原发性免疫缺陷病继发噬血细胞综合征1例

正原发性免疫缺陷病(primary immunodeficiency diseases,PID)是一组由遗传学因素引起的免疫功能缺失或减低的临床综合征,以易患感染、肿瘤、自身免疫病为特点。我院近期诊治了1例PID继发噬血细胞综合征的患者,现将该患者的临床资料报告如下。1病例资料患者,男,15岁,2014年4月24日因"间断发热、乏力4个月"入院。患者于入院前4个月无明显诱因出现发热,体温最高达40℃,伴头痛、流清     

自身免疫性肝炎误诊为肾综合征出血热1例

1病例资料 女性患者,55岁,主因发热12 d于2011年12月9日以发热原因待查:(1)泌尿系统感染;(2)结缔组织病人院.患者于入院前12 d突然出现发热,体温最高39.6℃,热前无发冷及寒战,无头痛、腰痛及眼眶痛.入院前1周出现四肢关节肿痛,以双侧膝关节明显,无四肢肌肉疼痛,无脱发及口腔溃疡.     

成人噬血细胞综合征1例并文献复习

噬血细胞综合征(hemophagocytic syndrome,HPS),本病罕见,早期因为缺乏特异性的临床症状及体征,容易造成误诊与漏诊。本院呼吸内科收治1例成人噬血细胞综合征患者,现结合文献复习如下:病例介绍患者,女,49岁,因反复发热9 d于2012年04月07日入院。9天前无明显诱因下出现畏寒、发热,最高体温达     

多杀巴斯德菌肺炎并文献复习

多杀巴斯德菌是一种小的革兰氏阴性球杆菌。能引起动物的原发和机会感染,人类感染较罕见,主要是通过与动物接触(尤其是猫、狗等动物的抓、咬伤)所致。近我们诊治1例由多杀巴斯德菌引起的重症肺炎合并败血症、急性呼吸窘迫综合征(ARDS)患者,现予报告并复习有关文献。1病例报告患者男性,16岁,学生。因轻咳、咯少量白粘痰半月,加重伴高热、咯脓血痰、胸痛、进行性胸闷、气急22 h而于2005年12月12日下午入院。患者病初伴有鼻塞、流涕,未诊治仍上学,于入院前1天受凉后咳嗽加重、咯黄脓痰及脓血痰、胸痛、气急,伴发热(体温39℃)、寒战,而于12日…     

伤寒并发格林-巴利综合征1例

作为报道表现为格林-巴利综合征(急性多发性神经根炎)的伤寒患者1例。病例介绍患者男,26岁。以持续发热、双下肢感觉异常3周入院。新近无疫苗接种、化疗、血清治疗及针灸史,也未与发热患者或瘫痪患者接触。一直居住在巴黎南部市郊。既往无任何病史。发热和感觉异常2周后出现双腿乏力,无尿潴留或尿失禁。体温     

发热待查患者的诊断分析

作者分析了1971～1975年的1,599例住院患者,其中持续发热38℃2天以上、入院时发热原因不明的16岁以上成人患者182例(11.4%)。本组患者男100例、女82例。其诊断分析如下: 本组患者确诊152例(84%):感染引起者129例(71%)、恶性肿瘤9例(5%)、自身免疫疾病5例(3%)、其它9例(5%)。以发热待查入院的46例患者中,25例(54%)入院后确诊,其中尿路感染(7例)占第1位,其次为肺炎(4例),肺外结核(4例)。最终诊断不明的30例患者中,约一半是     

慢性肝病患者腹水中的沙眼衣原体

迄今已知沙眼衣原体可引起非淋球菌性尿道炎、宫颈炎、输卵管炎、子宫内膜炎、附睾炎、新生儿结膜炎、直肠炎、肺炎。晚近尚有报导引起腹膜炎及青年妇女肝周围炎(Fitz-Hugh-Curtis综合征)。为了解此病原体在肝硬化细菌性腹膜炎中可能有的意义,作者对9例肝硬化腹水患者在作腹水常规检查与培养时进行了腹水中沙眼衣原体的检测。9例患者中7例系酒精性肝病,其中1例合并结肠腺癌。2例为坏死后性肝硬化。全部     

肾综合征出血热并肠功能衰竭二例

例1 男,28岁,因发热腹痛9 d、腹胀无尿3d以肾综合征出血热(HFRS)、急性肾功能衰竭入院.患者于入院前9 d出现发热、体温达39°C,伴右下腹疼痛,第3病日于当地医院诊为"急性阑尾炎"行阑尾切除术,术中发现阑尾充血水肿、腹腔大量血性渗液.     

