Pulmonary arterial smooth muscle cells (PASMC) were divided into a normoxic group (N), 2, 8 and 12 h hypoxic groups (H2, H8 and H12) and an AG490 plus 8 h hypoxic group (AG490). The expression of JAK1, JAK2, JAK3 and TYK2 mRNA was analyzed by reverse transcription-polymerase chain reaction (RT-PCR). STAT1 and STAT3 protein expressions were determined by Western blotting. The results showed that the levels of JAK1, JAK2 and JAK3 mRNA did not change significantly in the N group but were increased after 2 h exposure to hypoxia. JAK1, JAK2 and JAK3 mRNA expressions peaked at 8 h. It decreased at 12 h but remained above those in the N group. TYK2 mRNA was not found in either hypoxic or normal PASMC. The phospho-STAT1 and-STAT3 protein levels increased after 2 h exposure to hypoxia. They were about 2.8 and 4.1 times the N group, respectively, after 8 h. They decreased at 12 h but remained above those in the N group. AG490 inhibited phospho-STAT3 protein expression by about 25.5% at 8 h but did not block the expression of phospho-STAT1 protein. These findings suggest that hypoxia induces the expression of JAK1, JAK2, JAK3 and phospho-STAT1 and -STAT3 in PASMC. Hypoxia activates the JAKseSTATs signaling pathway, which may participate in the pathogenesis of hypoxic PASMC injury.

Allergen-specific CD4+ T-helper (Th) 2 cells are involved in the induction and effector phase of allergic asthma. It is well established that T cells activation requires interaction of T cell receptor (TCR) and MHC-peptide complex, as well as costimulatory signal delivered by antigen presenting cells (APCs). There is increasing evidence that CD80 (B7.1) and CD86 (B7.2), as the most important costimulatory molecules, are involved in the allergic immune responses. In the present study, we investigated the CD80 and CD86 expression of spleen-derived dendritic cells (DCs) in a murine model of allergic asthma. We first established a murine model of ovalbumin (OVA)-allergic asthma that showed unique histological characteristic of allergic inflammation in the lung, high serum OVA-specific IgE level, high numbers of eosinophils in the bronchoalveolar lavage (BAL) and high production of Type 2 cytokines in the splenic T cells. In this model, we found that CD80 were significantly upregulated on the spleen-derived DCs from OVA-sensitized and challenged mice compared with that from PBS-treated or non-treated mice, while CD86 is not different among three groups. Furthermore, we demonstrated that Th2 immune responses were elicited by these DCs with high expression of CD80, even to naı¨ve T cells from non-treated mice. Our results suggest that DCs in the spleen of allergic mice, via upregulation of CD80 might play a pivotal role in the maintenance and amplification of allergic immune response, namely Th2 immune response.

目的观察血红素氧合酶（HO）在慢性阻塞性肺疾病（COPD）患者中的表达及其变化。方法设COPD组、COPD合并肺癌组、单纯肺癌组及正常健康组。4组均进行血气分析和肺功能测定。应用紫外分光光度计间接测定动脉血一氧化碳血红蛋白（COHb）含量和肺脏HO-1的活性。用逆转录-聚合酶链反应检测肺脏和肺动脉组织HO mRNA表达水平。用免疫组化法测定肺脏组织HO蛋白的表达。结果COPD组和COPD合并肺癌组患者动脉血氧分压低于60 mm Hg（1 mm Hg=0.133 kPa），提示这两组患者均为I型呼吸衰竭患者。与正常健康组比较，这两组患者的肺一氧化碳弥散量、肺一氧化碳弥散量/肺泡通气量及1秒钟用力呼气容积占预计值的百分比均显著降低，残气容积/肺总量显著升高，提示这两组患者均患有中度COPD（Ⅱ级）。这两组患者的COHb明显高于单纯肺癌组和正常健康组（P<0.01），单纯肺癌组和正常健康组比较差异无显著性。COPD合并肺癌组患者胆红素生成量、肺脏及肺动脉组织HO-1mRNA吸光度值明显高于单纯肺癌组和正常健康组。HO-1免疫组化染色显示，COPD合并肺癌组非癌变肺组织肺泡壁细胞、肺内小血管和支气管壁细胞胞质HO-1的表达显著增强。结论COPD患者HO-1表达增多。

