一例疑似黏膜病死亡麋鹿消化及主要免疫器官病理组织学观察

应用常规石蜡切片,H.E染色,对临床初步诊断为黏膜病的一例死亡麋鹿(Elaphodus davidianus)的消化系统及脾、淋巴结进行病理组织学观察。结果表明,消化道的病变主要在黏膜层,黏膜上皮细胞脱落、坏死,固有层内毛细血管充血,炎性细胞浸润;脾主要表现为急性败血型,红髓充血、出血严重,白髓几乎完全消失;淋巴结坏死严重,组织结构被破坏,界限不明显,仅见淋巴细胞弥漫性分布于整个淋巴结内。病理组织学观察为临床诊断提供了形态学依据。     

嗜麦芽寡养单胞菌胞外产物对斑点叉尾损伤的病理学研究

采用硫酸铵盐析从嗜麦芽假单胞菌培养物中提取其胞外产物,通过腹腔注射方式,进行了嗜麦芽假单胞菌(P.maltophilia)胞外产物对斑点叉尾(Ictalurus punctatus)损伤的系统病理学研究。结果表明,嗜麦芽假单胞菌胞外产物具有较强的毒力,对斑点叉尾(42.5±4.4)g的半致死剂量(LD50)为3.21mg蛋白/kg体重。病鱼出现神经症状,腹部和下颌充血、出血,腹部膨大,腹腔内充满大量淡黄色或带血的腹水,胃肠道黏膜充血、出血,肠套叠,肝、脾、肾肿大等临床病变。组织学病变主要表现为全身多组织、器官水肿,出血、变性、坏死以及炎症反应,特别是脑、骨骼肌、肝、脾、肾和胃肠道的损伤较为严重。超微结构观察发现病鱼肝、脾、肾和骨骼肌等器官的细胞的超微结构均有较为严重的破坏,线粒体肿胀,嵴断裂或溶解消失,呈空囊状,内质网扩张,细胞核变形,染色质溶解或固缩;研究中还发现嗜麦芽假单胞菌胞外产物可致淋巴细胞凋亡,脾和肾间质内淋巴细胞均表现为细胞核染色质浓缩边移,或核固缩成一个或数个团块凝聚在核膜周边,形成凋亡小体。     

乙酸诱导建立大鼠急性直肠黏膜损伤模型的形态学观察

目的通过形态学观察评价乙酸诱导建立急性直肠黏膜损伤模型的效果。方法将含有4%乙酸溶液的棉签经SD大鼠肛门置入直肠1 min,置入深度为3 cm,诱导大鼠形成急性直肠黏膜损伤,并于损伤后0.5 h和1、4、6 d分别解剖大鼠,对直肠进行大体形态观察和组织病理学分析。结果损伤后大鼠6 d内全部存活,模型成功率为100%。损伤后0.5 h~1 d,大鼠直肠黏膜大体形态由充血、水肿和溃疡到合并出血,镜下形态见黏膜层由上皮组织坏死伴出血到黏膜组织全层坏死,腺体由部分留存到全无,黏膜下层由水肿到合并充血、出血,间质内由血管扩张充血到炎细胞浸润;损伤后4~6 d,直肠黏膜大体形态仍可见部分水肿和血丝,镜下形态见黏膜上皮有部分留存,损伤部位有炎性肉芽组织增生,黏膜充血、出血减轻。结论 4%乙酸作用于直肠1 min能成功诱导建立大鼠急性直肠黏膜损伤模型,该模型操作方便、成功率高、重复性好,损伤维持时间6 d以上,适合作为快速筛选直肠外用药物疗效的动物模型。     

荧光假单胞菌感染大鲵的病理损伤

通过对感染荧光假单胞菌(Pseudomonas fluorescents)发病的大鲵(Andrias davidianus)主要器官进行病理剖解和病理组织学观察,以明确大鲵感染荧光假单胞菌引起的病理学损伤特点。结果表明,大鲵感染荧光假单胞菌后,主要表现为腹部极度膨胀、腹水和严重胃肠道反应,严重者可见将胃呕吐至口腔;组织器官具有典型的病理变化,其主要靶器官为肾、肝、肠道、皮肤和肌肉。分别引起坏死性肾小球肾炎、肝炎。此外,还可引起轻微肠炎及皮炎。可在肾小管管腔内、肝细胞坏死灶内、肠道固有层内及皮肤肌肉中发现数量极多的杆状细菌。     

