免疫组化法检测人牙龈成纤维细胞TRAF6表达

目的:采用免疫组化法检测人牙龈成纤维细胞(HGFs)肿瘤坏死因子受体相关因子-6(TRAF-6)的表达及LPS的影响.方法:采用原代培养的人牙龈成纤维细胞,取3～8代细胞以LPS梯度浓度干预,24 h后观察干预后人牙龈成纤维细胞形态学的变化,并采用免疫组织化学的方法检测TRAF6在各组细胞中的表达.结果:TRAF-6在...     

IL-1β诱导人牙龈成纤维细胞TRAF6表达

目的 观察白细胞介素1β(IL-1β)干预人牙龈成纤维细胞中肿瘤坏死因子受体相关因子6(TRAF6)表达水平,为研究细胞因子对牙周组织的调控作用提供理论依据.方法 采用原代培养的人牙龈成纤维细胞,取3～8代细胞以不同浓度IL-1β进行于预,24 h后观察干预后人牙龈成纤维细胞形态学变化,采用免疫组织化学方法检测TRAF6在各组细胞中的表达:结果IL-1β干颅后,人牙龈成纤维细胞形态改变不明显;免疫组化结果显示,以0.1、0.5、1、5、10 ng/mL的IL-1β干预后,细胞中TRAF6呈阳性表达.并且随IL-1β干预浓度升高而增强,TRAF6蛋白表达量吸光度分别为(0.15±0.012)、(0.19±0.010)、(0.20±0.008)、(0.24±0.010)、(0.27±0.011).两两比较,差异均有统计学意义(均P＜0.01).结论 TRAF6表达水平变化提示,TRAF6可能是参与牙龈成纤维细胞功能调控的重要信号分子.     

纳米二氧化硅诱导巨噬细胞焦亡对肺成纤维细胞的影响

目的 探讨纳米二氧化硅(SiNPs)诱导巨噬细胞焦亡对原代肺成纤维细胞基质金属蛋白酶及成纤维细胞向肌成纤维细胞转分化的影响。方法 构建SiNPs致巨噬细胞焦亡模型后,采用纳米高光谱定位巨噬细胞中SiNPs、光学显微镜观察巨噬细胞SiNPs暴露后形态、Western blot检测焦亡相关蛋白表达。通过胰酶和Ⅳ型胶原酶消化法提取小鼠原代肺成纤维细胞;以光学显微镜和免疫荧光技术表征并鉴定原代肺成纤维细胞;体外构建SiNPs诱导巨噬细胞焦亡与原代肺成纤维细胞共培养模型。以正常巨噬细胞上清干预原代肺成纤维细胞作为MF组,焦亡巨噬细胞上清干预原代肺成纤维细胞作为PF组,采用qRT-PCR、Western blot技术分别检测原代肺成纤维细胞中MMP2、MMP9的mRNA水平和蛋白表达,免疫荧光、免疫细胞化学染色检测肌成纤维细胞标志物α-SMA蛋白表达。结果 纳米高光谱、形态学观察和Western blot检测结果显示, SiNPs 成功诱导J774A.1 巨噬细胞发生焦亡,光学显微镜观察发现,与胰酶消化法相比,Ⅳ型胶原酶法提取小鼠原代肺成纤维细胞的纯度更高;免疫荧光结果提示Ⅳ型胶原酶法获得的成纤维细胞波形蛋白呈现典型的微丝结构,细胞骨架结构完整。qRT-PCR 结果显示,PF组MMP2 和MMP9 mRNA水平较MF组增加(P<0.05), Western blot结果显示,PF组MMP2和MMP9蛋白表达水平较MF组升高(P<0.05), 免疫荧光结果显示,与MF组相比,PF组α-SMA红色荧光强度增加,免疫细胞化学染色为强阳性。结论 SiNPs诱导巨噬细胞焦亡能够促进原代肺成纤维细胞MMP2和MMP9表达水平上调,并促进成纤维细胞向肌成纤维细胞转分化。     

激光扫描共聚焦显微镜中荧光强度的测定条件研究

目的对应用激光扫描共聚焦显微镜进行荧光强度的测定条件做了详细的分析.方法选择和设置激光扫描共聚焦显微镜的各参数,对用间接免疫荧光法检测改性后的材料表面对人牙龈成纤维细胞分泌细胞外基质纤粘连蛋白FN和Ⅰ型胶原的影响进行荧光强度的定量.结果细胞在材料表面接种后FN的荧光染色强度在四组材料之间没有显著差异,说明材料表面化学成分的改变对FN的形成没有明显影响.但四组材料对Ⅰ型胶原分泌的影响有差异.结论选择和设置适合的激光扫描共聚焦显微镜中荧光强度的测定条件,可以真实有效的反映实验的结果.     

