小儿支气管肺炎患者中性粒细胞吞噬及细胞内杀菌功能与脂质过氧化关系的探讨

目的：探讨了小儿支气管肺炎患者血液中性粒细胞吞噬及细胞内杀菌功能与脂质过氧化的关系。方法：采用普通酵母菌对62例患者及35例正常人进行中性粒细胞吞噬和细胞内杀菌功能试验和化学比色法测定血浆丙二醛（MDA）、谷胱甘肽过氧化物酶（GSH—PX）含量，放免法测超氧化物歧化酶（SOD），并与35名正常健康人作比较。结果：小儿支气管肺炎患儿在治疗前中性粒细胞吞噬及细胞内杀菌功能均明显低于正常人（P〈0．01），S01）、GSH-PX低于正常人组（P〈0．01），而MDA显著地高于正常人组（P〈0．01），相关分析显示，中性粒细胞吞噬及细胞内杀菌功能与MDA呈显著负相关（r=-0．3118，-0．3024，P〈0．05），经10d治疗后则与正常人比较无显著性差异（P〉0．05）。结论：检测小儿支气管肺炎患儿血液中性粒细胞吞噬及细胞内杀菌功能与脂质过氧化的关系对临床诊断、治疗和预后观察有重要的临床价值。     

肝硬化患者中性粒细胞吞噬及细胞内杀菌功能

<正> 本文报道44例肝硬化患者中性粒细胞吞噬及细胞内杀菌功能的观察结果。一、临床资料: 本组44例肝硬化患者的诊断系根据临床症状、体征、肝功能异常及超声波检查等确诊。其中50％有肝炎史和/或HBsAg(+)。代偿期患者12例、失     

慢性重症乙型肝炎患者血糖和中性粒细胞吞噬及细胞内杀菌功能检测的临床意义

慢性重症乙型肝炎常伴有细胞免疫抑制、造成患者免疫功能的降低[1],而中性粒细胞又是细胞免疫的重要组成部分。为了进一步地探讨慢性乙型肝炎的免疫功能水平,本文对患者进行了血糖及中性粒细胞吞噬和细胞内杀菌功能的测定,现将结果报告如下。     

1型出血热患者中性粒细胞与淋巴细胞功能变化研究

目的 研究肾综合征出血热（ＨＦＲＳ）患者的淋巴细胞和中性粒细胞免疫功能变化及其相互间关系，进一步阐明发病机理。方法 采用Ｅａ、Ｅｔ花环形成，ＰＨＡ皮肤试验及中性粒细胞趋吞化，吞噬，ＮＢＴ还原等多种试验方法同时对３２例由Ｈａｎｔａａｎ病毒引起的姬鼠型ＨＦＲＳ患者的淋巴细胞和中性粒细胞免疫功能变化及其相互间关系进行动态测定。     

内毒素血症大鼠中性粒细胞功能的变化

以大肠杆菌内毒素静脉注入复制大白鼠内毒素血症模型。观察了该模型动物中性粒细胞(PMN)功能的变化。结果表明,内毒素血症时外周血白细胞计数降低;肺小血管内有白细胞聚集;PMN吞噬细菌及产生活性氧能力明显减弱;趋化性明显受到抑制;PMN在静止时释放β-葡萄糖醛酸酶(β-g)明显增加;此外,PMN的糖皮质激素受体数目明显减少,而血浆皮质酮含量明显增高。     

烧伤患者中性粒细胞趋化因子变化分析

目的:探讨烧伤患者外周血中性粒细胞趋化因子的变化.方法:选取2018年2月至2020年5月我院救治的烧伤患者56例为研究组,选取60例健康志愿者为对照组,使用琼脂糖趋化实验来检测两组患者中性粒细胞的趋化距离,用酶联免疫吸附测定法来检测患者趋化因子受体阳性表达情况,然后对患者的中性粒细胞趋化距离及趋化因子受体阳性表达情况进行比较.结果:研究组患者的中性粒细胞的趋化距离均明显短于对照组(p<0.05);研究组患者入院3d时中性粒细胞趋化因子受体(CXC-chemokine receptor 1,CXCR1)与(CXC-chemokine receptor 1,CXCR2)受体阳性率均明显低于对照组(p<0.05),重度烧伤组患者的入院3d时中性粒细胞趋化因子受体CXCR1与CXCR2受体阳性率明显高于轻、中度烧伤组(p<0.05).研究组患者的IL-6、IL-10及TNF-α的水平明显高于对照组.结论:烧伤患者早期外周血中性粒细胞的趋化功能存在障碍,这可能与中性粒细胞趋化因子(CXCR1与CXCR2)的阳性表达率降低的有关.     

