随着免疫抑制人群的增多、检测技术的发展, 深部真菌感染日益受到人们的关注。真菌中的曲霉属成了这些免疫功能低下患者致病性感染的重要原因, 而烟曲霉在侵袭性曲霉病例中最常见。侵袭力是烟曲霉菌极为重要的致病原因;病原菌侵入上皮、内皮细胞等组织细胞后才导致了可怕的侵袭性感染。从上世纪90 年代来, 对于侵袭的研究已逐步深入, 为探讨复杂的致病机制打下了基础。侵袭性烟曲霉病一般的致病过程认为是烟曲霉孢子被宿主吸入下呼吸道, 侵入呼吸道上皮细胞后发育成菌丝, 菌丝进一步生长, 可侵入血管、进入血液, 造成全身播散[ 1] 。因此曲霉与宿主细胞( 上皮细胞、内皮细胞等) 的相互作用成了致病过程的重要环节。目前对病原体与宿主细胞作用的研究取得了一些进展, 对阐明致病机制、研究治疗靶点等有重要意义。
Objective To investigate the effect of microRNA-22-3p (miR-22-3p) on the inflammation of human pulmonary microvascular endothelial cells (HPMEC) induced by lipopolysaccharide (LPS) by regulating the HMGB1/NLRP3 pathway. Methods miRNA microarray was taken from peripheral blood of patients with acute respiratory distress syndrome (ARDS) caused by abdominal infection and healthy controls for analysis, and the target miRNA was selected. miRNA mimics, inhibitor and their negative controls were transfected in HPMECs which were stimulated with LPS. Real time fluorescent quantitative polymerase chain reaction (RT-qPCR) and Western blot were used to detect the mRNA and protein levels of high mobility group box-1 protein (HMGB1) and nucleotide binding oligomerization segment like receptor family 3 (NLRP3). RT-qPCR and enzyme linked immunosorbent assay were used to detect the levels of inflammatory factors in the cells and supernatant. Results miRNA microarray showed that miR-22-3p was down-regulated in the plasma of patients with ARDS. Compared with the negative control group, after miR-22-3p over-expression, the protein and mRNA levels of HMGB1 and NLRP3 decreased significantly. Similarly, the level of cleaved-caspase-1 decreased significantly. At the same time, interleukin (IL)-6, IL-8 and IL-1β mRNA level in cytoplasm and supernatant were down-regulated by miR-22-3p mimics. After transfected with miR-22-3p inhibitor, the expression levels of HMGB1, NLRP3, caspase-1 protein and inflammatory factors were significantly up-regulated. Conclusion miR-22-3p is significantly downregulated in peripheral blood of ARDS patients caused by abdominal infection, which can inhibit the expression of HMGB1 and NLRP3 and its downstream inflammatory response in HPMECs.
Objective To observe the levels of von Willebrand factor ( vWF) expressed by human umbilical vein endothelial cells ( HUVECs) infected by aspergillus fumigatus ( AF) alone or treatment with cytochalasin D, N-cadherin monoclonal antibody, dexamethasone, respectively, so as to explore the mechanism of angioinvasion in invasive aspergillosis. Methods An in vitro model of HUVECs infected by AF hypha was established. The experiment included six groups, ie. a sham control group, a TNF-αgroup, an AF hypha group, a cytochalasin D group, a N-cadherin antibody group, and a dexamethasone group. Cell supernatants were collected to detect the levels of vWF at 2 h, 6 h, 12 h, and 18 h by enzyme linked immunosorbent assay ( ELISA) . Results Compared with that of vWF at 2 h, the level was higher at 18 h in the sham controlgroup and the TNF-αgroup, and higher at 6 h, 12 h, and 18 h in the other groups( P lt; 0. 05) . Compared with the sham control group, the level of vWF in each experiment group increased at 2 h, 6 h, 12 h, and 18 h except that in the N-cadherin antibody group at 2 h ( P lt; 0. 05) . The level of vWF in TNF-α group was higher than that in the AF hypha group at 2 h, but lower at 18 h. ( P lt; 0. 05) . The level of vWF was not significantly different between the cytochalasin D group and the AF hypha group at each time point. The level of vWF was lower in the N-cadherin antibody group than that in the AF hypha group at 2 h and 6 h ( P lt;0. 05) . The level of vWF was not significantly different between the dexamethasone group and the AF hypha group at each time point. Conclusion HUVECs infected by AF hypha overexpress vWF. N-cadherinmonoclonal antibody can reduce the expression of vWF, but cytochalasin D or dexamethasone has no significant effect on it.
Objective To study the advantages of heat and moisture exchangers compared with heated humidifiers in reducing the incidence of ventilator-associated pneumonia ( VAP) . Methods We searched PubMed as well as reference lists from publications to collect randomized controlled trials which comparing heat and moisture exchangers with heated humidifiers in preventing VAP for mechanically ventilated patients. Meta-analysis was performed using software Review Manager 5. 0. Results Fifteen randomized controlled trials were included. There was no difference in incidence of VAP among the patients managed with moisture exchangers or heated humidifiers ( OR1. 18, 95% CI [ 0. 96, 1. 44] ) . The subgroup of patients using moisture exchangers had lower VAP incidence compared with those using heated humidifiers without heated wire circuits ( OR 1. 39, 95% CI [ 1. 08, 1. 79] ) . There were no differences between the compared groups in mortality, length of intensive care unit stay, or duration of mechanical ventilation. Conclusion The available evidence indicates that moisture exchangers are superior to heated humidifiers without heated wire circuits, and not to heated humidifiers with heated wire circuits to prevent VAP.
ObjectiveTo summary the relationship between CD147 and the occurrence and development of hepatocellular carcinoma, and its roles in clinical diagnosis and treatment. MethodReferring to the related literatures in recent years at home and abroad, the concept of CD147, and its relationship with the occurrence, development, invasion, and metastasis of hepatocellular carcinoma were reviewed. ResultsCD147 plays a key role in the development, progress, invasion, and metastasis of hepatocellular carcinoma. CD147 can be used as a long-term outcome predictor for hepatocellular carcinoma patients and also began to show its in hepatocellular carcinoma target therapy. ConclusionThere are numerous studies about the relationship between CD147 and hepatocellular carcinoma, but still exists some problems to be further studied.