口服磷酸奥司他韦引起严重精神症状1例并文献复习

<正>病例资料患者,杜某某,男,70岁,系"咳嗽伴胸闷、发热4天"于2014年2月7日入院。入院前5天受凉后出现咳嗽、胸闷不适,伴有发热,体温最高39℃,外院输注头孢他啶3天,症状无好转。发病前1周内无禽类接触史,无发热病人以及禽流感病人接触史,周围接触者无类似病史。既往有高血压病史多年(口服复方降压片)。入院时查体:T:39.6℃,P:90     

造血干细胞移植的感染防治问题——附6例报告

本文报告6例造血干细胞移植病人感染的防治措施及临床结果。6例中3例感染发热,其中2例有感染的临床或生物学表现。另外3例经全环境保护(TEP)的病人,白细胞降至0无发热,但其中1例于移植后37天发生皮肤带状疱疹病毒(VZV)感染.病人均已恢复,未发生败血症和间质性肺炎(IP).     

全身免疫炎症指数与脑血管疾病相关性研究进展

免疫炎症反应在脑血管疾病的病理生理机制中发挥着重要作用.最新的研究表明,全身免疫炎症指数(SⅡ)作为一种新型的炎症标志物,综合多种炎性细胞,可以更全面地反映局部免疫和全身炎症反应的平衡状态,并与多种脑血管病(如脑梗死、脑出血、静脉窦血栓形成、颅内动脉瘤等)的发生、发展及临床预后相关,因其潜在的临床应用价值,越来越受临床...     

Pathways of mononuclear cell infiltration in rheumatoid synovitis

Summary The mononuclear cell infiltration which characterizes the chronic inflammatory reaction results from the migration of lymphocytes and monocytes through the endothelium of the postcapillary venule. The initial step in the emigration of these cells in their binding to the vascular endothelium. The binding capacity of the endothelial cell (EC) for lymphocytes and monocytes is increased by IFN-, IL-1, TNF, and TNF. Production of these cytokines by chronic inflammatory cells may be expected to amplify the chronic inflammatory reaction. Initiation of the chronic synovitis of rheumatoid and other chronic synovitides probably results from the interaction of antigen with sensitized T cells in the sublining region of the synovium. This interaction is facilitated by the presence of substantial numbers of DR+macrophage+accessory cells in the synovial interstitial space. It is likely that these accessory cells are bone marrow derived monocytes migrating to the synovial lining layer in response to chemotactic factors released by the hyperplastic synovial lining cells. Lymphocytes differ in their binding affinity for ECs, and more strongly binding lymphocytes may be preferentially bound. Since binding is the first step in lymphocyte emigration, this event may lead to the selection of more strongly binding lymphocytes in the perivascular infiltrate. The T cells present in the mononuclear cell infiltrates of rheumatoid arthritis, other chronic synovitides, and multiple sclerosis have been shown to be composed largely of the CDw29+CD4+, helper-inducer, memory cell subset. The predominance of this T-cell subset may result from its demonstrated greater binding affinity for ECs. The fact that this subset has been shown to react weakly with T-cell mitogens and strongly with soluble antigens, may explain two important properties of synovial fluid T cells in inflammatory disease: (1) their weak reactivity to T cells mitogens and (2) their strong reactivity to antigens. Thus, the hyperplasia of the synovial lining layer, which may be an important factor in the mobilization of accessory cells, and the increased EC binding of HI memory T cells may combine to facilitate the initiation and maintenance of chronic synovitis.     

Effect of proinflammatory interleukins on jejunal nutrient transport

AIM: We examined the effect of proinflammatory and anti-inflammatory interleukins on jejunal nutrient transport and expression of the sodium-glucose linked cotransporter (SGLT-1). METHODS: 3-O-methyl glucose and L-proline transport rates were examined in New Zealand White rabbit stripped, short circuited jejunal tissue. The effects of the proinflammatory cytokines interleukin (IL)-1alpha, IL-6, and IL-8, IL-1alpha plus the specific IL-1 antagonist, IL-1ra, and the anti-inflammatory cytokine IL-10 were investigated. In separate experiments, passive tissue permeability was assessed and brush border SGLT-1 expression was measured by western blot in tissues exposed to proinflammatory interleukins. RESULTS: The proinflammatory interleukins IL-6, IL-1alpha, and IL-8 significantly increased glucose absorption compared with control levels. This increase in glucose absorption was due to an increase in mucosal to serosal flux. IL-1alpha and IL-8 also significantly increased L-proline absorption due to an increase in absorptive flux. The anti-inflammatory IL-10 had no effect on glucose transport. The receptor antagonist IL-1ra blocked the ability of IL-1alpha to stimulate glucose transport. IL-8 had no effect on passive tissue permeability. SGLT-1 content did not differ in brush border membrane vesicles (BBMV) from control or interleukin treated tissue. CONCLUSIONS: These findings suggest that intestinal inflammation and release of inflammatory mediators such as interleukins increase nutrient absorption in the gut. The increase in glucose transport does not appear to be due to changes in BBMV SGLT-1 content.     

慢性阻塞性肺疾病与慢性炎症

慢性阻塞性肺疾病(chronic obstructive pulmonary disease,COPD)患病率高、病程长、病死率高,已成为严重的社会负担.小气道炎症是COPD的主要病变及导致肺功能进行性损害的主要原因,同时大量研究证明COPD患者存在系统性炎症,但目前对于COPD气道炎症与系统性炎症的关系尚不十分明确.     

