氧自由基介导血管内皮细胞与白细胞粘附的研究

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Total and differential leukocyte counts percentiles in normal pregnancy

OBJECTIVE: To establish leukocyte count and leukocyte differential percentiles in normal uncomplicated pregnancy. STUDY DESIGN: This retrospective longitudinal study was performed in an outpatient facility for routine antenatal care. The study population comprised of 726 healthy women from the 5th to the 41st week of pregnancy. Altogether, there were 1749 complete blood count evaluations, of which 481 were in the 1st trimester, 687 in the 2nd trimester and 581 in the 3rd trimester. The total and differential leukocyte counts were determined by an automated cell counter. RESULTS: The leukocyte and neutrophil counts gradually and significantly increased form the 1st to the 3rd trimester. The monocyte count increase became significant only during the 3rd trimester. The eosinophil count did not significantly change throughout pregnancy. The basophil count significantly decreased during the 2nd trimester and returned to 1st trimester values during the 3rd trimester. CONCLUSION: In this study, we provide total and differential leukocyte counts' mean+/-S.D., minimal and maximal values, and the 3rd, 5th, 10th, 50th, 90th, 95th, and 99th percentiles for entire pregnancy and for each trimester separately. These reference values should prove useful for diagnostic and research purposes.     

Acromioclavicular joint septic arthritis in an immunocompetent child: A case report

Septic arthritis of acromioclavicular (AC) joint is a rare entity. It is generally seen in patients who are immunocompromised. Only 15 cases have been reported till now, with only one case series of 6 patients. We report a case of septic arthritis of AC joint in an immunocompetent child. A 9 years old girl presented with history of pain in left shoulder for 4 days associated with fever. No history suggestive of any immunocompromised state was complained. On local examination, a swelling of around 3 cm in diameter was found over left AC joint region with raised local temperature, tenderness on palpation and positive response in fluctuation test. Total leukocyte count was 18.7 × 10⁹/L with 80% of neutrophils. Erythrocyte sedimentation rate (ESR) was 28 mm/1 h. C-reactive protein (CRP) was 12 mg/L. X-ray showed enlarged left AC joint space. Ultrasound revealed hypoechoic collection in the AC joint and the surrounding area. The aspirate was thick and purulent in nature, revealing Gram positive cocci at staining. Arthrotomy and thorough lavage of AC joint was done. Culture of the aspirate showed Methicillin Resistant Staphylococcus Aureus (MRSA) after 48 hours that was sensitive to amikacin, gentamicin, erythromycin and teicoplanin. Patient was symptom-free at 2 months of follow-up with no signs of osteomyelitis on the radiographs. Thus this is the first case of AC joint septic arthritis in healthy individual. Being proximal to the shoulder joint, AC joint septic arthritis can be confused with the shoulder joint septic arthritis. Thus, high index of suspicion is required for accurate diagnosis.     

Expression of Bcl-2 on leukocytes in prostatic fluid from patients with acute and chronic prostatitis

 In our continuing investigation to clarify the significance of leukocytosis and its prolongation in prostatic fluid (PF) from prostatitis patients, we investigated whether expression of the antiapoptotic gene Bcl-2 on leukocytes in prostatic fluid has any relation with prolonged leukocytosis in prostatitis. The subjects were eight patients with acute bacterial prostatitis (ABP) and eight with nonbacterial prostatitis (NBP) with a history of more than 2 years. Twelve micrograms of protein obtained from leukocytes in PF were subjected to Western blot analysis. Bcl-2 was expressed in seven of eight (87.5%) and six of eight (75.0%) patients with NBP and ABP, respectively. Quantitative density analysis of the Bcl-2 band did not show any statistically significant differences between patients with NBP and those with ABP. These results suggest that the expression of antiapoptotic Bcl-2 on leukocytes in PF is not a cause of leukocyte longevity in long-term prostatitis. Received: November 13, 2002 / Accepted: February 28, 2003     

实时荧光定量PCR测定人肿瘤坏死因子相关凋亡诱导配体基因表达

目的 建立检测人肿瘤坏死因子相关凋亡诱导配体(TRAIL)基因表达含量的实时荧光定量逆转录(FQ-RT)-PCR法,探讨其在健康对照者、乙型病毒性肝炎肝硬化患者及原发性胆汁性肝硬化(PBC)患者外周血单个核细胞(PBMC)中的表达状况.方法 设计TRAIL基因的特异性引物和TaqMan-MGB探针,以β-actin基因为内参,RT-PCR扩增目的 片段.胶同收纯化目的 片段,构建克隆载体作为定最模板,在ABI Prism7000型荧光定量分析仪上进行扩增,建立标准曲线;同时检测30名健康对照者、30例PBC患者及25例乙型病毒性肝炎肝硬化患者外周血PBMC中TRAIL基因的荧光强度和循环阈值,计算样本中TRAIL基因的起始拷贝数.结果 FQ-RT-PCR检测TRAIL mRNA的线性范围为103-106拷贝/ug RNA(r=-0.997);高浓度样本批内和批间变异系数(CV)分别为5.6%和6.3%.低浓度样本批内及批间CV分别为12.5%和14.6%.PBC患者TRAIL mRNA表达量为[(3.3±2.5)×105拷贝ug RNA],高于健康对照组[(0.5±0.2)×105拷贝/ug RNA],两组差异有统计学意义(t=5.994,P<0.01);乙型病毒性肝炎肝硬化患者TRAIL mRNA的表达[(2.1±0.9)×105拷贝/ug RNA]亦高于健康对照组,且差异有统计学意义(t=8.536,P<0.01),而两疾病组间差异无统计学意义(t=1.988,P>0.05).结论 成功建立检测TRAIL mRNA的FQ-RT-PCR法,并初步发现TRAIL mRNA在PBC及乙型病毒性肝炎肝硬化患者外周血PBMC中表达升高,这将对肝硬化肝损伤机制研究提供新的思路.     