广东乌龟五种器官的组织学观察

利用石蜡切片法对广东乌龟的心脏、肝脏、脾脏、肺和肾脏等组织器官进行了组织结构观察.结果显示,心肌纤维束状排列,可见闰盘结构.肝脏分3叶,肝内结缔组织很少,相邻肝小叶分界不清.肝血窦内含色素细胞.脾脏分被膜和实质两部分.实质可分为白髓和红髓.白髓包括椭球周围淋巴鞘(PELS)和动脉周围淋巴鞘(PALS).红髓由脾索和脾窦组成.未发现淋巴小结和生发中心.肺为一对长形扁平囊.支气管黏膜上皮为假复层柱状纤毛上皮.细支气管的黏膜为单层柱状纤毛上皮.肺泡囊状.肾脏由肾小体、颈段、近曲小管、中间段、远曲小管、收集管等部分构成.颈段和中间段均由单层纤毛立方上皮细胞构成.近曲小管、远曲小管和收集管均由单层柱状上皮细胞构成.     

家兔生后外周淋巴器官的组织形态学研究

本文探讨了不同发育阶段家兔淋巴结和脾的组织学年龄性变化,研究结果表明:1.初生时期淋巴结和脾脏均未达到成年水平,淋巴结皮质较薄,且呈弥散性;髓质琉松,含结缔组织较多,淋巴细胞稀少。2.具有生发中心的淋巴小结和脾小体在30日龄时出现。3.网状纤维在淋巴结主要分布于淋巴小结的外周;在脾白髓区域的网状纤维丰富而粗大。     

益生菌抑制肠上皮细胞凋亡与新生儿坏死性小肠结肠炎

新生儿坏死性小肠结肠炎（NEC）是新生儿时期严重的肠道炎症性疾病,早产儿低出生体重儿尤为高危,死亡率居高不下,其病理生理复杂,目前公认的病因包括早产、肠壁缺氧缺血、肠道喂养和肠道细菌感染等,其病理改变以肠黏膜片状坏死甚至肠壁全层坏死为特征。近年研究发现,肠上皮细胞凋亡是NEC早期肠上皮细胞死亡的主要形式,是NEC进一步发展的必经阶段。     

鼠痘的病理诊断及分析

鼠痘是由鼠痘病毒引的实验小鼠的一种烈性传染病,分为急性和慢性两型,但大部分为隐性感染。鼠痘的病理组织学特点是,出现皮疹,肝脏、脾脏、肠道、淋巴结、肾脏等出现程度不同的灶性坏死,在这些损伤部位的上皮细胞和内皮细胞出现境界清楚、周围有晕、成群存在、嗜酸性胞浆内包涵体．利用鼠痘抗体,通过免疫酶组织化学染色,可以对组织内鼠痘病毒进行定位诊断。电镜下,在肝脏等组织内可观察到鼠痘病毒颗粒。     

应用绿色荧光蛋白标记迟缓爱德华菌感染斑马鱼

目的建立斑马鱼模型研究迟缓爱德华菌的致病性及感染途径。方法应用绿色荧光蛋白标记迟缓爱德华菌,追踪观察其感染斑马鱼的动力学过程及病理组织学变化。结果病理组织学检查以肝脏水肿变性,肝细胞萎缩、坏死、脱落,脾脏散在增生性结节、充血、水肿、淋巴细胞大量缺失等病变为主;感染后,该菌先后在斑马鱼肠道、鳃和皮肤中定植。结论斑马鱼可作为研究迟缓爱德华菌致病性的动物模型。肠道、鳃和皮肤可能是迟缓爱德华菌先后感染斑马鱼的主要途径。     

朱鹮幼雏大肠杆菌病的病理组织学观察

对一例大肠杆菌病死亡的5日龄朱鹮进行了系统的病理组织学观察。结果发现：肺内小静脉充血、出血,肺间质有大量的炎性细胞浸润。肝脏血管有“血管套”现象,肝细胞变性、坏死。肾小管上皮细胞变性、坏死,肾内炎性细胞浸润。心肌间隔增宽,肌纤维断裂。脑中有“卫星化”和“嗜神经”现象。小脑蒲肯野氏细胞肿胀。各段消化管上皮均有不同程度的轻微脱落和局部炎性细胞浸润。胰腺、气管无明显变化。     