pHGF对人中性粒细胞吞噬功能的影响

我们曾报道，从乳猪肝脏提取的促肝细胞生长因子（ｐＨＧＦ）能增强小鼠中性粒细胞的吞噬功能，本文进而用吞噬杀菌试验、化学发光技术和促凝血活性试验证明，ｐＨＧＦ也能显著增强人中性粒细胞的吞噬和杀菌功能。     

HIV-1感染与吞噬细胞活性的降低与重建

HIV-1以巨噬细胞和中性粒细胞作为播散的载体和病毒复制的存贮器：巨噬细胞和中性粒细胞表面表达两种主要的HIV-1协同受体（CXCR4和CCR5）,能分别与HIV病毒亲嗜性毒株x4和R5结合。HIV-1病毒膜蛋白（gp120、gp41）能降低这些细胞的吞噬功能并改变他们的调节功能,这可能是AIDS患者易产生合并感染和重复感染（如呼吸道、肠道感染和HIV-1痴呆）的原因。高效抗逆转录病毒疗法（HAART）能显著改善单核／巨噬细胞和中性粒细胞的化学趋化活性和生物活性,改善这些细胞的功能,降低继发感染的发生率。     

Elmo1上调中性粒细胞胞外诱捕网的形成

探讨Elmo1在中性粒细胞胞外诱捕网(neutrophil extracellular trap,NET)形成过程中的作用机制。分别提取WT小鼠和Elmo1敲除小鼠的中性粒细胞后,用PMA诱导NET形成。运用激光扫描共聚焦显微镜对NET的形成进行观察,用多功能酶标仪读取荧光强度值并进行定量分析。为了进一步探索Elmo1调节NET形成的分子机制,我们用Western blotting检测了NET形成过程中相关信号通路的激活情况,包括p38和Akt。结果发现,Elmo1敲除的条件下,NET的形成明显减少。同时,在Elmo1敲除小鼠的中性粒细胞中,PMA诱发的p38和Akt的激活也显著降低。抑制p38、Akt后,WT和Elmo1敲除型小鼠之间NET形成的差异消失。说明Elmo1通过p38和Akt参与上调NET的形成。上述结果提示Elmo1参与上调NET形成。     

Circadian structure of rat neutrophil phagocytosis

Published findings regarding the time structure of phagocytosis appear to be partly discordant. In addition, this feature has not yet been evaluated in rats, although the rat is an important biomodel used for haematological preclinical biomedical studies. Thus, we examined selected characteristics using rats in order to help elucidate the above-mentioned controversies and to provide further complete data on the haematology of this biomodel. The ingestion of foreign particles (HEMA) or large cells (yeast), the reduction of nitroblue tetrazolium salts (NBT) in rat circulating neutrophils and their migration were evaluated. We found circadian variations in the following characteristics of neutrophil phagocytosis: (i) phagocytic activity; the concentration of engulfed particles and phagocytic index decreases late in the day and peaks in the morning; (ii) NBT reduction; a rise being observed at noon and a fall in the evening. The acrophase for phagocytosis of larger yeast cells was earlier (small hours) than that of smaller HEMA particles (in the morning). Chemotactically oriented migration showed a significant increase in the afternoon, but we have not found a statistically significant fit for the cosine function of this characteristic. No circadian rhythm was present in spontaneous migration. Our findings support the opinion that changes in phagocytic characteristics are a part of the circadian system of the immune system in laboratory rats. By comparing our data with the literature it seems that discrepancies in the courses of the circadian rhythms can be at least partly caused by different laboratory procedures as well as by different acrophases for the various elements of phagocytosis.     

Leptin modulates neutrophil phagocytosis of Klebsiella pneumoniae

Leptin is a pleiotropic hormone-cytokine known to regulate energy homeostasis and immune function. Neutrophils from leptin-deficient mice exhibited impaired phagocytosis of Klebsiella pneumoniae opsonized with serum containing complement and reduced CD11b expression that could be restored with exogenous leptin. These results suggest that leptin is required for normal neutrophil complement-mediated phagocytosis of bacteria.     

