Immunomodulatory effect of Hypoderma lineatum antigens: in vitro effect on bovine lymphocyte proliferation and cytokine production

This study examines the immunomodulatory effect of a crude larval extract (CLE), obtained from first stage larvae (L1) of H. lineatum , and the purified fractions hypodermin A (HyA), HyB and HyC. Proliferative responses of peripheral blood mononuclear cells (PBMC) from uninfested and previously infested cattle and the production of the cytokines IL-10, IL-4 and IFN-γ, in response to concanavalin A (Con A), were determined. The stimulation index of peripheral blood mononuclear cells from uninfested cattle was significantly lower than that from infested animals with the different antigens assayed. The HyA was the antigen that most inhibited the proliferative response, followed by the HyB, the HyC and the CLE. This hypodermin provoked an increase of IFN-γ and a suppression of IL-10 production that would support a Th1-like cytokine response. The HyB reduced the production of IL-10 stimulated by the Con A in cultures from infested animals. The HyC did not modulate the production of cytokines. Finally, the CLE induced a marked suppression in the production of the different cytokines in cultures from naïve and previously sensitized animals. Our results indicate that Hypoderma larval secretions are comprised of different components (hypodermins) that individually induce distinct but partially overlapping modulatory responses.     

套式PCR对HIV—l env基因检测的敏感度分析

采用套式PCR对含HIV—1膜蛋白基因的B亚型质粒和HIV—1感染者外周血单核细胞(PBMC)进行env基因部分片断的扩增,套式PCR可使常规PCR的敏感性提高100至1000倍,常规PCR只扩增出12份PBMC中的2份样品,套式PCR则扩增出全部样品中HIV—1膜蛋白基因片断.     

肿瘤患者自体血浆诱导树突状细胞的实验研究

目的探讨以实体瘤患者自体血浆替代胎牛血清诱导外周血单核细胞(PBMC)来源的树突状细胞(DC)的可行性,为临床应用提供实验依据。方法以血细胞分离机分离经动员的实体瘤患者外周血单核细胞(PBMC),在自体血浆(AP)、胎牛血清(FCS)等培养条件下,加入rhGM-CSF、rhIL-4和nrhTNF-α培养7~9 d诱导成为树突状细胞,进行细胞形态、表型及刺激T细胞增殖能力分析。结果在不同血清条件下,PBMC经诱导后均出现典型的树突状细胞形态和超微结构;但流式细胞术分析显示,以自体血浆培养的DC共刺激分子CD86为(74.09±0.92)%,MHCⅡ类分子HLA-DR为(91.73±1.96)%,显著高于FCS培养的DC;并且同种混合淋巴细胞反应结果显示AP-DC具有更高效的刺激T细胞活化增殖的能力。结论以AP代替FCS,实体瘤患者PBMC可被诱导为表型更成熟的DC;该方法既可去除异种蛋白干扰,又利于DC成熟,可作为临床应用DC的培养途径。     

慢性乙型肝炎病人血液单核细胞中HBV标志物的检出

本文报告在慢性乙型肝炎38例的外周血单核细胞(PBMC)和T、B淋巴细胞中检测到HBV标志物阳性29例(76.3％)。其中17例病人的PBMC中HBsAg,HBeAg和HBV-DNA阳性者分别为4,2和14例。21例病人分离出T,B淋巴细胞,其中T细胞中HBsAg,HBeAg与HBV-DNA阳性分别为2,2和1例;B细胞中分别为3,6,1例。血清HBV标志物阳性的病人其PBMC中这些标志物的检出率(13/15例)明显高于血清抗HBc和抗HBe阳性的稳定期病人(3/7例)。提示HBV可能感染和损害慢性乙型肝炎病人的淋巴细胞,这也许是乙型肝炎病人免疫功能异常的原因之一。     

The relationship between blood leptin level and bone density is specific to ethnicity and menopausal status