石英对肺成纤维细胞增殖信号的影响及氧化苦参碱的拮抗作用

目的通过体外实验探讨石英-肺泡巨噬细胞(AM)培养上清液联合氧化苦参碱(OM)对肺成纤维细胞增殖信号的影响。方法对SD大鼠乳鼠肺成纤维细胞进行原代培养和传代培养,传至4~5代后,用石英-AM培养上清液刺激成纤维细胞,培养一定时间,用氯氨T法检测细胞中羟脯氨酸的含量;用免疫细胞化学技术测定成纤维细胞膜Gq蛋白的表达;用流式细胞技术检测成纤维细胞内Ca2+的含量。结果与空白对照组比较,石英-AM培养上清液作用于成纤维细胞不同时间羟脯氨酸含量明显增高(P0.05);Gq表达量相对值以及细胞内游离Ca2+荧光强度(F)值明显增高(P0.05),且随作用时间的延长呈现逐渐升高趋势。上清液联合OM后,与上清液单独作用组比较,羟脯氨酸含量降低,差异有统计学意义(P0.05)。结论石英-AM培养上清液对成纤维细胞增殖和胶原合成有促进作用,这种促进作用可能与成纤维细胞膜上Gq蛋白介导的信号传导通路有关。中药OM抑制纤维化的作用可能与成纤维细胞膜上Gq蛋白介导的Ca-IP3通路有关。     

0.2 mT工频磁场引起人羊膜成纤维细胞微丝骨架重组

目的探讨50Hz工频磁场对人羊膜成纤维细胞微丝装配的影响,并分析磁场对肌动蛋白和表皮生长因子受体蛋白表达的影响。方法将人羊膜成纤维细胞分别用0．1、0．2．0．3、0．4、0．5mT,50Hz工频磁场辐照30min,以异硫氰四甲基罗丹明一鬼笔环肽标记细胞微丝并在显微镜下观察分析微丝形态的变化。用荧光光谱及紫外光谱检测法测定细胞内微丝总含量,用激光共聚焦显微镜逐层扫描的方法观测细胞微丝骨架的高度,用扫描电镜观测细胞外部形态等方法进一步分析磁场对细胞微丝骨架及细胞形态的影响。用Western blotting检测去垢剂不可溶的蛋白的表达量以分析磁场作用的可能机制。结果人羊膜成纤维细胞经不同强度工频磁场辐照30min后,只有0．2mT工频磁场辐照显著导致细胞中平行排列的微丝应力纤维减少,诱导细胞周边出现致密微丝外周带并伸出丝状伪足,停止辐照2h后微丝形态恢复,伪足消失。光谱检测发现胞内微丝总含量无显著变化。激光共聚焦显微镜逐层扫描观测到0．2mT磁场辐照使细胞微丝骨架平均高度由（12．37±1．28）μm降低到（9．97±0．38）μm（t=6．96,P〉0．05）。扫描电镜图像显示磁场辐照使细胞更为扁平,有足状伪足出现。Western blotting检测到磁场辐照后细胞骨架中去垢剂不可溶部分的肌动蛋白和表皮生长因子受体含量与对照组相比,分别升高（16．8±2．3）％（t=16．68,P〈0．05）和（31．2±4．1）％（t=17．10,P〈0．05）。结论0．2mT工频磁场短时辐照影响了人羊膜成纤维细胞微丝骨架的形态,此效应可随磁场撤销而解除,且可能与磁场诱导了细胞膜上表皮生长因子受体聚簇有关。     

乳鼠成纤维细胞在人血清中的存活与增殖的研究

目的：本研究旨在证明人血清直接培养乳鼠成纤维细胞是可行的。方法：将乳鼠成纤维细胞分别在胎牛血清及人血清中培养,通过在显微镜下观察成纤维细胞形态及密度,同时用MTT比色法检测吸光度来对比成纤维细胞在胎牛血清及人血清中的增殖活性。结果：两种实验方法均显示：两组成纤维细胞在第一天的增殖活性无显著性差异,第四天人血清组的成纤维细胞增殖明显比胎牛血清组活跃。结论：乳鼠成纤维细胞在人血清中不仅可以存活,而且有增殖行为。     