Requirements of transcription factor Smad-dependent and -independent TGF-β signaling to control discrete T-cell functions

TGF-β modulates immune response by suppressing non-regulatory T (Treg) function and promoting Treg function. The question of whether TGF-β achieves distinct effects on non-Treg and Treg cells through discrete signaling pathways remains outstanding. In this study, we investigated the requirements of Smad-dependent and -independent TGF-β signaling for T-cell function. Smad2 and Smad3 double deficiency in T cells led to lethal inflammatory disorder in mice. Non-Treg cells were spontaneously activated and produced effector cytokines in vivo on deletion of both Smad2 and Smad3. In addition, TGF-β failed to suppress T helper differentiation efficiently and to promote induced Treg generation of non-Treg cells lacking both Smad2 and Smad3, suggesting that Smad-dependent signaling is obligatory to mediate TGF-β function in non-Treg cells. Unexpectedly, however, the development, homeostasis, and function of Treg cells remained intact in the absence of Smad2 and Smad3, suggesting that the Smad-independent pathway is important for Treg function. Indeed, Treg-specific deletion of TGF-β-activated kinase 1 led to failed Treg homeostasis and lethal immune disorder in mice. Therefore, Smad-dependent and -independent TGF-β signaling discretely controls non-Treg and Treg function to modulate immune tolerance and immune homeostasis.     

Endothelial Semaphorin 7A promotes neutrophil migration during hypoxia

Recent studies identified basic biological principles that are shared by the immune and the nervous system. One of these analogies applies to the orchestration of cellular migration where guidance proteins that serve as a stop signal for axonal migration can also serve as a stop signal for the migration of immune-competent cells. The control of leukocyte migration is of key interest during conditions associated with inflammatory tissue changes such as tissue hypoxia or hypoxic inflammation. Semaphorins are members of these axon guidance molecules. Previously unknown, we report here the expression and induction of semaphorin 7A (SEMA7A) on endothelium through hypoxia-inducible factor 1α during hypoxia. This induction of SEMA7A translates into increased transmigration of polymorphonuclear neutrophil granulocytes across endothelial cells. Extension of these findings demonstrated an attenuated extravasation of polymorphonuclear neutrophil granulocytes in Sema7a-deficient mice from the vasculature during hypoxia. Studies using chimeric animals identified the expression of Sema7A on nonhematopoietic tissue to be the underlying cause of the observed results. Taken together, our findings demonstrate that neuronal guidance proteins do not only serve as a stop signal for leukocyte migration but also can propagate the extravasation of leukocytes from the vascular space. Future anti-inflammatory strategies might be based on this finding.     

Tolerance to apoptotic cells is regulated by indoleamine 2,3-dioxygenase

Tolerance to self-antigens present in apoptotic cells is critical to maintain immune-homeostasis and prevent systemic autoimmunity. However, mechanisms that sustain self-tolerance are poorly understood. Here we show that systemic administration of apoptotic cells to mice induced splenic expression of the tryptophan catabolizing enzyme indoleamine 2,3-dioxygenase (IDO). IDO expression was confined to the splenic marginal zone and was abrogated by depletion of CD169(+) cells. Pharmacologic inhibition of IDO skewed the immune response to apoptotic cells, resulting in increased proinflammatory cytokine production and increased effector T-cell responses toward apoptotic cell-associated antigens. Presymptomatic lupus-prone MRL(lpr/lpr) mice exhibited abnormal elevated IDO expression in the marginal zone and red pulp and inhibition of IDO markedly accelerated disease progression. Moreover, chronic exposure of IDO-deficient mice to apoptotic cells induced a lupus-like disease with serum autoreactivity to double-stranded DNA associated with renal pathology and increased mortality. Thus, IDO limits innate and adaptive immunity to apoptotic self-antigens and IDO-mediated regulation inhibits inflammatory pathology caused by systemic autoimmune disease.     

Elevated cyclic AMP and PDE4 inhibition induce chemokine expression in human monocyte-derived macrophages

Macrophages are central mediators of the innate immune system that can be differentiated from monocytes upon exposure to cytokines. While increased cyclic adenosine monophosphate (cAMP) levels are known to inhibit many lipopolysaccharide-elicited macrophage inflammatory responses, the effects of elevated cAMP on monocyte/macrophage differentiation are not as well understood. We show here that during differentiation, cAMP agonists can cause a large increase in the mRNA and protein levels of several of the pro-inflammatory CXCL and CCL chemokines. The cAMP mediator-exchange protein activated by cAMP (Epac) contributes substantially to the increase in these chemokines. These chemokines are known to play an important role in the regulation of immune responses, particularly regarding the pathogenesis of asthma and chronic obstructive pulmonary disorder. We also found that a selective cAMP-degrading phosphodiesterase (PDE) 4 inhibitor can potentiate the chemokine expression elicited by low-dose forskolin or Prostaglandin E2 (PGE₂). These data suggest that chemokine receptor antagonists administered in conjunction with a PDE4 inhibitor may improve both the efficacy and safety of PDE4-inhibitor therapy for chronic inflammatory disorders.