实验性自身免疫性睾丸炎病理变化及肥大细胞改变

目的 观察和分析BALB/c小鼠自身免疫性睾丸炎后病理改变及肥大细胞(MC)的数量、分布等变化.方法 BALB/c雄性小鼠72只,随机分为6组,每组12只,其中5组为模型组,行单侧睾丸动脉结扎,在结扎后2h开通血管,分别在开通后12h、1周、2周、3周、4周处死,取睾丸和附睾;另一组为对照组,不做任何处理,直接取睾丸和附睾进行对比.结果 TB染色显示对照组侧睾丸MC基本上只见于白膜下面,睾丸间质中几乎不存在或仅偶见MC.模型组侧小鼠睾丸白膜、睾丸间质、睾丸纵隔以及附睾中均可见MC.其中附睾中MC的数量最多,依次是纵隔、白膜、睾丸间质.模型组MC的数量和分布与对照组比较差异具有显著性.HE染色显示:随着缺血后再灌注的时间延长,组织病理变化逐渐减轻.结论 自身免疫性睾丸炎模型组MC数量高于对照组,睾丸组织病理变化随时间延长逐渐减轻,具有相对的可恢复性.     

自身免疫性睾丸炎对精子特异性酶和生育功能的影响

目的 :研究自身免疫性睾丸炎对精子特异性酶和生育功能的影响。　方法 :复制豚鼠实验性变态反应性睾丸炎 (EAO)模型 ,采用酶动力学分光光度法和明胶固定底物薄膜法 ,观察EAO状态下精子顶体蛋白酶、透明质酸酶、精子胞质乳酸脱氢酶、附睾尾部精子和睾丸组织形态的变化。　结果 :EAO造成附睾精子顶体酶系中顶体蛋白酶、透明质酸酶和乳酸脱氢酶活性下降、附睾尾部精子质量下降、睾丸生精细胞发生退行性病变。　结论 :EAO明显影响雄性豚鼠生育力 ,睾丸生精细胞和附睾精子可能是主要作用环节。     

腮腺炎性睾丸炎

腮腺炎性睾丸炎是青春期及成年男性流行性腮腺炎最常见的并发症,可引起睾丸萎缩、生精功能障碍,并极易导致男性不育.本文从病理生理学、诊断、治疗、预后等方面对腮腺炎性睾丸炎与男性不育的关系进行综述.     

结直肠癌组织中巨噬细胞因子的分子生物学作用

巨噬细胞因子（macrophage cytokine,MCK）是由单核-巨噬细胞合成分泌的一类具有广泛生物学活性的小分子蛋白质,在体内的作用非常复杂,既可以参与机体的炎症反应、免疫应答、免疫调节,又有抗肿瘤和促进肿瘤生长的双重作用。近年来,发现MCK可以通过增加肿瘤组织中胸苷磷酸化酶（thymidine phosphorylase,dThdPase）的表达而使5＇-脱氧氟尿苷（商品名氟铁龙,5＇-DFUR）转化为5-氟尿嘧啶5-FU,起到细胞毒性作用。现将MCK在结直肠癌组织中的表达,和它在肿瘤的生长、浸润、转移、治疗中的重要作用进行综述。     

腮腺炎睾丸炎对睾丸的损伤及其治疗

流行性腮腺炎(腮腺炎)是由腮腺炎病毒(mumps virus,MuV)引起的一种急性呼吸道传染病,是小儿和青少年常见病,约18％～30％伴发睾丸炎,但实际可能超过这个数字[1].病毒除易侵犯腮腺,对生殖器官、神经组织和胰腺等也有侵犯,特别容易侵犯男孩的睾丸组织,引起病毒性睾丸炎,单侧受累约占2/3,双侧占1/5～1/3.30％的患者发生睾丸组织的广泛破坏和萎缩,生精功能发生不可逆的破坏[2].对于腮腺炎睾丸炎(parotiditis orchitis)生精细胞内包涵体的检出未见报道,笔者在临床生精细胞检测中,发现生精细胞被病毒感染后形成包涵体[3],现介绍如下.     

流行性腮腺炎性睾丸炎的无精子症与防治策略

睾丸炎是青春期、成人男性流行性腮腺炎(EM)患者的常见并发症,已往认为流行性腮腺炎性睾丸炎(EMO)一般不引起或很少引起男性不育症。近年来,随着青少年、成人EM发病率的上升和相关研究的深入,EMO所致的无精子症病例日渐增多,成为临床无精子症最常见的原因之一。本文通过国内外文献,就EMO睾丸萎缩、无精子症发病率、临床检测、预后和防治策略等进展进行阐述。     

