Summary： This study investigated the expression of interleukin-17 （IL-17） and T cell immunoglobulin mucin and domain-containing molecule-3 （Tim-3） in bronchoalveolar lavage fluid （BALF） of asthmatic mice and th...Summary： This study investigated the expression of interleukin-17 （IL-17） and T cell immunoglobulin mucin and domain-containing molecule-3 （Tim-3） in bronchoalveolar lavage fluid （BALF） of asthmatic mice and the effect of dexamethasone （DEX） on these factors. Thirty-six mice were randomly divided into three groups： normal group, asthmatic group and DEX group. The mouse model of asthma was es- tablished by sensitization with ovalbumin in both the asthmatic and DEX groups. The levels of IL-6, IL-10, IL-17 and TGF-β were measured in BALF by enzyme-linked immunesorbent assay （ELISA）. The mRNA expression level of Tim-3 was detected by reverse transcription polymerase chain reaction （RT-PCR）. The ratio of Tim-3＋CD4＋ cells to total CD4＋ cells in BALF was determined by flow cy- tometry. Differential inflammatory cells in BALF were detected. The correlations among IL-17, IL-6, IL-10, Tim-3 and inflammatory cells were analyzed. The results showed that the levels of IL-17, IL-6 and Tim-3 were substantially increased and the IL-10 level decreased in BALF in the asthmatic mice, which was significantly reversed by DEX treatment. IL-17 expression was positively correlated with IL-6 and Tim-3 expression and the number of inflammatory cells but negatively with IL-10 expression. These results indicate that the increased expression of IL-17 and Tim-3 in BALF may be implicated in the occurrence and development of asthmatic inflammation; the mechanism by which DEX suppresses asthmatic airway inflammation involves down-regulation of IL-17 and Tim-3 levels.展开更多
During human pregnancy, progesterone induced decidual cells protect against hemorrhage: 1) as endovascular trophoblast breech and remodel uterine blood vessels;and 2) in the third stage of labor following preterm and ...During human pregnancy, progesterone induced decidual cells protect against hemorrhage: 1) as endovascular trophoblast breech and remodel uterine blood vessels;and 2) in the third stage of labor following preterm and term delivery. De- cidual cells promote hemostasis through enhanced expression of tissue factor (TF), the primary initiator of hemostasis via thrombin generation, and plasminogen activator inhibitor-1, which inactivates tissue type plasminogen activator, the primary fibrinolytic agent. Abruptions (decidual hemorrhage) produce excess thrombin which acts as autocrine/paracrine inducer of decidual cell expressed matrix metalloproteinases and of neutrophil chemoattractant and activator, interleukin-8. The latter mediates aseptic abruption-related neutrophil infiltration. During abruptions, decidual cell and neutrophil-derived proteases effectively degrade the decidual and fetal membrane extracellular matrix to promote preterm premature rupture of the membranes and preterm delivery (PTD). Decidual cell-derived thrombin weakens the amniotic membrane and lowers decidual cell-expressed progesterone receptor levels by increasing phospho-ERK1/2 signaling. The resulting functional progesterone withdrawal accompanies PTD.展开更多
基金supported by grants from the National Natural Science Foundation of China(No.81200006)the Natural Science Foundation of Hubei Province(No.2010CDB08804)+1 种基金Wuhan Health Bureau Foundation(No.WX11B10)supported by Wu Jieping Medical Fund(No.32067501285)
文摘Summary： This study investigated the expression of interleukin-17 （IL-17） and T cell immunoglobulin mucin and domain-containing molecule-3 （Tim-3） in bronchoalveolar lavage fluid （BALF） of asthmatic mice and the effect of dexamethasone （DEX） on these factors. Thirty-six mice were randomly divided into three groups： normal group, asthmatic group and DEX group. The mouse model of asthma was es- tablished by sensitization with ovalbumin in both the asthmatic and DEX groups. The levels of IL-6, IL-10, IL-17 and TGF-β were measured in BALF by enzyme-linked immunesorbent assay （ELISA）. The mRNA expression level of Tim-3 was detected by reverse transcription polymerase chain reaction （RT-PCR）. The ratio of Tim-3＋CD4＋ cells to total CD4＋ cells in BALF was determined by flow cy- tometry. Differential inflammatory cells in BALF were detected. The correlations among IL-17, IL-6, IL-10, Tim-3 and inflammatory cells were analyzed. The results showed that the levels of IL-17, IL-6 and Tim-3 were substantially increased and the IL-10 level decreased in BALF in the asthmatic mice, which was significantly reversed by DEX treatment. IL-17 expression was positively correlated with IL-6 and Tim-3 expression and the number of inflammatory cells but negatively with IL-10 expression. These results indicate that the increased expression of IL-17 and Tim-3 in BALF may be implicated in the occurrence and development of asthmatic inflammation; the mechanism by which DEX suppresses asthmatic airway inflammation involves down-regulation of IL-17 and Tim-3 levels.
文摘During human pregnancy, progesterone induced decidual cells protect against hemorrhage: 1) as endovascular trophoblast breech and remodel uterine blood vessels;and 2) in the third stage of labor following preterm and term delivery. De- cidual cells promote hemostasis through enhanced expression of tissue factor (TF), the primary initiator of hemostasis via thrombin generation, and plasminogen activator inhibitor-1, which inactivates tissue type plasminogen activator, the primary fibrinolytic agent. Abruptions (decidual hemorrhage) produce excess thrombin which acts as autocrine/paracrine inducer of decidual cell expressed matrix metalloproteinases and of neutrophil chemoattractant and activator, interleukin-8. The latter mediates aseptic abruption-related neutrophil infiltration. During abruptions, decidual cell and neutrophil-derived proteases effectively degrade the decidual and fetal membrane extracellular matrix to promote preterm premature rupture of the membranes and preterm delivery (PTD). Decidual cell-derived thrombin weakens the amniotic membrane and lowers decidual cell-expressed progesterone receptor levels by increasing phospho-ERK1/2 signaling. The resulting functional progesterone withdrawal accompanies PTD.
