大鼠建立全小肠异位移植模型,分4组,每组24只.A组:同基因移植组(BN→BN);B组:异基因移植组(F344/N→BN);C组:F344/N→BN异基因移植+TGF-β1基因转染imDC;D组:F344/N→BN异基因移植+TGF-β1基因转染imDC+FK506.术后3、5、7 d各处死6只,取出移植肠.行免疫组化检测Bcl-2和Bax表达,TUNEL及电镜观察细胞凋亡.同期进行移植肠组织病理学检查.结果 C组中Bcl-2在术后有轻度下降,而Bax的表达则略有升高,但明显低于B组,差异有统计学意义(P＜0.05);D组术后Bcl-2及Bax的表达与A组无明显差异.C组的凋亡细胞数在术后逐渐增加,但数量始终较少,与B组比较差异有统计学意义(P＜0.05);D组仅见少量凋亡细胞.结论 经TGF-β1基因转染的imDC预处理受体可以抑制细胞凋亡,从而减轻小肠移植术后急性排斥反应的程度.     

腺泡细胞凋亡在大鼠胰腺移植急性排斥反应中的意义

目的：观察移植胰腺的腺泡细胞凋亡及其与急性排斥反应的关系。方法：选用SD和Wistar大鼠进行全胰十二指移植。实验分为同基因移植组（Wistar→Wistar）和异基因移植组（SD→Wistar）两组。于术后第3d、5d和7d分批处死受体，取移植胰腺标本用HE染色和原位末端标记（TUNEL）技术检测移植胰腺切片，进行排斥反应的病理学评分和计数凋亡指数（AI）。结果：发生凋亡的细胞主要是腺泡细胞，同基因移植组胰腺有散在的腺泡细胞凋亡，AI在术后无明显变化。异基因移植组胰腺腺泡细胞凋亡在术后第3d、5d和7d逐渐升高，AI与急性排斥反应的病理学评分成正相关。结论：细胞凋亡与移植胰腺急性排斥反应的严重程度显著相关，凋亡指数可作为判断移植物损伤程度的指标，对急性排斥反应的诊断有一定的参考价值。     

供体凋亡/坏死细胞对大鼠脾移植急性排斥反应的作用研究

目的 探讨供体凋亡与坏死细胞对大鼠脾移植急性排斥反应的作用及机制.方法 建立大鼠异位脾移植模型后,随机分为4组:A组输注生理盐水2 ml;B组输注供者凋亡细胞5×106;C组输注正常供体细胞悬液5×106;D组输注5×106坏死细胞.术后不同时间点每组取大鼠8只进行指标测定.结果 移植后脾出现排斥反应并逐渐加重,D组最为严重,A组和C组次之,B组最为轻微.各组移植脾匀浆和受体血清中IFN-γ水平逐步增加,为B组低于A组,而D组高于A组,A组与C组相似.B组大鼠移植脾匀浆和血清中TGF-β水平明显升高,其他各组TGF-β1水平持续于较低水平.凋亡细胞抑制混合淋巴细胞反应,而坏死细胞则作用相反.结论 供体细胞能够影响大鼠脾移植急性排斥反应,可能与细胞因子偏移和受体同种免疫反应性改变有关.     

猪肝肠联合移植免疫耐受的实验研究

目的 研究猪肝肠联合移植中肝移植物对同源小肠移植物免疫耐受的作用.方法 70头杂交长白猪分为4组,A、B、C组为辅助性同种异体肝肠联合移植(每组20头);D组为节段性间种异体小肠移植(10头).移植后A、D组未用免疫抑制剂治疗,B、C组分别采用常规剂量和小剂量的环孢素和甲基强的松龙治疗.结果 A组术后小肠移植物较D组排斥反应时间延迟,程度明显减轻(P＜0.05).常规剂量的B组与小剂量的C组在术后存活时间、排斥反应开始时间以及排斥反应程度方面差异无统计学意义(P＞0.05).结论 猪同种异体肝肠联合移植中肝移植物可以诱导同源小肠移植物免疫耐受.     

Apoptosis and CD8 and CD54 cell expression in rat small bowel transplantation

The importance of activated CD8 cells expressing IL-2R in small bowel and other organ rejection has been reported. Some authors even consider that a positive correlation might be demonstrated between the number of apoptotic enterocytes and the degree of graft rejection. In addition, moderate to intense activation of endothelial molecules in small bowel allograft in rats has been reported in chronic rejection. The aim of the present paper is to ascertain, in a heterotopic small bowel transplantation (HSBT) in rats, whether CD3, CD4, CD8, and CD54 cell expression in the allograft infiltrates shows some relationship with allograft enterocyte apoptosis when rejection is present. Wistar Furth male rats were allotted to two groups: group A was the control group without transplantation; group B received a heterotopic small bowel allograft from Fisher rats and an im dose of FK506 (0.25 mg/kg/day). A significant increase of CD8, CD54 cell receptor expression, and apoptosis in the group undergoing HSBT showed rejection. No significant differences have been observed in the variables under study between the control and HSBT without rejection groups or in CD3 and CD4 among the three groups. We observed a significant correlation between apoptosis and rejection, between CD8 and CD54 with apoptosis and with rejection, and between CD8 and CD54. This indicates that the activation of endothelial molecules and cells may play an important role in established HSBT chronic rejection. We consider that this study may contribute to the knowledge of small bowel allograft chronic rejection and its immunomodulation.     

