肠血管活性多肽对多器官功能障碍综合征大鼠肠淋巴细胞归巢的影响

为观察肠血管活性多肽 (VIP )对大鼠肠缺血再灌注致多器官功能障碍综合征 (MODS )时 ,肠淋巴细胞归巢至肠相关淋巴细胞 (GALT )的调节以及对MODS转归的影响。本研究用微型无创动脉夹夹住大鼠肠系膜动脉根部 4 5min ,松夹后再灌注6h ,制备MODS模型。将VIP分别从股静脉输入和从腹腔注入大鼠体内。收集肠淋巴液 ,计数淋巴细胞总数及T、B淋巴细胞比例 ,了解淋巴细胞进入血循环状况。体外用51Cr标记肠淋巴细胞 ,回输入大鼠体内 ,用γ计数器检测各器官组织内的51Cr 肠淋巴细胞 ,了解肠淋巴细胞归巢。检测血及肠淋巴TNF α、内毒素 ;测定血D 乳酸、谷丙转氨酶 (ALT )、肌肝 (Cr)、血氧分压 ;观察重要器官组织学改变 ,评价VIP对MODS时各脏器形态及功能改变。结果显示 ,VIP使MODS大鼠肠粘膜迁移至血循环肠淋巴细胞总数 [(0 4 2± 0 18)× 10 7/h]较未予处理的MODS组 [(0 2 8± 0 15 )× 10 7/h]显著增加 (P <0 0 5 ) ,以T细胞数上升明显。VIP减少了MODS大鼠归巢至肠粘膜的肠淋巴细胞 ,Peyer淋巴结及小肠分布的51Cr 细胞量分别占总51Cr量的 2 14 %± 1 4 9%、 1 5 8%± 0 4 2 % ,显著低于未予处理的MODS组 (5 0 4 %± 1 2 3%和 3 2 3%± 1 6 9% ,P <0 0 1及P <0 0 5 )。外源性给予MODS大鼠VIP后 ,肠淋巴     

肠血管活性多肽或生长抑素抑制大鼠肠CD8~+淋巴细胞归巢

为观察肠血管活性多肽 (VIP )及生长抑素 (SST )对大鼠肠淋巴细胞在肠相关淋巴组织归巢的影响 ,本实验将 18只大鼠随机分为三组 ,每组 6只 ,分别从股静脉输入生理盐水、VIP组或SST ,从肠系膜淋巴管插管引流淋巴液。结果显示 ,大鼠经静滴VIP或SST后 ,5h内肠系膜淋巴管淋巴细胞总数降低 (P <0 0 5 ) ;肠淋巴液量和对照组比较无显著改变 (P >0 0 5 ) ;每毫升淋巴液中细胞数降低 (P <0 0 5 )。VIP组和SST组肠淋巴液中CD8+ 细胞比例降低 (P <0 0 5 )。两实验组回肠粘膜CD8+ 细胞数降低 (P <0 0 5 )。VIP或SST能减少肠粘膜CD8+ 淋巴细胞与其他器官及系统免疫的沟通 ,也抑制从其他器官及系统免疫中归巢至肠粘膜的CD8+ 细胞     

麻醉大鼠肠淋巴循环的研究

探讨肠淋巴循环的研究方法、参数及正常值，为淋巴学研究提供参考。方法：通过微循环显微电视技术，对７５只大鼠进行肠系膜淋巴微循环研究，同时采用肠淋巴管插管方法对６０只大鼠实施肠淋巴管插管，测定大鼠肠淋巴流量、淋巴蛋白输出量和肠淋巴管压力。结果：麻醉大鼠肠系膜淋巴管静态口径为１０３．８９± ７．１８μｍ，自主收缩频率为６０．１± ０．２２次／ｍｉｎ，淋巴管收缩分数（ＩｎｄｅＩ）为０．５６± ０．０３，总收缩活性指数（Ｉｎ－ｄｅｘⅡ）为１．７７±０．０９，肠淋巴流量为１０．７４±０．４９μｌ／ｍｉｎ，肠淋巴管压力为１．８５± ０．１７ ｋＰａ。结论：肠系膜淋巴管口径、收缩性参数及淋巴流量的测定，可用于淋巴循环的研究。     