人Kv1.5通道基因转染人胚胎肾细胞的研究

目的建立表达人Kv1.5通道的细胞模型。方法采用Lipofactamine 2000脂质体将人Kv1.5通道基因转染人胚胎肾细胞(HEK293),通过荧光显微镜和全细胞膜片钳技术观测人Kv1.5通道基因的表达。结果pcDNAHKv1.5真核表达载体转染HEK293细胞2d后,荧光显微镜可观察到人Kv1.5通道表达;3d后全细胞膜片钳技术记录到人Kv1.5通道基因编码的通道电流。结论pcDNAHKv1.5真核表达载体转染HEK293细胞为人Kv1.5通道的研究提供了良好的真核细胞表达系统和细胞模型。     

间接荧光抗体试验在主要寄生虫病监测中的应用进展

间接荧光抗体试验(IFAT)是通过将荧光素与抗人免疫球蛋白或其他第二抗体在不影响抗体免疫特性的情况下，用化学方法结合起来，制备成荧光抗体。当作为检测用的未标记的抗原(或抗体)与待测标本中相应的抗体(或抗原)结合成抗原一抗体复合物时，加入荧光抗体与之结合形成免疫荧光复合物，即可在荧光显微镜下显示亮绿色荧光，从而间接地显示出待测标本中存在着相应抗体(或抗原)。IFAT最早用于寄生虫病的血清     

电穿孔法介导转染老年人成纤维细胞参数的优化

目的探究采用电穿孔法将质粒pGenesil-1(简称p G)转染老年人成纤维细胞,从中寻找最佳的参数。方法采用电穿孔法将能表达G418抗性蛋白和增强型绿色荧光蛋白(EGFP)的质粒p G转染老年人成纤维细胞。荧光显微镜下观察EGFP表达并测定转染效率、细胞存活率;通过G418筛选得到稳定转染的细胞。结果本实验室电穿孔法介导的老年人成纤维细胞转染的最佳电转条件:电压:240 V;电容:750μF;DNA剂量:8μg。48 h后电穿孔法的转染率接近30%。结论用电穿孔法将质粒pG稳定转染老年人成纤维细胞耗时短,有利于在体外对老年人成纤维细胞进行后续实验。     

Monocyte CD14 response following endotoxin exposure in cotton spinners and office workers

BACKGROUND: Monocyte cell surface CD14 acts as the major lipopolysaccharide (LPS) binding structure, and as such is of interest in the etiology of LPS induced disease. METHODS: The objective was to assess change in monocyte cell surface CD14 and CD4+ CD25+ lymphocytes in a group of cotton workers exposed to LPS over a working week, and to compare this to changes in office workers. Twenty-five cotton workers and nine office workers were studied. Monocyte CD14 fluorescence was measured by flow cytometry, on samples taken pre-shift on a Monday morning (baseline/pre-exposure), and subsequently after 6 and 72 hr. The majority of cotton workers were exposed to at least 1 EU/m(3) of endotoxin over a working shift, and some highly exposed (between 100 and 400 EU/m(3)). RESULTS: After 6 hr of work in the mill, cotton workers developed a significant upregulation in CD14 in comparison to office workers (P = 0.016), whereas CD14 expression had returned to levels not significantly differing from the office workers at 72 hr after first work exposure (P = 0.426). CONCLUSIONS: We propose that CD14 expression on monocytes may help to determine the mechanism of action of lipopolysaccharide in producing respiratory ill health, and may ultimately play a role in monitoring the health effect associated with LPS exposure in the workplace.     