Intestinal tight junction in allograft after small bowel transplantation

INTRODUCTION: In the intestinal physical barrier, tight junctions between intestinal epithelial cells play a central role. There is increasing evidence that rejection after small bowel transplantation promotes intestinal barrier injury to allografts. Our aim was to study the morphological changes of tight junctions in allografts during rejection. METHODS: Small bowel transplantation was performed using the F344 to Lewis rat model. Animals were divided into three groups: isogeneic controls, acute rejection group, and chronic rejection group. Allograft rejection was characterized by hemotoxylin and eosin staining of mucosal tissue sections. Tight junctions in grafts were investigated by transmission electron microscopy. RESULTS: Acutely rejected allografts showed severe mucosal injury and completely loosened tight junctions, while chronically rejected allografts revealed less mucosal injury and remained with partial integrity of their tight junctions. CONCLUSION: Our study demonstrated for the first time the morphological alterations of tight junctions in allograft mucosa during acute and chronic rejections, suggesting disruption of tight junctions was relative to the intestinal inflammatory processes.     

Effect of FTY720 and ex vivo graft irradiation in rat small bowel transplantation: apoptosis of crypt cells and lymphocytes

OBJECTIVE: We investigated the extent of apoptosis in crypt cells and Peyer's patches (PPs) during small bowel allograft rejection in rats to examine the effect of FTY720 and ex vivo graft irradiation during rejection. MATERIALS AND METHODS: Orthotopic small bowel transplantations (SBT) were performed from Brown Norway (BN) rats to Lewis (LEW) rats. Four groups of SBT animals were studied on days 3, 5, and 7 after operations: untreated allograft, allograft with FTY720, allograft with irradiation, and allograft with FTY720+irradiation. Cryostat sections were prepared from the grafts, including PPs. An in situ end-labeling (ISEL) technique was used to detect apoptotic cells. Indirect immunoperoxidase staining was also performed using monoclonal antibodies against rat Fas/FasL. RESULTS: The graft survival was prolonged in the FTY720-treated groups. In the FTY720-treated group, the number of ISEL-positive enterocytes was significantly down-regulated on days 3, 5, and 7 compared with the untreated allograft group. The number of ISEL-positive mononuclear cells was also significantly down-regulated compared with the untreated allograft group. The FTY720 the radiation and the FTY720+irradiation treated groups showed significantly down-regulated numbers of Fas/FasL-positive enterocytes on day 7 compared with the untreated allograft group. Fas/FasL-positive mononuclear cells were also significantly down-regulated in the allograft compared with the untreated allograft group. CONCLUSIONS: FTY720 and ex vivo graft irradiation prevented up-regulation of the number of apoptotic enterocytes, lymphocytes, and Fas/FasL-positive lymphocytes, and also prolonged small bowel allograft survival. Combination FTY720 and ex vivo graft irradiation did not affect graft survival and apoptotic cell expression compared with the FTY720 only group. These findings suggest that FTY720 may prevent both rejection-associated and sepsis-induced apoptosis during the late phase of small bowel graft rejection.     

Phenotypic and functional characteristics of intestinal intraepithelial lymphocytes during acute rejection of small intestinal allografts

Infiltration of a transplanted organ by host lymphoid cells is the hallmark of acute rejection. However, after intestinal transplantation, physiological lymphocyte migration may lead to host cell infiltration of the graft even in the absence of rejection. It is unclear whether this lymphocyte migration also involves the intraepithelial compartment of the graft or whether infiltration there is indicative of acute rejection. We demonstrate here that host cell infiltration of the intestinal mucosa occurs both during acute rejection of a small bowel allograft and, to a lesser extent, when rejection is prevented by immunosuppression with FK506. The infiltrating host cells consisted of CD3 ⁺ T cells with a predominant CD4^–CD8 ⁺ phenotype resembling intraepithelial lymphocytes (IELs). Functional studies showed that the nonspecific cytolytic activity of IELs was not affected by acute rejection or by immunosuppression with FK506. These findings indicate that host cell infiltration of the intestinal mucosa does not connote an ongoing acute rejection. Furthermore, the decreased mucosal barrier function during acute rejection of intestinal allgrafts is probably not due to impaired cytolytic activity of IELs. Received: 10 March 1997 Received after revision: 6 November 1997 Accepted: 19 November 1997     

小肠移植排斥反应期移植肠粘膜细胞凋亡的研究

目的 明确移植肠上皮细胞凋亡在小肠移植排斥反应中的意义及诊断价值。方法 选用近交系大鼠Ｆ３４４／Ｎ和Ｗｉｓｔａｒ／Ａ进行全小肠异位移植,实验分４组。第１组：非基本对照 ;第２组;同基因移植组;第３组;异基因移植组;第４组;异基因移植加环孢霉素Ａ治疗组。术的第３、５、７天取移植肠进行病理学检查,采用ＴｄＴ介导的脱氧核苷酸原位末端标记法（ＴＵＮＥＬ）检测移植肠上皮细胞凋亡。结果 病理学检查显示第３组大     