胃肠多肽对肠粘膜肥大细胞稳定性的影响

目的 :为了探讨P物质 (SP)、生长抑素 (SST)、血管活性肠肽 (VIP)等胃肠多肽对离体的大鼠肠粘膜肥大细胞 (IM MC)释放组胺及颗粒的影响。方法 :采用胶原酶消化分离并纯化大鼠肠粘膜肥大细胞 ,加不同浓度胃肠多肽孵育 ,测定细胞及上清液组胺浓度 ,计算组胺释放率 ,透射电镜观察细胞超微结构变化。结果 :①正常大鼠IMMC的组胺自然释放率为 (2 2 86±3 2 2 ) %。②SP促进大鼠IMMC组胺释放 ,其效应与SP浓度呈正相关 ,r=0 983,P <0 0 1。SP促使IMMC总组胺量显著高于对照组 ,P <0 0 1。③SST显著降低IMMC组胺释放率 ,其效应与SST浓度呈负相关 ,r=- 0 991,P <0 0 1。但IMMC总组胺量与对照组比较无显著变化 ,P >0 0 5。④在浓度为 1× 10 - 5～ 1× 10 - 8mol L范围内 ,随VIP浓度降低 ,IMMC组释放率呈剂量相关性升高。但继续降低VIP浓度至 1× 10 - 9mol L时 ,IMMC组胺释放率降低至自然分泌状态 ,随着VIP浓度的继续降低 ,组胺释放无明显变化。结论 :SP、SST分别以剂量依赖方式促进和抑制IMMC组胺释放。VIP对IMMC稳定性的影响取决于不同的VIP浓度范围。     

受体淋巴细胞向小肠移植物相关淋巴组织迁移的实验研究

目的：动态分析移植小肠各淋巴组织内供、受体淋巴细胞的表型及免疫状态，以推断其在小肠移植排斥反应中的作用。 方法： 小鼠小肠移植后2、4、6 d，观测移植物排斥病理形态变化，流式细胞术分析移植物肠系膜淋巴结（MLN）、派氏结（PP）、粘膜上皮细胞间淋巴组织（IEL）与固有层淋巴组织（LPL）中淋巴细胞中供、受体淋巴细胞的比例及激活状态。 结果:在移植后6 d，组织学观测到移植物开始出现排斥征象；移植后2、4 d，移植肠MLN、PP内受体来源的淋巴细胞迅速取代供体细胞，而移植肠IEL与LPL内受体来源的淋巴细胞比例增加速度略慢，但在移植后6 d也基本取代供体细胞；在移植后4 d，受体来源的T细胞表达激活分子CD69与CD25的比例达到89.8%±3.4％和84.5%±10.2％，显著高于供体T细胞与受体自身肠道中的T细胞。 结论:移植小肠内的淋巴组织在移植后早期即被受体来源的淋巴细胞迅速取代并激活，抑制这一过程可应用于缓解排斥反应。     

腹泻型肠易激综合征模型大鼠肠道Cajal间质细胞的变化及意义

目的：通过检测肠壁组织中酪氨酸激酶受体C-kit蛋白（C-kit）的表达及分布，观察Cajal间质细胞在腹泻型肠易激综合征模型大鼠小肠、回盲部及结肠中的变化，并初步探讨其变化在肠易激综合征中的意义。方法：通过对新生大鼠结直肠扩张（colorectal distension，CRD）制备肠易激综合征模型，40 d后观察大便性状；通过腹壁回撤反应(abdominal withdrawal reflex，AWR)评分评估内脏敏感性；小肠、回盲部及结肠组织常规HE染色，光镜下观察病理学变化；免疫组化检测肠壁组织中C-kit的表达及分布。结果：实验组大鼠大便Bristol评分明显升高；在相同压力的直肠刺激下AWR评分明显高于对照组；小肠、回盲部及结肠组织的C-kit表达显著增强。结论：新生大鼠结直肠扩张可以制备肠道分泌、运动和内脏敏感性均增强的肠易激综合征模型；Cajal间质细胞可能在腹泻型肠易激综合征发病中有重要的意义。     