心理弹性量表信度和效度评价及应用

目的通过对心理弹性量表简表(RS-14)信度和效度的评价,探讨该量表应用于中国成年居民心理弹性测量的可行性,为临床患者进行心理弹性评估提供特异性测量工具。方法采用整群抽样方法,抽取福建省部分市、县、乡镇各级卫生院医务从业人员以及福州市鼓楼区军门社区居民446人,使用翻译为中文版的RS-14进行测量,对该量表信度及效度进行考评。结果RS-14量表包含14个条目,2个公因子,分别为个人能力和积极认知,共解释总方差的60.755%;RS-14总分与SF-36总分呈正相关(r=0.513,P<0.001);1周前后2次测量RS-14总分呈正相关(r=0.812,P=0.000);奇数组和偶数组2个半量表得分呈正相关(r=0.890,P<0.001);整体量表内部一致性Cronbach's α系数为0.928;不同社会支持利用度者心理弹性得分差异有统计学意义(F=23.781,P=0.000)。结论RS-14量表具有较好的信度和效度,可作为测量中国普通成年人心理弹性高低的可靠工具,但该量表是否应用于中国肿瘤患者仍需进一步的深入研究。     

Parenteral Nutrition Rapidly Reduces Hepatic Mononuclear Cell Numbers and Lipopolysaccharide Receptor Expression on Kupffer Cells in Mice

Background: Parenteral nutrition (PN) reduces the number of hepatic mononuclear cell (MNCs) and impairs their function, resulting in poor survival after intraportal bacterial challenge in mice. Our recent animal study demonstrated resumption of enteral nutrition after PN to rapidly restore hepatic MNC numbers (in 12 hours) and lipopolysaccharide (LPS) receptor expression on Kupffer cells (in 48 hours). The present study examined the time courses of hepatic MNC number reductions and LPS receptor expression changes in mice receiving PN. Methods: Male mice (n = 49) from the Institute of Cancer Research were divided into chow (n = 8), PN0.5 (n = 8), PN1 (n = 8), PN2 (n = 9), PN3 (n = 9), and PN5 (n = 7) groups. The chow group was given chow with an intravenous saline infusion. The PN groups were fed parenterally for 0.5, 1, 2, 3, or 5 days following the chow‐feeding courses. After 7 days of nutrition support, hepatic MNCs were isolated and counted. The expression of LPS receptors on Kupffer cells was analyzed by flow cytometry. Results: Hepatic MNC numbers rapidly reached their lowest level in the PN0.5 and PN1 groups but were somewhat restored thereafter and remained stable after the third day, without significant differences between any 2 of the PN groups. CD14 and Toll‐like receptor 4/MD‐2 expressions both showed significant reductions in the PN1 group compared with the chow group and gradually decreased to their lowest levels in the PN5 group. Conclusions: PN administration rapidly reduces hepatic MNC numbers and LPS receptor expression on Kupffer cells.     

青蒿琥酯对中暑内毒素血症小鼠腹腔巨噬细胞内CD14和Toll样受体4的影响

目的探讨青蒿琥酯对中暑内毒素血症小鼠腹腔巨噬细胞内CD14和Toll样受体4 (TLR4)表达的影响。方法昆明种小鼠随机分为常温组、高温组、生理盐水组和青蒿琥酯组(均按60 mg/kg连续5 d腹腔注射),常温组在干球温度25℃±0．5℃、相对湿度43%±5%的条件下暴露2 h,其他组在干球温度35℃±0．5℃、相对湿度65%±5%的条件下热暴露,观察不同时间点(1、2 h)小鼠腹腔巨噬细胞内CD14和TLR 4 mRNA的表达及血浆中肿瘤坏死因子α(TNF-α)的含量。结果常温组CD14和TLR 4 mRNA表达分别为0．34%±0．047%和0．31%±0．062%；高温1 h组分别为0．53%±0．085%和0．45%±0．049%,与常温组的差异均有统计学意义(P＜0．01),并在2 h时呈现继续升高的趋势；生理盐水1 h组CD14和TLR4表达升高,但在2h时有轻度下降；青蒿琥酯1 h组CD14和TLR4的表达则分别为0．26%±0．051%和0．25%±0．084%,并在2 h有轻微的下降。各组TNF-α含量的变化呈现出与CD14、TLR 4变化基本一致的趋势。结论青蒿琥酯能明显降低内毒素信号转导通路上CD14和TLR 4的表达,减少TNF-α的产生,这可能是其抗中暑内毒素血症的机制之一。     

A novel amino acid site closely associated with the neurovirulence of live,attenuated Japanese encephalitis vaccine (SA14-14-2 strain)