Immune responses of graft mesenteric lymph node in small bowel transplantation

BACKGROUND: The high proportions of lymphoid tissues are thought to be one of the underlying factors inducing severe allograft rejection following small bowel transplantation. Mesenteric lymph nodes (MLN) contained in the intestinal graft are not only a source of donor-derived professional antigen-presenting cells, but also offer a field for immune interaction between donor and host cells. We investigated immune responses in graft MLNs with or without FK506 to develop a novel strategy to control small bowel allograft rejection. MATERIALS AND METHODS: Heterotopic small bowel transplantations were performed from Brown Norway donors to Lewis recipients. Changes in population of lymphocytes, expressions of costimulatory molecules, apoptosis, and cytokine profiles in graft MLNs were evaluated. RESULTS: The increase in apoptotic cells and cytokine responses relating to rejection in the graft MLNs developed prior to those in graft jejunum. While donor lymphocytes in graft MLNs were rapidly replaced to host-derived lymphocytes independent of FK treatment, increase in CD8(+) T cells in host population was seen only in recipients without FK506 treatment. The expressions of B7 molecules on donor cells in graft MLNs were significantly lower in the recipients with FK treatment. CONCLUSIONS: Immune responses in graft MLNs have significant impact on the outcome of the small bowel allograft. Apoptosis of graft MLN cells was well correlated with and ahead of progression of acute rejection. Modulation of costimulatory molecules on donor-derived MLN cells in the allograft and specific suppression of host CD8(+) T cells are possible ways to control severe rejection after allogeneic small bowel transplantation.     

Preservation injury and acute rejection of rat intestinal grafts: Protection afforded by pyruvate

Pyruvate has been shown to prevent intestinal mucosal injury after ischemia-reperfusion. The aim of the present study was to determine whether pyruvate can (1) prevent postreperfusion mucosal injury occurring after intestinal preservation and subsequent transplantation and (2) exert a protective effect on the intestinal graft mucosa during acute rejection. Preservation mucosal injury was evaluated, after 2 hours of reperfusion, by comparing grafts transplanted in a rat syngeneic combination (ACI to ACI) after 2 hours of cold preservation using pyruvate (n = 6) or placebo (n = 6). Mucosal parameters obtained during acute rejection (allogeneic combination: ACI to Lewis) were compared between placebo-treated (n =6) and pyruvate-treated (n = 6) animals. Tissue injury was evaluated by histopathologic examination, oxygen free radical production by luminol-enhanced chemiluminescence, and degree of neutrophil infiltration by myeloperoxidase staining. After reperfusion of the preserved grafts and during acute rejection, mucosal oxygen free radical levels and the number of infiltrating neutrophils were significantly (P <0.05) increased in the untreated grafts, whereas there was a statistically significant inhibition of these parameters in those treated with pyruvate. Mucosal injury, seen after reperfusion of the preserved grafts, was prevented by pyruvate. The histopathologic abnormalities observed in the untreated grafts during rejection were also significantly reduced by pyruvate. Treatment with pyruvate before cold preservation of intestinal grafts, in this rat model, reduced reperfusion mucosal injury, neutrophil infiltration, and oxygen free radical production. Oxygen free radicals were produced in the mucosa of the graft during acute rejection and their production was reduced by pyruvate, which exerted a protective effect on the rejecting allograft mucosa.     

Small bowel allografts maintained by administration of bombesin while under immunosuppression

Background/Purpose: The aim of this study was to determine if Bombesin (BBS) could help maintain the mucosal villus state in small bowel allografts without inducing acute rejection under immunosuppression. Methods: Allogeneic small bowel transplantation was performed heterotopically in rats (n = 12). All rats received daily administration of FK506 from postoperative day 0 to day 28. On postoperative day 14, rats were divided into 2 groups of 6 rats each, and administered BBS or normal saline as a control. After 2 weeks of treatment, the rats were killed, and the graft mucosal villus state was evaluated by H[amp ]E staining, and crypt cell proliferation analysis was performed using immunohistochemistry with proliferative cell nuclear antigen (PCNA). Results: Villi were thin, and villus blunting was marked in the control group. The BBS group showed that the villi of the grafts were well maintained, and the volume of the lamina propria mucosa was adequately preserved. The PCNA labeling index of crypt cells in the control group was 40.06 [plusmn] 3.36 (mean [plusmn] SD) and that in the BBS group was 61.02 [plusmn] 4.27. There was a significant difference (P [lt ] .001) between the 2 groups. Conclusions: BBS maintained allograft epithelial cells and the volume of the lamina propria intestinal mucosa, stimulating proliferation of crypt cells under immunosuppression without inducing acute rejection. J Pediatr Surg 38:83-87.