痢疾杆菌口服免疫小鼠肠道相关淋巴组织中CD45R~+和CD45RB~+细胞动态变化的观察

为了解肠道相关淋巴组织（GALT）对痢疾杆菌口服免疫的应答状况,分离了Shigella fiexneri四次免疫后Balb/c 小鼠牌（SP）、肠系膜淋巴结（MLN）、Peyer’s结（PP）、固有膜（LP）和上皮内（IE）淋巴细胞,对末次免疫后1～13d内免疫组与对照组GALT中的CD45R~+和CD45RB~+细胞群作了FACS分析。结果免疫后起初7d IE和LPCD45R~+细胞增加而MLN和PP CD45R~+细胞减少。CD45RB~+LPL在起初4d增加,而CD45RB~+IEL总是低于对照。CD45RB~(lo)/CD45RB~(hi)比例在SP和MLN中几乎无变化,但在PP中先降至最低后上升并超过对照。LP中主要为CD45RBD~(lo),IE中主要为CD45RB~(hi)。这些结果在一定程度上反映了粘膜淋巴细胞CD45表达的组织特异性及在痢疾杆菌免疫后B细胞、记忆细胞和辅助细胞的功能状态和变化趋势。     

肝细胞生长因子对重症急性胰腺炎小鼠肠黏膜屏障保护作用

目的探讨肝细胞生长因子（HGF）对重症急性胰腺炎（SAP）小鼠肠黏膜屏障功能障碍修复作用及机制,以及肠道干细胞在黏膜损伤修复中的作用。方法健康雄性昆明小鼠60只,按数字表法随机分成正常对照（NC）组10只、SAP组25只和HGF组25只。酶耦联紫外分光光度法检测血清D哥L酸水平,肠系膜淋巴结、胰腺、肝脏、脾脏及肺组织细菌培养,流式细胞仪检测肠上皮细胞增殖指数,免疫组化染色法检测小肠隐窝干细胞变化。结果SAP组血清D-乳酸值为（11．17±1．90）mg／L,较NC组（4．87±0．73）mg／L和HGF组（7．30±0．88）mg／L高,差异均有统计学意义（F=78．20,P值均〈0．01）。胰腺、肠系膜淋巴结、肝脏、脾脏、肺脏细菌培养器官移位率SAP组（50％,40／80）高与NC组（14％,7／50）和HGF组（29％,29／100）（χ^2=7．427,χ^2=4．112,P值均〈0．01）。肠黏膜上皮细胞增殖指数SAP组较NC组和HGF组明显下降（F=42．71,P值均〈0．05）,HGF组与NC组比较则明显升高（P〈0．01）。SAP组小肠隐窝干细胞数（1．26±0．87）个,低于NC组（2．16±0．90）个和HGF组（2．50±0．96）个,差异均有统计学意义（F=8．34,P值均〈0．01）。结论HGF可促进肠黏膜上皮细胞的增殖,降低肠道通透性及肠道细菌移位率,减轻急性胰腺炎小鼠肠黏膜的损伤。     

重症胰腺炎大鼠肠道免疫功能改变及精氨酸的调节作用

目的：探讨重症急性胰腺炎（Severe Acute Pancreatitis，SAP）大鼠肠道黏膜免疫功能变化及L-精氨酸（L-Arg）对SAP大鼠肠道黏膜免疫功能的影响。方法：成年、雄性Wistar大鼠随机分为胰腺炎组、假手术组和L．精氨酸治疗组。分别于造模后24、48和72小时取标本检测：鲎试剂法检测大鼠门静脉血内毒索水平、免疫组化方法检测并计数小肠黏膜固有层内CD3、CD4、CD8阳性T淋巴细胞百分数、放射免疫法检测盲肠内容物中分泌型IgA（sIgA）含量。结果：SAP组大鼠各时段门静脉血内毒素水平显著升高，回肠末段黏膜固有层CD3^＋、CD4^＋T淋巴细胞百分数明显减少，CD^＋／CD8^＋T淋巴细胞比值降低，盲肠内容物sIgA含量明显降低；与SAP组比较，L-精氨酸组大鼠各时段门静脉血内毒素水平明显降低，回肠末段黏膜固有层CD3^＋、CD4^＋T淋巴细胞百分数明显增加，CD4^＋／CD8^＋T淋巴细胞数比值升高，盲肠内容物SIgA含量增加。结论：SAP大鼠早期即发生肠黏膜免疫功能明显下降，可能是导致肠道内毒素移位的主要原因，L-精氨酸可以改善SAP大鼠肠道黏膜免疫功能，降低SAP大鼠肠道内毒索移位发生。     