STUDIES ON LYMPHOCYTES

Continuous extracorporeal irradiation of the circulating blood (ECIB) of from 3 to 501/2 hr duration was used to study in the calf the differential depletion of lymphocytes from spleen, lymph nodes and thymus as compared to blood and thoracic duct lymph. The cell content of tissues was measured by planimetry and/or test point analysis. Lymphocyte depletion by ECIB from various lymphoreticular organs, and from different areas within a given organ, was less than in the circulating blood or the thoracic duct lymph and varied from one site of a lymphoreticular organ to another. The degree of depletion with time followed an exponential function with at least two components. The first component corresponded to a relatively rapid fall and the second to a very slow reduction in lymphocyte content. The former is related to the elimination of an easily mobilizable pool of lymphocytes while the latter corresponds to a more sessile mass of lymphocytes which exchange with blood lymphocytes very slowly. Elimination of the easily mobilizable pool of lymphocytes by ECIB from all tissues studied was observed within 10–15 hr, indicating that the rate of exchange with blood is similar for this group of cells in various lymphoreticular tissues. The size, however, of the easily mobilizable vs the more sessile pools of lymphocytes may vary considerably, the best estimates for the former being as follows (in per cent of total lymphocyte mass): lymph node medulla, less than 10%; lymph node cortex plus paracortical zone, 18% (depletion mainly paracortical); red pulp of the spleen, 37%; densely populated white pulp of the spleen, 55%; and loosely populated white pulp of the spleen, 60%. In comparison, the approximate fractions of lymphocytes originating fromthe easily mobilizable pools in various lymphoreticular tissues plus the cells already circulating a t the onset of EClB correspond to 64% for the thoracic duct lymph and 78% for the circulating blood respectively. These findings are discussed in relation to production, recirculation and life span of lymphocytes, and immune reactions.     

Septicemic listeriosis in a reindeer calf

Septicemic listeriosis is described in a 2-day-old reindeer calf (Rangifer tarandus tarandus) from a local zoo. The gross and microscopic lesions were typical of disease caused by bacterial septicemia. Major lesions included necrosis of the liver, lung, adrenal gland, spleen, and lymph node. The diagnosis was suspected by special histopathological stains and confirmed by isolation of Listeria monocytogenes from multiple organs. This is the first report of listeriosis in a reindeer.     

Antigenic relationship between medullary thymocytes and a subpopulation of peripheral T cells in the rat: description of a masked antigen.

Using differentially absorbed rabbit antisera to rat thoracic duct cells, an antigen is described which normally is expressed on the surface of T cells in thoracic duct lymph and lymph node, but which exists in a masked form on medullary thymocytes and apparently not at all on cortical thymocytes. This antigen is termed the rat masked thymocyte antigen (RMTA). RMTA on medullary thymocytes can be unmasked mechanically by sectioning in a cryostat or enzymatically by treating with neuraminidase. Trypsin destroys or removes RMTA. Nearly all the T cells in thoracic duct lymph and lymph node are RMTA⁺, whereas only 58–66% of T cells in spleen are RMTA⁺. RMTA⁺ T cells, which are cortisone resistant, reside in the paracortex and periarteriolar sheath regions of lymph node and spleen. RMTA^? T cells, which are cortisone sensitive, appear to reside in the red pulp of spleen. The results suggest that (i) two antigenically distinct populations of T cells exist in the rat, RMTA⁺ and RMTA^? T cells, (ii) medullary thymocytes are the immediate precursors of RMTA⁺ T cells, and (iii) cortical thymocytes may be the immediate precursors of RMTA^? cells.     