Japanese encephalitis (JE) poses a serious threat to the world’s public health yet without a cure, the only way to prevent Japanese encephalitis virus (JEV) infection is vaccination. Live attenuated vaccine (SA14-14-2 strain) is the most widely used JE vaccine, and clinical data have confirmed its safety and effectiveness. Eight sitesassociated with virulence in the Envelope (E) protein are often the focus of quality control of JE vaccine. However, sequences retrieved from NCBI, as well as our previous results showed that the wild strain SA14 may harbor two different amino acids at amino acid residue 244 of the E glycoprotein (E244), and it may be related to virulence. In this study, we introduced a single mutation at nt1708 (G → A) in the full-length cDNA clone of SA14-14-2, replacing a Gly with Glu at amino acid residue 244 of the E glycoprotein, and successfully constructed the mutant virus (JEV E244). JEV E244 exhibited a similar plaque morphology and growth characteristics to JEV SA14-14-2 in cell culture. However, it had lethal neurovirulence in mice and could enter the brain following intraperitoneal inoculation. Moreover, the virulence of JEV E244 in the context of vaccine in mice is significantly different from that of the JEV E244 alone. These results suggested that E244 site should be included in the assessment of the genetic stability of the attenuated JE vaccine. The detection of minor mutations in vaccine population and influence on the safety of vaccine is discussed.     

Immunologic response to inhaled endotoxin: changes in peripheral cell surface markers in normal individuals

Monocyte cell surface CD14 increases following both in vitro challenge with lipopolysaccharide (LPS) and exposure to organic dusts. We investigated 9 volunteers, mean age 39 years (range, 29-53 years). Each inhaled increasing concentrations of lipopolysaccharide (0.5 microg, 5.0 microg, and 20 microg). Monocyte cell surface CD14 (expressed as mean linear fluorescence) was measured before and after using flow cytometry. Upregulation of CD14 (up to 6 hours after LPS exposure) did not differ significantly between LPS (mean, 35.8; standard deviation [SD]; 54.3), n = 7 after 20 l g LPS) in comparison to placebo (39.3 [49.0]; n = 7). Maximum mean (SD) percentage CD14 upregulation up to 6 hours after challenge differed, but not significantly between those experiencing a clinically significant event (58.4 [49.2]) in comparison to those who did not (13.8, [43.2]; P = 0.27). Two individuals with a marked clinical response developed marked CD14 upregulation after exposure to LPS.     

Naturally-occurring human serum antibodies to inner core lipopolysaccharide epitopes of Neisseria meningitidis protect against invasive meningococcal disease caused by isolates displaying homologous inner core structures

Sera from healthy infants (under 1 year old), toddlers (3-4 years) and adults (18-65 years) were assayed for their ability to bind to inner core (ic) lipopolysaccharide (LPS) epitopes of Neisseria meningitidis. Antibodies (Abs) reacting to inner core structures, including different substitutions of the first heptose (HepI) and second heptose (HepII) residues of the LPS backbone, truncated and fully extended LPS glycoforms, were detected and for each structure, these inner core antibodies showed an age-related pattern of acquisition. A novel column-based methodology was used to affinity purify IgG antibodies in which purified inner core LPS (derived from a mutant MC58) was covalently linked to Sepharose 4B. Comparison of reactivity before and after affinity purification of the pooled sera showed that the purified Abs bound to the surface of N. meningitidis organisms displaying truncated and extended LPS with a homologous inner core region, promoted the deposition of C3b, were opsonophagocytic in vitro and decreased bacteraemia when used to passively protect infants rats. In addition, the purified Abs were bactericidal in vitro against the mutant strain displaying truncated LPS with a homologous inner core region. These results demonstrate that naturally occurring serum human antibodies to N. meningitidis LPS can access inner core epitopes of encapsulated organisms with a fully extended LPS.     

Bacterial cell envelopes (ghosts) but not S-layers activate human endothelial cells (HUVECs) through sCD14 and LBP mechanism.