114例非何杰金氏淋巴瘤病理及免疫组织化学研究

使用免疫组化方法，按国际工作分类（ＷＦ）方案，对长春地区１１４例非何杰金氏淋巴瘤进行组织学分析。结果表明，Ｂ系淋巴瘤９３例（８１．６％），其中弥漫型大无裂细胞性淋巴瘤发病率最高（４４例，３８．６％），小淋巴细胞性淋巴瘤发病率最低（３例，２．６％）。Ｔ系淋巴瘤２１例（１８．４％），以淋巴母细胞性淋巴瘤最多见（１０例，８．８％）。原发部位结性占５４．４％，以颈部淋巴结发病率最高，其次为肠系膜及后腹膜淋     

肠肌成纤维细胞与IBD相关肠纤维化

 肠纤维化是炎症性肠病(inflammatory bowel disease, IBD)的并发症,肠肌成纤维细胞是肠纤维化的关键细胞。肠肌成纤维细胞及其与炎症细胞的相互作用在IBD相关肠纤维化发生中起重要作用。     

Gastric and intestinal mixed and solely intestinal types of intestinal metaplasia in the human stomach

To generate a novel understanding of Intestinal metaplasia (IM) on the basis of cellular differentiation status, a total of 132 gastric surgical specimens were studied using gastric and small intestinal cell markers by much histochemical and Immunohistochemical techniques. The cases were divided into two types: (i) gastric and intestinal (GI) mixed type; and (ii) solely intestinal (I) type, with the reference to the presence of gastric and/or intestinal cell markers. The GI mixed type was subdivided into six subtypes: (i) a subtype consisting of surface mucous (Su), pyloric gland (Py), Intestinal absorptive (Ab), and goblet (Go) cells, but lacking Paneth (Pa) cells, GI(Pa-); (ii) a GI(Pa-) subtype without Py cells, GI(Py-, Pa-); (iii) a GI(Pa-) subtype without Su cells, GI(Su-, Pa-); (iv) a GI(Su-, Pa-) subtype with Pa cells, GI(Su-, Pa+); (v) a Gi(Pa-) subtype with Pa cells, GI(Pa+); and (vi) a GI(Pa+) subtype without Py cells, GI(–, Pa+).The I type was subdivided Into: (I) a subtype consisting of cells with Ab and Go cells, I(Pa-); and (ii) a I(Pa-) subtype with Paneth cells, I(Pa+). The GI mixed subtypes, except for the GI(Py-, Pa-) and GI(Py-, Pa+), were characterized by Intestinalized gastric plts connected with underlying pyloric glands. Immunohistochemical staining of proliferating cell nuclear antigen (PCNA) revealed a common prolifemtive cell zone between the two. The GI mixed type, especially the GI(Pa-) subtype, predominated in the pyloric mucose, while the I type was most frequent In the fundle region, suggesting that the pathogenesis of IM differs between these two locations. The results of the study confirm that IM is an abnormal and unstable differentiation status between the stomach and small Intestine.     

Importance of the intestinal inflammatory reaction in salmonella-mediated intestinal secretion.

The ability of Salmonella typhimurium to invade the intestinal epithelium is essential to the pathogenesis of salmonella-induced intestinal secretion. This invasion is accompanied by an intense acute inflammatory reaction. The present study tests the hypothesis that the acute inflammatory reaction may have a role in the pathogenesis of salmonella-induced secretion. Two groups of rabbits infected with S. typhimurium were studied: normal animals and animals pretreated with nitrogen mustard. Nitrogen mustard depletes the polymorphonuclear leukocyte pool and thereby prevents the formation of an acute inflammatory reaction. In vivo ligated ileal loops were constructed and infected 72 h after nitrogen mustard administration when polymorphonuclear leukocytes were undetectable. Nitrogen mustard treatment markedly inhibited salmonella-induced secretion. Ileal histology in normal animals infected with S. typhimurium revealed an intense acute inflammatory reaction, while in animals pretreated with nitrogen mustard only a rare polymorphonuclear leukocyte was seen. The antisecretory effect of nitrogen mustard was not merely a nonspecific effect since nitrogen mustard treatment did not inhibit cholera toxin-induced secretion and did not alter either ileal morphology nor the activities of various intestinal enzymes in normal animals. Nitrogen mustard also did not alter the virulence of the inoculated S. typhimurium. These data suggest that the mucosal inflammatory reaction induced by salmonella invasion may be important to the pathogenesis of the salmonella secretory process. The mechanism by which the inflammatory reaction stimulates secretion is not known.     