人体胸腺和周围淋巴器官内T细胞亚群和NK细胞分布的研究

本文用多种Ｔ细胞和ＮＫ细胞单抗和免疫组织化学的ＡＢＣ技术,在冰冻切片上对人扁桃体、淋巴结、牌和胸腺内Ｔ细胞亚群和ＮＫ细胞的分布进行了检测。结果显示,ＣＤ５、ＣＤ８、ＣＤ４、ＣＤ３和ＡＩＧ３阳性细胞主要分布在扁桃体,淋巴结的副皮质区、脾的动脉周围淋巴鞘和胸腺,但各种抗体的反应强度不同。从各种Ｔ细胞工群的染色强度和形状看,胸腺髓质部的胸腺细胞相当于周围淋巴器官内的胸腺依赖区。胸腺内Ｔ细胞在分化过程中,质膜上的抗原也有相应变化。ＮＫ细胞主要分布在淋巴小结的生发中心,淋巴结和扁桃体的副皮质区,脾的红髓以及胸腺的筋质部。这些不同的分布,说明ＮＫ细胞不仅与淋巴小结的活动有关,可能还参与机体的免疫调节功能。     

Immunohistochemical analysis of human peripheral blood and lymphoid tissues using monoclonal antibodies immunoreactive with non-lymphoid cells

Immunoperoxidase methods were used to study human peripheral blood and lymphoid tissues using a panel of monoclonal antibodies to non-lymphoid cells. The majority of peripheral blood monocytes were immunoreactive for LeuM1, LeuM2, LeuM3 and LeuM5. Rare peripheral blood monocytes were immunoreactive for R4/23. The different antibodies showed characteristic patterns of immunoreactivity in peripheral lymphoid tissues. LeuM1 was immunoreactive with scattered cells in the paracortex of lymph node and tonsil and with many cells in the marginal zone of the spleen. LeuM2 was immunoreactive with endothelial cells in lymph node and tonsil. A few cells in the red pulp of the spleen were immunoreactive for LeuM2. LeuM3 and R4/23 showed distinctive immunoreactivity in germinal centers of secondary follicles, giving a "lacy" pattern. LeuM3 was also immunoreactive with endothelium in lymph node and tonsil and with sinus lining cells in lymph node. LeuM5 was immunoreactive with macrophages in the germinal center, fibroblastic reticulum cells in the mantle zone and interdigitating reticulum cells in the paracortex of lymph node and tonsil.     

3H-deoxythymidine incorporation in graft-versus-host disease in the Norway rat. II. Autoradiographic studies.

A sequential analysis was made of various areas within the lymph nodes and spleen of newborn Brown Norway (BN) rats suffering from graft-versus-host disease (GVHD) subsequent to an allogeneic injection of adult Lewis (L) lymph node cells (experimental). One micron thick autoradiographs were compared between such experimental and control littermates having received the same number of syngeneic adult BN cells. Both experimental and control animals received tritiated deoxythymidine (3HdT) one hour before killing. The autoradiographs revealed a 2.25 and 2.50 times higher thymidine labeling index of lymphocytes in the deep cortex of mesenteric lymph nodes and white pulp of the spleen, respectively, for experimental animals. The experimental effect occurred within one day. The majority of the labeled cells in experimental animals were large lymphoblasts with prominent nucleoli. The labeling index within these areas remained significantly higher than control values until day 8 in the spleen and through day 14 within the lymph nodes. However, differences in labeled cells present in high powered microscopic fields reached a peak on day 3 within compartments in experimental animals but fell significantly below control values by day 9 owing to a pronounced disappearance of both small and large lymphocytes from these areas, and a decreased intensity of individual cell labeling as the reaction progressed. In contradistinction the concentration of labeled cells present in high powered microscopic fields of lymph nodes' medulla became 3.13 times controls by day 4. Most of these labeled cells contained a more basophilic cytoplasm than those found in the deep cortex and some were distinctly plasma cell precursors. In contrast to the deep cortex their concentration remained approximately three times control values until death. The data indicates that the major proliferative events within the spleen and lymph nodes in neonatal rat GVHD are initially restricted to donor cell localization areas of these tissue compartments. Subsequently the GVHD-related events may be attributed to other areas and possibly cell types. Thus any proliferation contributing to splenomegaly in the latter stages of GVHD appears to occur in the red pulp and that contributing to lymph node enlargement a medullary response.     

