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MiR-146b protects against the inflammation injury in pediatric pneumonia through MyD88/NF-κB signaling pathway.

MiR-146b通过MyD88/NF-κ b信号通路保护小儿肺炎炎症损伤。

  • 影响因子:1.61
  • DOI:10.1080/23744235.2019.1671987
  • 作者列表:"Zhang L","Dong L","Tang Y","Li M","Zhang M
  • 发表时间:2020-01-01
Abstract

:Background: Pneumonia is a common respiratory disease worldwide that can be prevented and treated. However, it is considered to be the leading cause of children death. The present study was aimed to explore the functional role and molecular mechanism of miR-146b in the inflammation injury in pediatric pneumonia.Materials and methods: The lipopolysaccharide (LPS)-induced pulmonary injury cell model was established in WI-38 human lung fibroblasts cells. QRT-PCR and Western blot was applied to detect miR-146b and MyD88 expression. ELISA assay was used to analyze the production of pro-inflammatory factors. Cell viability was evaluated by CCK-8 assay. The apoptosis proteins and the downstream genes of NF-κB pathway were detected by Western blot.Results: we displayed that miR-146b was down-regulated, whereas MyD88 was up-regulated in the serum of children patients with pneumonia and in WI-38 cells treated with LPS. Moreover, re-expression of miR-146b suppressed the production of inflammatory factors in the serum of pneumonia patients and WI-38 cells treated with LPS. In addition, elevating miR-146b expression increased WI-38 cell viability and reduced cell apoptosis. More importantly, bioinformatics analysis revealed that MyD88 was a target of miR-146b and could overturn the protective effect of miR-146b on the inflammation injury in LPS-injured WI-38 cells. Furthermore, miR-146b over-expression inhibited the activation of NF-κB signaling pathway by suppressing MyD88.Conclusion: miR-146b attenuated the inflammation injury in pediatric pneumonia through inhibiting MyD88/NF-κB signaling pathway. These preliminarily findings further deepened our understanding of this mechanism and identified new potential therapeutic targets for pediatric pneumonia.

摘要

背景: 肺炎是世界范围内常见的呼吸道疾病,可以预防和治疗。然而,它被认为是儿童死亡的主要原因。本研究旨在探讨miR-146b在小儿肺炎炎症损伤中的作用及分子机制。材料和方法: 在WI-38 人肺成纤维细胞中建立脂多糖 (LPS) 诱导的肺损伤细胞模型。应用QRT-PCR和Western blot检测miR-146b和MyD88 表达。ELISA法分析促炎因子的产生。通过CCK-8 测定法评价细胞活力。通过Western blot检测凋亡蛋白和NF-κ b通路下游基因。结果: 我们显示在肺炎患儿血清和LPS处理的miR-146b细胞中,WI-38 下调,而MyD88 上调。此外,miR-146b的再表达抑制了肺炎患者和用LPS处理的WI-38 细胞的血清中炎性因子的产生。此外,升高miR-146b表达增加WI-38 细胞活力和减少细胞凋亡。更重要的是,生物信息学分析显示MyD88 是miR-146b的靶标,并且可以推翻miR-146b对LPS损伤的WI-38 细胞的炎症损伤的保护作用。此外,miR-146b过表达通过抑制MyD88 抑制NF-κ b信号通路的激活。结论: miR-146b通过抑制MyD88/NF-κ b信号通路减轻小儿肺炎的炎症损伤。这些初步发现进一步加深了我们对这一机制的理解,并确定了小儿肺炎的新的潜在治疗靶点。

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影响因子:14.71
发表时间:2020-02-01
来源期刊:Nature immunology
DOI:10.1038/s41590-019-0571-2
作者列表:["Adrover JM","Aroca-Crevillén A","Crainiciuc G","Ostos F","Rojas-Vega Y","Rubio-Ponce A","Cilloniz C","Bonzón-Kulichenko E","Calvo E","Rico D","Moro MA","Weber C","Lizasoaín I","Torres A","Ruiz-Cabello J","Vázquez J","Hidalgo A"]