Leptin, the obesity hormone, has been linked to bone mineralization and tumorigenesis. In addition, both bone mineral density (BMD) and postmenopausal breast cancer are associated with obesity, but the interrelationships between obesity, leptin, BMD, and breast cancer are not yet clear. In particular, there is little published research comparing white and black women in terms of these variables. We obtained blood specimens for leptin analysis from a group of 320 breast cancer patients and controls with an ethnic composition of 49% white women and 51% black women. Distal and proximal radial BMD (DBMD and PBMD) were measured by dual-energy X-ray absorptiometry, and age- and ethnicity-specific standardized scores (Z-scores) were calculated for bone density. Blood leptin levels were determined by radioimmunoassay. Blood leptin level was not linked to breast cancer risk. Leptin levels were significantly higher in black women than in white women and were also significantly higher in obese and overweight women than in normal-weight women. Black women weighed more and had a higher body mass index (BMI) than white women. After controlling for BMI, leptin was correlated with DBMD ( r = .17; P < .05) and PBMD ( r = .21; P < .05) in whites, but not in blacks. Leptin was also correlated with both distal and proximal Z-scores in postmenopausal women ( r = .14 and .13; P < .05). Thus leptin may be a predictor for BMD in a population that is prone to have a low BMD, and this relationship is independent of the effect of body weight on leptin levels. Our results suggest that ethnicity and menopausal status should be considered when comparing results from different studies.     

Myalgic Encephalomyelitis/Chronic Fatigue Syndrome – Evidence for an autoimmune disease

Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS) is a frequent and severe chronic disease drastically impairing life quality. The underlying pathomechanism is incompletely understood yet but there is convincing evidence that in at least a subset of patients ME/CFS has an autoimmune etiology. In this review, we will discuss current autoimmune aspects for ME/CFS. Immune dysregulation in ME/CFS has been frequently described including changes in cytokine profiles and immunoglobulin levels, T- and B-cell phenotype and a decrease of natural killer cell cytotoxicity. Moreover, autoantibodies against various antigens including neurotransmitter receptors have been recently identified in ME/CFS individuals by several groups. Consistently, clinical trials from Norway have shown that B-cell depletion with rituximab results in clinical benefits in about half of ME/CFS patients. Furthermore, recent studies have provided evidence for severe metabolic disturbances presumably mediated by serum autoantibodies in ME/CFS. Therefore, further efforts are required to delineate the role of autoantibodies in the onset and pathomechanisms of ME/CFS in order to better understand and properly treat this disease.     

Responses in extracellular and intracellular calcium and magnesium in aldosteronism

We hypothesized the hypercalciuria and hypermagnesuria that accompany aldosteronism could be pharmacologically attenuated to prevent shifts in extracellular and intracellular levels of these divalent cations and the adverse outcomes associated with them. Accordingly, rats administered aldosterone/salt treatment (ALDOST) were cotreated with either hydrochlorothiazide (Hctz), to selectively reabsorb urinary Ca2+, or with Hctz plus spironolactone (Hctz+Spi), where Spi retards the excretion of these cations in both urine and feces. We monitored urinary excretion and responses in extracellular and intracellular Ca2+ and Mg2+, together with indices of oxi/nitrosative stress in plasma and ventricular tissue. At 4 weeks ALDOST we found the following: (1) hypercalciuria was reduced by Hctz and normalized by Hctz+Spi, and this combination, unlike Hctz alone, also rescued hypermagnesuria; (2) the decrease in plasma-ionized [Ca2+]o was not seen with Hctz or Hctz+Spi, whereas Spi cotreatment protected against a decline in [Mg2+]o; (3) the Ca2+ loading of peripheral blood mononuclear cells and cardiac tissue was not seen with Hctz+Spi; and (4) the induction of oxi/nitrosative stress, expressed as reduced plasma alpha1-antiproteinase activity and activation of gp91(phox) subunit of NADPH oxidase in inflammatory cells invading intramural coronary arteries of the right and left ventricles, together with vascular fibrosis, was completely prevented by Spi cotreatment. In rats with aldosteronism, cotreatment with Hctz+Spi more effectively (vis-à-vis Hctz alone) protects against adverse iterations in extracellular and intracellular concentrations of Ca2+ and Mg2+, as well as the appearance of oxi/nitrosative stress to prevent the proinflammatory vascular phenotype.