Differential response of B cells in the lymph node and the spleen to bacterial lipopolysaccharide

In vivo polyclonal activation of B cells in the lymph nodes and the spleens of mice injected with bacterial lipopolysaccharide (LPS) was compared. The peak of anti-trinitrophenylated sheep red blood cells plaque-forming cell (PFC) response in the lymph node was reached 6-8 days after the injection of LPS while that in the spleen was reached at 2 days. The maximal increase in the total number of Ig-producing cells in the lymph node also occurred at the later stage. These differences in time courses of polyclonal activation of B cells between the lymph node and the spleen were not due to the absence of B cells in the lymph node, migration of PFC from the spleen to the lymph node, or qualitative differences of B cells. This phenomenon was dependent on the environmental difference between the lymph node and the spleen, because B cells from the lymph node could respond to LPS rapidly in the spleen. Further, the polyclonal activation of B cells was accelerated in the lymph nodes of mice receiving prior injection of LPS. In in vitro cultures of lymph node cells of those mice, a significant amount of interleukin-1 could be detected by stimulation of LPS. It was possible that the delayed activation of B cells in the lymph node was due to the time lag necessary for construction of the environmental condition suitable for activation of B cells, whereas in the spleen this condition can be provided without delay.     

Trichinella spiralis: the influence of short chain fatty acids on the proliferation of lymphocytes, the goblet cell count and apoptosis in the mouse intestine

This study was carried out to determine the influence of short chain fatty acids (SCFA) on spleen and mesenteric lymph node lymphocyte proliferation, goblet cells and apoptosis in the mouse small intestine during invasion by Trichinella spiralis. BALB/c mice were infected with 250 larvae of T. spiralis. An SCFA water solution containing acetic, propionic and butyric acids (30:15:20 mM) was administered orally starting 5 days before infection and ending 20 days post infection (dpi). Fragments of the jejunum were collected by dissection 7 and 10 dpi, and were examined for apoptotic cells in the lamina propria of the intestinal mucosa, and for goblet cells. The proliferation index of the cultured spleen and mesenteric lymph node lymphocytes with MTT test was also determined. The orally administered SCFA solution decreased the proliferation of mesenteric lymph node lymphocytes in the mice infected with T. spiralis at both examination times, but did not influence the proliferative activity of the spleen cells. Seven dpi, both in the spleen and mesenteric lymph nodes, the highest proliferation index of concanavalin A (Con A)-stimulated lymphocytes was found in the group of uninfected animals receiving SCFA animals. This tendency could still be seen 10 dpi in the mesenteric lymph nodes but not in the spleen, where the proliferation index in this group had significantly decreased. In vitro studies revealed, that butyric and propionic acids added to the cell cultures suppressed the proliferation of Con A-stimulated mesenteric lymph nodes and spleen lymphocytes taken from uninfected and T. spiralis-infected mice. Acetic acid stimulated proliferation of splenocytes taken from uninfected mice but did not affect lymphocyte proliferation in mesenteric lymph nodes from uninfected or infected mice. Orally administered SCFA increased the number of goblet cells found in the epithelium of the jejunum 7 dpi, but this number had decreased 10 dpi. The number of apoptotic cells in the lamina propria of the intestinal mucosa of animals infected with the T. spiralis and receiving SCFA was also lower, particularly 10 dpi. The above results show that SCFA can participate in the immune response during the course of trichinellosis in mice.     

Correlation of cytotoxicity with experimental allergic encephalomyelitis.

Cytotoxicity of immune lymph node cells in experimental allergic encephalomyelitis (EAE) was maximal 9 days after injection of encephalitogenic emulsion. The ability of these cells to passively transfer EAE was also maximal at this time. Immune spleen cells were more cytotoxic than lymph node cells 9 days after injection; however, these cells did not passively transfer EAE. Twelve days after injection of encephalitogenic emulsion immune spleen cells passively transferred EAE with resulting mild histopathologic lesions. At this time the spleen cells were 50% more cytotoxic than comparable lymph node cells. Cyclophosphamide suppressed the development of clinical EAE and the development of cytotoxic lymphoid cells. It also reduced clinical signs and cytotoxic activity of lymph node cells. Spleen cell cytotoxic activity was enhanced by Cyclophosphamide. It was concluded that cytotoxic activity of lymph node and spleen cells was correlated with the ability of these cells to produce EAE. Lymph node cell populations differed qualitatively and/or quantitatively from immune spleen cell populations in EAE. Capacity to passively transfer EAE coincided with the maximal Cytotoxicity of the lymphoid cells from each tissue.