Impact of perfluorooctanesulfonate and perfluorooctanoic acid on human peripheral leukocytes

Perfluorinated compounds (PFCs), such as perfluorooctanesulfonate (PFOS) and perfluorooctanoic acid (PFOA), are xenobiotics that can be detected worldwide in the environment, wildlife, and humans. So far, the immunotoxicity of PFCs has only been investigated in rodents, but not in humans. In this study, we explore the impact of PFOS and PFOA on selected functions of human leukocytes in vitro. PFOS induced a significant decrease of natural killer-cell activity and reduced the release of the pro-inflammatory cytokine TNF-α following lipopolysaccharide (LPS)-stimulation. Furthermore, the plasma PFOS concentrations (2.09-8.98 ng/ml) found in our study subjects correlated positively with the LPS-stimulated IL-6 release. PFOA augmented significantly calcitriol-induced monocytic differentiation of the HL-60 cell line. Additionally, there was a significant linear relationship between LPS-stimulated TNF-α and IL-6 release, and the plasma PFOA (1.20-6.92 ng/ml) concentrations of the study subjects. In conclusion, the investigated PFCs affect human immune cells mainly with regard to natural killer-cell cytotoxicity and the pro-inflammatory cytokine release by stimulated macrophages.     

外周血白细胞与糖尿病肾病进展关系的研究

将473例肌酐正常的2型糖尿病肾病（DN）患者根据尿白蛋白／肌酐分为微量白蛋白尿组（DNl组,246例）和大量白蛋白尿组（DN2组,227例）,结果显示,DN2组WBC、单核细胞、CRP较DNl组显著增加[（6．8±1．7）×109／L比（6．3±1．5）×109／L,（0．49±0．23）×109／L比（0．32±0．21）×109／L,（4．1±1．1）mg／L比（1．7±0．3）mg／L,均P〈0．05]。多元线性回归分析显示,WBC、单核细胞、LDL—C和淋巴细胞是尿白蛋白／肌酐升高的独立影响因素。     

Neutrophils are the predominant cell-type to associate with Burkholderia pseudomallei in a BALB/c mouse model of respiratory melioidosis

A variety of studies have implicated neutrophils and the rapid induction of cytokine in the host response in melioidosis. Here a BALB/c mouse model of infection with aerosolised Burkholderia pseudomallei K96243 has been used to understand the immune response to infection in this model and verify other infection models that show rapid growth of bacteria, colonisation of tissues and periphery, induction of cytokines and influx of neutrophils. Uniquely, this study has also determined the association of B. pseudomallei to host cells in vivo using flow cytometric techniques. Neutrophils were found to be the predominant cell-type exhibiting B. pseudomallei antigens during infection and it is likely that bacteria have been internalised. This data confirms that neutrophils are likely to play an important and active role in fighting infection with B. pseudomallei.     

Understanding the interaction between psychosocial stress and immune-related diseases: a stepwise progression

For many years, anecdotal evidence and clinical observations have suggested that exposure to psychosocial stress can affect disease outcomes in immune-related disorders such as viral infections, chronic autoimmune diseases and tumors. Experimental evidence in humans supporting these observations was, however, lacking. Studies published in the last 2 decades in Brain, Behavior and Immunity and other journals have demonstrated that acute and chronic psychological stress can induce pronounced changes in innate and adaptive immune responses and that these changes are predominantly mediated via neuroendocrine mediators from the hypothalamic-pituitary-adrenal axis and the sympathetic-adrenal axis. In addition, psychological stress has predicted disease outcomes using sophisticated models such as viral challenge, response to vaccination, tracking of herpesvirus latency, exploration of tumor metastasis and healing of experimental wounds, as well as epidemiological investigations of disease progression and mortality. These studies have contributed significantly to our understanding that the neuroendocrine-immune interaction is disturbed in many pathophysiological conditions, that stress can contribute to this disturbance, and that malfunction in these communication pathways can play a significant role in the progression of disease processes. There are, however, significant gaps in the extant literature. In the coming decade(s), it will be essential to further analyze neuroendocrine-immune communication during disease states and to define the specific pathways linking the central nervous system to the molecular events that control important disease-relevant processes. This knowledge will provide the basis for new therapeutic pharmacological and non-pharmacological behavioral approaches to the treatment of chronic diseases via specific modulation of nervous system-immune system communication.