Cocaine inhibits human neutrophil phagocytosis and phagolysosomal acidification in vitro

Cocaine, used intravenously, increases the risk of infections, but its effects on neutrophil phagocytosis have not been examined in vitro. Human neutrophils were suspended in cocaine hydrochloride 0, 1, 10, 50, 100 or 200 microg/ml in Hank's balanced salt solution to which was added a phagocytic meal of killed Saccharomyces cerevisiae stained with the pH indicator dye bromcresol purple. Yeast per phagocytosing neutrophil and the percent neutrophils phagocytosing yeast were reduced in neutrophils treated with cocaine 100 and 200 microg/ml (P < 0.05). When examined for percent of yeast phagocytosed after 10 minutes, neutrophils treated with cocaine 1-200 microg/ml demonstrated a decrease (P < 0.05). However, at 60 minutes only neutrophils treated with cocaine 50 and 100 microg/ml still showed a decrease in percent of yeast phagocytosed. Phagolysosomal acidification was impaired in neutrophils treated with 50, 100 and 200 microg/ml cocaine. Thus, cocaine inhibits neutrophil phagocytosis and phagolysosomal acidification in vitro, offering a reason for cocaine users/abusers to have impaired host defense and to be potentially at higher risk for infections.     

Modification of the neutrophil Fc receptor by neutrophil granule products: its significance for phagocytosis and bactericidal activity

Preincubation of neutrophils with various amounts of autologous neutrophil granule products induced a dose-dependent decrease in neutrophil Fc receptor expression. However, neutrophil granule products did not affect the neutrophil phagocytic and bactericidal activities.     

Leukotriene B4 augments neutrophil phagocytosis of Klebsiella pneumoniae

Neutrophils play a critical role in the clearance of bacteria from the lung and other organs by their capacity for phagocytosis and killing. Previously, we identified an important role for the leukotrienes in rat alveolar macrophage phagocytosis of Klebsiella pneumoniae. In this report, we explored the possibility that the leukotrienes play an important role in phagocytosis by neutrophils as well. Inhibition of endogenous leukotriene synthesis by 5-lipoxygenase knockout in mice or by pharmacologic means in human peripheral blood neutrophils attenuated phagocytosis of opsonized K. pneumoniae. Reduced phagocytosis was also observed in human neutrophils pretreated with a leukotriene B4 receptor but not a cysteinyl-leukotriene receptor antagonist. While leukotriene B4 reconstituted defective phagocytosis in leukotriene-deficient neutrophils and enhanced phagocytosis in neutrophils capable of leukotriene synthesis, leukotriene C4, leukotriene D4, 5-hydroperoxyeicosatetraenoic acid, and 5-oxo-eicosatetraenoic acid were ineffective. To determine the opsonin dependence of the leukotriene B4 augmentation of phagocytosis, we assessed the ability of leukotriene B4 to modulate neutrophil phagocytosis and the adherence of sheep erythrocytes opsonized with immunoglobulin G or the complement fragment C3bi. While leukotriene B4 augmented both Fc receptor- and complement receptor-mediated phagocytosis, increased adherence to leukotriene B4-treated neutrophils was limited to complement opsonized targets. In conclusion, we have identified a novel role for leukotriene B4 in the augmentation of neutrophil phagocytosis mediated by either the Fc or complement receptor.     

Kinetic studies on phagocytosis IV. Cellular defects and humoral inhibition as causes of impaired neutrophil phagocytosis in sarcoidosis

Kinetic measurements of the serum-independent uptake of IgG-coated or complement-opsonized latex particles have been performed in 58 patients with sarcoidosis. The mean rate for phagocytic uptake of IgG particles was 0·56 min^-1 which was not different from that of the controls (0·59 min^-1). The phagocytosis of complement-opsonized particles was in the patient group 0·53 min^-1 and significantly (P<0·001) reduced compared to the rate of the controls (mean rate 0·94 min^-1), indicating neutrophil C3b-receptor dysfunction in sarcoidosis. PMNs from patients with sarcoidosis were not stimulated by the presence of autologous serum in contrast to PMNs from normals and in individual cases even a reduced uptake was found. More than one-third of the sarcoid sera also inhibited the phagocytosis of normal PMNs indicating the presence of a phagocytosis-inhibitory activity in sarcoid sera. Patients with more severe lung affection as estimated by measurements of total lung capacity, central airway obstruction, small airway function and pulmonary X-ray changes had a more reduced PMN phagocytosis in the presence of autologous serum than those with minor signs of lung affection (P<0·05). The phagocytosis-inhibitory activity of sarcoid serum was also more pronounced in those individuals who had high pulmonary score (P<0·05) or radiographic stage II-IV sarcoidosis (P<0·01). No correlation was found between serum levels of lactoferrin or lysozyme and any of the phagocytic variables while elevated β₂-microglobulin levels were associated with more pronounced serum-mediated inhibition of PMN phagocytosis (P<0·05). The relevance of these findings to the pathogenesis of granuloma formation in sarcoidosis is discussed.     