大鼠非特异性睾丸炎模型的建立及生精上皮的变化

目的:探讨大鼠生精上皮在非特异性炎症状态下的变化。方法:20只成年W istar雄性大鼠随机分为2组(对照组和实验组),对照组腹腔注射生理盐水(1 m l/kg),实验组注射细菌内毒素(LPS),剂量为1 mg/kg,两组均隔1 d注射1次,距第1次注射10 d后取材。HE染色观察睾丸组织的病理改变,免疫组化方法探讨生精上皮内增殖细胞核抗原(PCNA)、α连接素的变化。结果:实验组睾丸组织有明显炎性改变;生精上皮内PCNA表达量显著降低:每个生精小管(仅精原细胞着色的小管)阳性细胞个数为(59±5)个,比对照组明显减少(P<0.01),而这种小管占总管数的比例显著升高(P<0.01),为0.673±0.054;实验组大鼠睾丸内α连接素表达量亦减少(P<0.01),阳性反应颗粒平均光密度为0.150±0.014。结论:睾丸炎症时精原细胞增殖和生精上皮内细胞间粘附力度均减弱,这可能是睾丸炎导致男性不育的原因之一。     

69例布鲁氏菌病性睾丸炎的调查报告

目的:了解布鲁氏菌病性睾丸炎(简称布病性睾丸炎)的流行病学特征、临床表现、诊断和治疗,为布病性睾丸炎的临床防治提供可靠依据。方法:采用回顾性调查法,根据门诊病例和患者住院病例病历记录进行数据整理与统计学分析。结果:布病性睾丸炎占布病患者的6.67%,流行病学特点显著,密切接触羊群的职业高发,年龄越大发病率越高,季节发病高峰在4~7月份,地区分布差异显著。全部患者睾丸局部有红肿热痛症状。45例患者勃起功能障碍100%,患者生育能力在患病期间受到短期影响。全身症状以发热、恶寒、出汗、关节痛等为主,睾丸双侧肿大多于单侧。患病初期容易误诊。口服药物以盐酸多西环素片、利福平胶囊为主,盐酸多西环素注射液、利福霉素注射液或利福平注射液静脉点滴可选用任何1种,按疗程正规治疗均可治愈,但部分患者可复发。结论:布病性睾丸炎有明显的流行病学特点,临床表现以睾丸局部红肿热痛为主,睾丸炎虽为一过性疾病,但患病期间可影响睾丸生精,临床治疗以口服药和静脉给药相结合,同时采取对症处理。     

重组干扰素α－2b治疗腮腺炎性睾丸炎11例报告

重组干扰素α－２ｂ治疗腮腺炎性睾丸炎１１例报告熊洁，熊升远，徐英民关键词干扰α－２ｂ，睾丸炎，流行性腮腺炎中图法分类号Ｒ６９７．２２男子患流行性腮腺炎最常见的并发症是睾丸炎，发病后可引起睾丸萎缩。如双侧睾丸萎缩，可导致男子不育症［１］。Ｅｒｐｅｎｂａ...     

Increased testosterone production in vitro by Leydig cells from rats with severe autoimmune orchitis

We have previously observed (M. O. Suescun et al. , 1994, Journal of Andrology , 15 , 442–448) that rats with autoimmune orchitis (EAO) exhibit increased testosterone production in vitro by isolated testes. The aim of the present study was to determine whether the increase in testosterone production correlated with an enhanced number of Leydig cells and/or enhanced steroidogenic capacity per Leydig cell. For this purpose, EAO was induced in adult Sprague-Dawley rats by active immunization with testicular homogenate and adjuvants. At 80 days after the primary immunization, 60% of rats presented with severe testicular damage characterized by sloughing of the seminiferous epithelium, seminiferous tubule atrophy and interstitial mononuclear cell infiltration. At 160 days after the first immunization, testicular lesions were more severe. A morphometric study, by light microscopy, showed an increase in the number of Leydig cells in rats with EAO (45% increase at 80 days and 50% at 160 days). By electronmicroscopy, testicular sections of rats with EAO revealed the presence of numerous Leydig cells closely associated with macrophages. Most Leydig cells exhibited ultrastructural features of active steroid secreting cells.
The steroidogenic capacity of Percoll-purified Leydig cells from testes of rats with EAO, killed at 80 and 160 days, was evaluated. Leydig cells from rats with EAO exhibited an enhanced steroidogenic response to hCG in vitro at 80 days (38%) and an increase in basal (77%) and post-hCG testosterone production (115%) at 160 days compared to controls. However, these cells were less sensitive to hCG. In conclusion, the results indicate that the enhancement of in-vitro testosterone production observed in rats with EAO is accounted for both by the increased number of Leydig cells and by the increased testosterone production of each Leydig cell.     

Adoptive transfer of murine autoimmune orchitis with sperm-specific T lymphoblasts

A protocol was successfully developed for reproducibly transferring experimental autoimmune orchitis (EAO) to naive recipient mice with sperm-specific T lymphoblasts. Cell donors were Balb/c mice immunized about 12 days earlier with homologous epididymal sperm capacitated in vitro with complete Freund's adjuvant. Draining lymph node cells were collected and subjected to a second challenge with the same sperm antigen in vitro. Sperm-specific T lymphoblasts were isolated on Percoll density gradients and propagated in the presence of interleukin-2 for 3 days and then were transferred intraperitoneally to naive recipients. As few as 3 x 10(6) sperm-specific T lymphoblasts were able to transfer EAO, which began on day 7 as infiltration of lymphocytes and macrophages and on days 14 to 21 developed to degenerative changes of spermatids and exfoliation of germinal epithelium. These pathologic alterations resemble a delayed type of hypersensitivity. The results show that sensitized T lymphoblasts can mediate an antigen-specific, mononuclear cell-invasive lesion in autoimmune orchitis.     