Bacterial cell-envelopes (called ghosts) and surface layers (S-layers) are discussed to be used as vaccines and/or adjuvants, consequently it is necessary to find out which immunomodulatory mediators are induced in human cells. The present work focuses on the effects of ghosts (Escherichia coli O26:B6), S-layers (Bacillus stearothermophilus) in comparison with LPS and antibiotic-inactivated whole bacteria (E. coli O26:B6) on human umbilical vein endothelial cells (HUVEC) with regard to the release of interleukin 6 (IL-6) and the expression of surface E-selectin and the role of lipopolysaccharide binding protein (LBP), soluble CD14 (sCD14) and serum for this activation.Endothelial cells responded to ghosts, whole bacteria and LPS with IL-6 release up to 15000 pg/ml and surface E-selectin expression, while in contrast the response to S-layers with IL-6 release up to 500 pg/ml was very weak. Compared to LPS, 10-100-fold higher concentrations of bacterial ghosts and whole bacteria were required to induce the cytokine synthesis and E-selectin expression. IL-6 release and E-selectin expression of HUVECs were reduced in the absence of serum and equivalent to unstimulated samples. We have also studied the role of CD14 and LBP for the activation of endothelial cells using antiCD14 and antiLBP antibodies (Ab). AntiCD14 and antiLBP Ab both inhibited IL-6 release and E-selectin expression in a dose dependent manner after stimulation with ghosts, whole bacteria and LPS but had no effect on S-layers stimulated cells. AntiCD14 Ab inhibited more effectively than antiLBP Ab. These findings suggest that bacterial ghosts but not S-layers activate HUVECs through sCD14 and LBP dependent mechanisms.     

Neutralizing epitopes mapping of human adenovirus type 14 hexon

Human adenoviruses 14 (HAdV-14) caused several clusters of acute respiratory disease (ARD) outbreaks in both civilian and military settings. The identification of the neutralizing epitopes of HAdV-14 is important for the surveillance and control of infection. Since the previous studies had indicated that the adenoviruses neutralizing epitopes were likely to be exposed on the surface of the hexon, four epitope peptides, A14R1 (residues 141–157), A14R2 (residues 181–189), A14R4 (residues 252–260) and A14R7 (residues 430–442) were predicted and mapped onto the 3D structures of hexon by homology modeling approach. Then the four peptides were synthesized, and all the four putative epitopes were identified as neutralizing epitopes by enzyme-linked immunosorbent assay (ELISA) and neutralization tests (NT). Finally we incorporated the four epitopes into human adenoviruses 3 (HAdV-3) vectors using the “antigen capsid-incorporation” strategy, and two chimeric adenoviruses, A14R2A3 and A14R4A3, were successfully obtained which displayed A14R2 and A14R4 respectively on the hexon surface of HAdV-3 virions. Further analysis showed that the two chimeric viruses antiserum could neutralize both HAdV-14 and HAdV-3 infection. The neutralization titers of anti-A14R4A3 group were significantly higher than the anti-KLH-A14R4 group (P = 0.0442). These findings have important implications for the development of peptide-based broadly protective HAdV-14 and HAdV-3 bivalent vaccine.     

Effects of airway exposure to nanoparticles on lung inflammation induced by bacterial endotoxin in mice

BACKGROUND: Although adverse health effects of particulate matter with a diameter of < 100 nm (nanoparticles) have been proposed, molecular and/or experimental evidence for their facilitation of lung inflammation in vivo is not fully defined. OBJECTIVE: In the present study we investigated the effects of nanoparticles on lung inflammation related to bacterial endotoxin [lipopolysaccharide (LPS) ] in mice. RESULTS: We intratracheally administered vehicle, two sizes (14 nm, 56 nm) of carbon black nanoparticles (4 mg/kg) , LPS (2.5 mg/kg) , or LPS plus nanoparticles and evaluated parameters for lung inflammation and coagulation. Nanoparticles alone induced slight lung inflammation and significant pulmonary edema compared with vehicle. Fourteen-nanometer nanoparticles intensively aggravated LPS-elicited lung inflammation and pulmonary edema that was concomitant with the enhanced lung expression of interleukin-1beta (IL-1beta) , macrophage inflammatory protein-1alpha (MIP-1alpha) , macrophage chemoattractant protein-1, MIP-2, and keratinocyte chemoattractant in overall trend, whereas 56-nm nanoparticles did not show apparent effects. Immunoreactivity for 8-hydroxyguanosine, a marker for oxidative stress, was more intense in the lungs from the LPS + 14-nm nanoparticle group than in those from the LPS group. Circulatory fibrinogen levels were higher in the LPS + plus 14-nm nanoparticle group than in the LPS group. CONCLUSIONS: Taken together, evidence indicates that nanoparticles can aggravate lung inflammation related to bacterial endotoxin, which is more prominent with smaller particles. The enhancement may be mediated, at least partly, via the increased local expression of proinflammatory cytokines and via the oxidative stress. Furthermore, nanoparticles can promote coagulatory disturbance accompanied by lung inflammation.