Changes in the kinetics of intracellular IFN-gamma production in TB patients during treatment

The role of T lymphocyte cytokine responses in tuberculosis (TB) still needs clarification. This study aimed to define interferon-gamma (IFN-gamma) responses longitudinally in HIV-negative TB patients during treatment, compared to those of healthy volunteers. Flow cytometric intracellular IFN-gamma determinations after CD3 stimulation were done in parallel with lymphocyte proliferation assays in response to mycobacterial antigen. Percentages of IFN-gamma-producing CD8 and CD4 T lymphocytes in patients at diagnosis were significantly higher than in controls but normalized during treatment. Additional kinetic studies suggested accelerated IFN-gamma production in patients at diagnosis, compared to controls and treated patients. Lymphocyte proliferation was below normal in patients at diagnosis and increased rapidly with decreasing bacterial load during treatment. We conclude that T cell IFN-gamma response kinetics in TB patients suggest a pre-activated state at diagnosis, which changes during treatment. At diagnosis intracellular IFN-gamma or lymphocyte proliferation was not an indicator for treatment response.     

Role of alpha-hemolysin for the in vitro phagocytosis and intracellular killing of Escherichia coli

The role of alpha-hemolysin for the elimination of Escherichia coli by phagocytes in vitro was investigated using sets of isogenic strains which included wild-type alpha-hemolytic strains, derived strains with a reduced production of alpha-hemolysin and derived nonhemolytic strains. Phagocytosis and intracellular killing of the bacteria by human blood granulocytes or monocytes were measured using growth inhibition techniques. alpha-hemolytic strains were phagocytosed and killed to a lesser extent than isogenic strains with a reduced production of alpha-hemolysin and isogenic nonhemolytic strains. The results obtained with granulocytes were similar to those obtained with monocytes although the elimination of bacteria by monocytes was less than that by granulocytes. These results strongly suggest that production of alpha-hemolysin is a means by which E. coli counteracts the activity of phagocytes by injuring these cells with the toxin.     

Function of phagocytosis and intracellular killing of peripheral neutrophils in Kawasaki disease

NBT (Nitroblue Tetrazolium) test was performed in 17 patients with Kawasaki disease to examine the function of phagocytosis and intra-cellular killing of neutrophils. The value was high compared to other pediatric patients. Activation with Proteus OX-2 antigen before NBF test showed a significant higher level than other proteus antigens, which correspond in serum level. With previous electronmicroscopic observation of rickettsia-like body in biopsy specimen, these findings suggest the existence of an agent in Kawasaki disease which shares antigenicity with Proteus OX-2.     

Monocytes in inflammatory bowel disease: phagocytosis and intracellular killing.

The ability of peripheral blood monocytes from patients with ulcerative colitis and Crohn's disease to phagocytose and kill a standard strain of Staphyloccus aureus has been studied. Using lysostaphin, a rapidly acting muralytic enzyme, phagocytosis could be accurately differentiated from intracellular killing. When compared with normal healthy individuals and patients with gastrointestinal diseases not thought to be immunologically mediated, monocytes from patients with inflammatory bowel disease showed a statistically significant increase in the number of bacteria phagocytosed in 2 hours. There was no difference, however, between patients with Crohn's disease and those with ulcerative colitis. For all groups studied, more than 95% of ingested organisms were killed, and there was no difference between groups. These results suggest that peripheral blood monocytes in patients with Crohn's disease and ulcerative colitis are activated. It is unlikely that the granulomata of Crohn's disease result from a defect in the microbicidal function of the monocyte/macrophage system.