Accumulation of donor-specific cytotoxic T cells in intestinal lymphoid tissues following intestinal transplantation

Utilizing a rat model of semiallogeneic intestinal transplantation, recipients were evaluated for accumulation of donorspecific cytotoxic T cells in spleen, mesenteric lymph nodes, Peyer's patches, lamina propria, and intraepithelial lymphocytes using limiting dilution analysis. Naive animals exhibited a low frequency of cytotoxic T cells in spleen and mesenteric lymph nodes with minimal activity detected in Peyer's patches and intraepithelial lymphocytes, but no detectable activity in lamina propria. Orthotopic intestinal transplantation resulted in significant increases in cytotoxic T-cell activity in recipient Peyer's patches as early as Day 6 and by Day 8 in spleen, mesenteric lymph nodes, lamina propria and intraepithelial lymphocyte populations. Graft lamina propria and intraepithelial lymphocytes exhibited significant cytotoxic T-cell activity as early as 4 days following transplant. The highest donorspecific cytotoxic T-cell activity was observed in graft intraepithelial lymphocytes on Day 8 posttransplant. These studies demonstrate rapid expansion of donor-specific cytotoxic T cells which migrate to the graft site within 4 days after semiallogeneic intestinal transplantation.     

Solitary intestinal fibromatosis in the newborn. Rare cause of neonatal intestinal obstruction

We describe a case of solitary fibromatosis of the ileum in an infant. Intestinal fibromatosis is a rare cause of intestinal obstruction in the newborn. The disease is poorly characterized and has been rarely reported under this name. The differential diagnosis is discussed with particular attention to inflammatory fibroid polyps, neurofibromatosis, and sarcoma. Reasons of a theoretical and practical nature are outlined that recommend the term "solitary intestinal fibromatosis" as the most appropriate name for this disease.     

Histopathogenesis of intestinal metaplasia: minute lesions of intestinal metaplasia in ulcerated stomachs.

Minute lesions of intestinal metaplasia composed of a few metaplastic tubules were observed in the gastric mucosa during routine histological examination of gastrectomy specimens. The histological findings indicated that these lesions might be an initial stage of more advanced intestinal metaplasia. Accordingly, more than 18,000 serial sections in 10 stomachs with chronic ulcers were examined to clarify the histopathogenesis of the intestinal metaplasia. It was concluded from the three dimensional reconstruction of minute intestinal metaplasia lesions that these lesions originated during the regenerative process of healing of gastric erosions. The lesions were roughly globoid with a depression on the surface. It is thought that with continuous formation and healing of gastric erosions, more extensive intestinal metaplasia lesions would be formed by an increase in size and confluence of these focal minute intestinal metaplasia lesions.     

Dysregulation of laminins in intestinal inflammation

Laminins are structural components of basement membranes that regulate and control many cellular functions. Changes in basement membrane composition play significant roles in etiology of diseases. Inflammatory bowel diseases are conditions that lead to defects in the mucosal barrier which includes the basement membrane underlying the epithelium. This review will summarize the main findings related to the involvement of laminins and of the laminin-binding receptors in inflammatory conditions such as Crohn's disease and ulcerative colitis. We will review the current literature devoted to studies in humans (immunolocalisation, genetic factors, microarray data), as well as experimental cell models that show that laminins contribute to the inflammation process probably linked to the deregulation of proinflammatory cytokines.     

Immunoglobulin-containing cells in the intestinal mucosa and immunoglobulins in the intestinal juice in children

The numbers of immunoglobulin-containing cells in the mucosae of the small intestine and rectum were counted by a direct immunofluorescence technique in biopsy specimens from children. Immunoglobulins in the intestinal juice of the same patients were quantified by electroimmunodiffusion. In all biopsy specimens IgA-containing cells predominated. These cells were more numerous in the specimens from children over 2 years of age than in those of younger ones. The cells seemed to be fairly evenly distributed along the intestinal tract. The number of IgM-containing cells did not change with age in the group studied.

In the intestinal juice the mean content of IgA was higher than that of the other immunoglobulins. More IgM and less IgA were found in the juice of infants under 2 years of age than in that of older children.

The results suggest that quantitatively the IgA-producing system of the gut is not fully developed in infancy, whereas the reverse is true for the cells producing IgM.