METHODS::The antimicrobial functions of neutrophils are facilitated by a defensive armamentarium of proteins stored in granules, and by the formation of neutrophil extracellular traps (NETs). However, the toxic nature of these structures poses a threat to highly vascularized tissues, such as the lungs. Here, we identified a cell-intrinsic program that modified the neutrophil proteome in the circulation and caused the progressive loss of granule content and reduction of the NET-forming capacity. This program was driven by the receptor CXCR2 and by regulators of circadian cycles. As a consequence, lungs were protected from inflammatory injury at times of day or in mouse mutants in which granule content was low. Changes in the proteome, granule content and NET formation also occurred in human neutrophils, and correlated with the incidence and severity of respiratory distress in pneumonia patients. Our findings unveil a 'disarming' strategy of neutrophils that depletes protein stores to reduce the magnitude of inflammation.

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翻译标题与摘要 下载文献
影响因子:2.81
发表时间:2020-01-05
DOI:10.3390/ijerph17010356
作者列表:["Yang LC","Suen YJ","Wang YH","Lin TC","Yu HC","Chang YC"]

METHODS::Pneumonia is a common respiratory infectious disease that involves the inflammation of the pulmonary parenchyma. Periodontal disease is widespread and correlated with pneumonia. However, the relationship between periodontal treatment and clinical infectious outcomes in patients with pneumonia has remained undetermined. The aim of this study was to investigate the association between periodontal treatment and the risk of pneumonia events in the Taiwanese population. A nationwide population-based cohort study was conducted using data from the Taiwanese National Health Insurance Research Database (NHIRD). A total of 49,400 chronic periodontitis patients who received periodontal treatment from 2001 to 2012 were selected. In addition, 49,400 healthy individuals without periodontal diseases were picked randomly from the general population after propensity score matching according to age, gender, monthly income, urbanization, and comorbidities. The Cox proportional hazard regression analysis was adopted to assess the hazard ratio (HR) of pneumonia between the periodontal treatment cohort and the comparison cohort. The average ages of the periodontal treatment and comparison groups were 44.25 ± 14.82 years and 44.15 ± 14.5 years, respectively. The follow up durations were 7.66 and 7.41 years for the periodontal treatment and comparison groups, respectively. We found 2504 and 1922 patients with newly diagnosed pneumonia in the comparison cohort and the periodontal treatment cohort, respectively. The Kaplan-Meier plot revealed that the cumulative incidence of pneumonia was significantly lower over the 12 year follow-up period in the periodontal treatment group (using the log-rank test, p < 0.001). In conclusion, this nationwide population-based study indicated that the patients with periodontal treatment exhibited a significantly lower risk of pneumonia than the general population.

翻译标题与摘要 下载文献
影响因子:2.89
发表时间:2020-04-01
DOI:10.1016/j.ijid.2020.01.038
作者列表:["Ngocho JS","Horumpende PG","de Jonge MI","Mmbaga BT"]

METHODS:OBJECTIVE:To describe the treatment of community-acquired pneumonia (CAP) in children under five years in Tanzania. METHODS:Between January and December 2017, children aged 2-59 months with chest radiography-confirmed CAP were enrolled. The parents were interviewed to collect information on the patients and home-based medication. Clinical information was derived from the patient files. Nasopharyngeal swab and blood samples were collected for isolation of the causative pathogens. Swab samples were analysed by quantitative PCR whereas blood samples were tested using BacT/Alert 3D. RESULTS:Overall, 109 children with CAP were included in this analysis. Provision of care to most children was delayed (median = 4.6 days). A quarter (26.6%) were given unprescribed/leftover antibiotics at home. Only one child had positive bacterial culture. Referrals were associated with nasopharyngeal carriage of Streptococcus pneumoniae (p = 0.003) and Haemophilus influenzae (p = 0.004). Of all admitted children, more than a quarter (n = 29) did not need to be hospitalised and inappropriately received injectable instead of oral antibiotics. CONCLUSION:We found high rates of home treatment, particularly with antibiotics. Appropriate health care was delayed for most children because of home treatment. Efforts are needed at the community level to improve awareness of antimicrobial resistance.

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肺炎方向

肺炎是指终末气道、肺泡和肺间质的炎症。可由细菌、病毒、真菌、寄生虫等致病微生物,以及放射线、吸入性异物等理化因素引起。临床主要症状为发热、咳嗽、咳痰、痰中带血,可伴胸痛或呼吸困难等。

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