New experimental model for adoptive transfer of murine autoimmune orchitis

Previous studies demonstrated that experimental autoimmune orchitis (EAO) was produced in C3H/He mice with very high incidence by subcutaneous (s.c.) injections of viable syngeneic testicular germ cells (TC), without resorting to any adjuvants or immunopotentiators. Using this EAO model, a new and simple protocol was developed for adoptive transfer of EAO. Cell donors were C3H/He mice that received s.c. injections twice with TC alone. Spleen cells from the donors were stimulated in vitro with TC, propagated in interleukin-2 containing medium, then injected i.p. to naive recipient mice. This procedure induced severe orchitis and hypospermatogenesis with or without inflammation in epididymis and vas deferens in the recipients at high incidence. Elimination of all T cells or CD4+ T cells before the transfer produced no histopathological signs in the recipients whereas that of the CD8+ T cells or B cells had no inhibitory effect on the disease transfer, indicating that the effector cells are CD4+ T cells.     

Effect of ketotifen fumarate on experimental autoimmune orchitis and torsion of the spermatic cord

The aim of this work was to study effects of ketotifen fumarate(KF)on prevention of tissue damage in testes of rats with experimental autoimmune orchitis(EAO)and on the contralateral testis in a model of prolonged testicular cord torsion(TCT).Rats with EAO or TCT were injected intraperitoneally once daily with KF or saline solution(vehicle group).Incidence and severity of testicular damage were evaluated by histopathology using an EAO score or a Johnsen score.Mast cells(MC)were identified by histochemistry and quantified.In EAO model,KF significantly reduced severity of histopathological testicular damage compared to rats in the vehicle group.KF also reduced the number of testicular MC compared to vehicle group.Similarly,in TCT model,multifocal damage of the contralateral testis was observed 30 days after testicular torsion characterized by sloughing of the germinal epithelium,seminiferous tubule atrophy,and interstitial edema.Focal signs of inflammation and fibrosis of seminiferous tubular walls were also observed.In contrast,sections of contralateral testis of rats injected with KF and killed 30 days after surgery showed normal histological features.A significant decrease in the number of MC was observed in rats treated with KF compared to untreated animals.In conclusion,we demonstrated that treatment with KF reduced testicular inflammatory process and MC infiltrates in both EAO and TCT models.The results suggest a promising treatment for infertile male patients with testicular pathologies associated with inflammation and germ cell loss.     

Phenotypic characterization of lymphocytic cell infiltrates into the testes of rats undergoing autoimmune orchitis

Experimental autoimmune orchitis (EAO) was induced in adult Wistar rats by active immunization with a testicular homogenate (TH) and adjuvants. Fifty per cent of the immunized rats developed EAO. Testicular damage became evident at 50 days after the primary immunization and increased in severity at 80 days. Phenotypic characterization of T-cell subsets (CD4+ and CD8+) and Ia+ cells was performed on cryostat sections of testis obtained from normal rats, rats immunized with adjuvant (control group) and rats immunized with TH and adjuvants (experimental group) at 50 and 80 days. Labelled cells were only detected in the interstitial area; no labelled cells were observed inside the seminiferous tubules with any of the monoclonal antibodies used (W3/25, OX-8, OX-6). A significant increase in the numbers of CD4+ and CD8+, as well as of Ia+ cells, were observed in the testis of rats with severe EAO at 80 days after the first immunization. Rats of the same experimental group without testicular damage showed no major differences compared to rats from the control group, with the exception of a lower number of CD8+ cells. Variations in the lymphocyte subsets in lymph nodes draining the site of immunization showed the opposite pattern to that observed in the testis. In conclusion, these data suggest the traffic of specifically sensitized lymphocytes from lymph nodes to the testis and an active role of CD4+, CD8+ and Ia+ cells in the pathogenesis of EAO in the rat.     

T cell regulation of autoimmune interstitial nephritis

Research in organ-specific autoimmunity has been greatly facilitated over the past decade by advances in cellular and molecular immunology. Such studies have greatly expanded our understanding of autoimmune effector mechanisms and the nature of the target antigens recognized by these mediators. Another facet of organ-specific autoimmunity concerns the definition of those factors that determine host susceptibility to disease. This review outlines studies performed in two models of autoimmune interstitial nephritis that focus on issues of susceptibility and tolerance to parenchymal self antigens. In both models, antigen-specific regulatory T cells modulate the effector limb of the nephritogenic immune response and the pattern of interstitial injury. This modulation can be either stimulatory or inhibitory. The dominant regulatory effect is linked to genes in the major histocompatibility locus and is tightly correlated with disease expression. Regulatory T cells which inhibit the nephritogenic immune response can also be cultured in vitro and are highly efficacious as a therapeutic modality. These studies provide both the background and requisite reagents for delineating the mechanism(s) underlying antigen-specific T cell regulation.