目的 通过观察大鼠常压缺氧肺动脉高压模型肺组织信号传导与转录活化因子（STATs）的表达水平，探讨其在低氧性肺动脉高压（HPH）形成过程中参与的可能机制。方法健康成年雄性Wistar大鼠60只，随机分为缺氧组和健康对照组，缺氧组大鼠复制HPH模型。用逆转录（RT）-聚合酶链反应（PCR）和Northern hlot检测2组大鼠肺组织STATsmRNA的表达水平，免疫组化检测大鼠肺组织STATs蛋白的含量。结果RT-PCR扩增显示，缺氧1周大鼠肺组织STAT 1、STAT 2、STAT 3、STAT 5 mRNA表达水平升高，缺氧2周表达水平最高，缺氧3周表达水平降低，但明显高于健康对照组；且缺氧2周的表达水平高于其他缺氧时间（P<0. 05）；STAT 4未检出。Northern blot显示，缺氧2周大鼠肺组织STAT 1、STAT 3、STAT 5 mRNA表达高于其他缺氧时间（P<0.01）。缺氧3周大鼠肺组织STAT 3和STAT 5组化染色可见，肺泡壁细胞、支气管壁细胞、小血管壁细胞及巨噬细胞的胞核呈紫蓝色；图像定量分析显示，缺氧3周大鼠肺组织STAT 3和STAT 5蛋白表达含量最高，缺氧4周含量降低.但仍高于健康对照组（P<0.01）。结论大鼠常压缺氧肺动脉高压模型肺组织STATs mRNA和蛋白表达增高，提示STAT可能参与了HPH的发病机制。

目的研究缺氧肺动脉高压（HPH）肺组织中白细胞介素6（IL-6）及Janus激酶（JAKs）表达的变化。方法 雄性Wistar大鼠60只，随机分为缺氧1周（H1）、缺氧2周（H2）、缺氧3周（H2）、缺氧4周（H4）和常氧（N）组，每组12只。常压缺氧舱复制HPH大鼠模型。应用逆转录一聚合酶链反应（RT-PCR）检测肺组织IL-6和JAKs mRNA的表达水平；免疫组化法检测肺组织JAKs蛋白的含量和细胞形态学变化。结果 （1）H1、H2和H3组大鼠肺组织IL-6 mRNA水平（分别为1.67±0.09、2.26 +0.12、1.55 +0.11）显著高于N组（1.20±0.11，P均<0.01）；Hl、H2和H3组大鼠肺组织JAKI mRNA水平（分别为2.11 ±0. 09、2.85 +0. 12、2.36±0.13）显著高于N组（1.62±0.10，P均<0.O1）;H1、H2和H3组大鼠JAK2 mRNA水平（分别为1.41±0.07、2.02±0.13、1.36±0.09）显著高于N组（1.01±0.09，P均<0.01）；H1、H2和H3组大鼠肺组织JAK3 mRNA水平（分别为0.86±0.11，1.45±0.10、0.91±0.13）显著高于N组（0.55±0.08，P均<0.01）；H1、H2组大鼠肺组织TYK2 mRNA水平（分别为1.36±0.10，1.76±0.11）显著高丁.N组（0.57±0.07，P均<0.01）；其中H2组大鼠肺组织表达IL-6和JAKs mRNA水平显著高于H1组和H2组（P均<0.01）；（2）H2组肺组织JAKI和JAK3组织化学染色可见，肺泡壁细胞、支气管壁细胞、小血管壁细胞以及巨噬细胞的胞浆呈棕黄色；TIGER图像定量分析表明，H3组JAKl（5.36±0.32）和JAK3（4.88±0.29）蛋白表达显著高于N组（分别为1.52±0.18，1.22±0.09；P均<0.01）。结论HPH大鼠肺组织中IL-6和JAKs mRNA和蛋白表达升高，说明IL-6/JAKs通路参与了HPH的发病机制。

要急性肺损伤和急性呼吸窘迫综合征是指由心源性以外的各种肺内外致病因素所导致的急性、进行性缺氧性呼吸衰竭。近年来，对急性肺损伤和急性呼吸窘迫综合征的命名和定义进行了更新和规范，对发病机制有了新的认识，提出了临床诊断标准和综合治疗措施。随着对急性肺损伤和急性呼吸窘迫综合征的深入研究，从炎症失控、调控着手去认识发病机制，采取针对性治疗，可望取得突破性进展。

急性呼吸窘迫综合征（acute respiratory distress syndrome， ARDS）是一种灾难性疾病，从其提出至今，已对其进行了大量的基础和临床研究。在1994年美欧联席会议（AECC）上对该综合征的定义达成了共识，并提出其本质是肺部炎症和通透性增加的综合征，使人们对该综合征的认识有了一个大的飞跃。现就近年ARDS的主要研究进展综述如下[l，2]。

目的研究脂多糖结合蛋白（LBP）抑制肽对内毒素（LPS）诱导的人单核巨噬细胞株U937细胞表达CD14的影响。方法佛波脂（PMA）诱导U937成熟后分为5组：正常对照组、LPS组（100ng/mL LPS+100ng/mL thLBP）、低剂量抑制肽组、中剂量抑制肽组及高剂量抑制肽组，后3组分别给予10、100和1000ng/mL抑制肽。用RT-PCR和蛋白定量方法（Westem blot）测定CD14 mRNA和蛋白的表达，ELISA测定培养上清液中肿瘤坏死因子-a（TNF-a）的含量。结果LBP抑制肽显著抑制LPS刺激后U937细胞CD14的mRNA与蛋白表达，同时也抑制了TNF-a的分泌，较LPS组有显著差异。结论LBP抑制肽通过抑制由CD14介导的LPS信号跨膜转导和TNF-a的分泌，对LPS所致疾病如脓毒血症、急性肺损伤可能有潜在的治疗作用。