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| 1 | 姜黄素对急性呼吸窘迫综合征大鼠肺组织及气道重塑的影响显示文摘目的探讨姜黄素对气管内雾化脂多糖诱导的急性呼吸窘迫综合征(ARDS)大鼠肺组织纤维化及支气管杯状细胞的影响。方法将24只Sprague Dawley成年雄性大鼠分为对照组(仅气管内雾化等容积等渗NaCl溶液)、ARDS组(气管内雾化脂多糖4 mg/kg)、姜黄素组(复制ARDS模型30 min前腹腔注射姜黄素50 mg/kg),每组各8只。模型复制5 d后计算各组大鼠肺组织湿干重比值(W/D)、支气管肺泡灌洗液(BALF)中肿瘤坏死因子α(TNF-α)、Ⅲ型前胶原(PCⅢ)的含量。Western-blotting检测各组大鼠肺组织Toll样受体4(TLR4)及核因子κBp65(NF-κBp65)蛋白表达水平。同时,采用Masson染色观察肺组织胶原纤维分布,阿利新蓝-过碘酸-雪夫(AB-PAS)染色观察支气管杯状细胞和黏液的情况。结果各组大鼠肺组织W/D,BALF中TNF-α、PCⅢ的含量,肺组织NF-κBp65及TLR4蛋白表达的比较,差异均有统计学意义(F=136.155、139.639、95.353、94.034、67.540,P均<0.001)。且与对照组比较,ARDS组和姜黄素组肺组织W/D[(3.99±0.16)、(5.53±0.15)、(4.81±0.24)],BALF中的TNF-α[(61±5)、(219±25)、(157±21)ng/L]和PCⅢ[(0.67±0.22)、(61.66±11.95)、(35.62±9.64)μg/L]含量,肺组织中NF-κBp65及TLR4蛋白表达水平均显著升高,且ARDS组更高(P均<0.05)。Masson染色显示,ARDS组肺间质呈广泛胶原纤维沉积,姜黄素组肺间质呈轻度弥漫性胶原纤维沉积。AB-PAS染色可见,ARDS组支气管上皮杯状细胞化生、姜黄素组支气管上皮杯状细胞轻度化生。结论姜黄素可以逆转脂多糖诱导的ARDS大鼠气道杯状细胞化生,改善肺组织纤维化,可能与抑制TLR4/NF-κB信号通路、改善肺部炎症反应有关。 | 杨茂宪 姚明 徐龙生 沈鹏 陈文宇 王倩倩 施云超 | 2021 | 中华危重症医学杂志(电子版)2021，14，5： | 2 |
| 2 | Alveolar macrophages:Achilles’heel of SARS-CoV-2 infection显示文摘The coronavirus disease 2019(COVID-19)pandemic has caused more than 6.3 million deaths to date.Despite great efforts to curb the spread of severe acute respiratory syndrome coronavirus 2(SARS-CoV-2),vaccines and neutralizing antibodies are in the gloom due to persistent viral mutations and antiviral compounds face challenges of specificity and safety.In addition,vaccines are unable to treat already-infected individuals,and antiviral drugs cannot be used prophylactically.Therefore,exploration of unconventional strategies to curb the current pandemic is highly urgent.Alveolar macrophages(AMs)residing on the surface of alveoli are the first immune cells that dispose of alveoli-invading viruses.Our findings demonstrate that M1 AMs have an acidic endosomal pH,thus favoring SARS-CoV-2 to leave endosomes and release into the cytosol where the virus initiates replication;in contrast,M2 AMs have an increased endosomal pH,which dampens the viral escape and facilitates delivery of the virus for lysosomal degradation.In this review,we propose that AMs are the Achilles’heel of SARS-CoV-2 infection and that modulation of the endosomal pH of AMs has the potential to eliminate invaded SARS-CoV-2;the same strategy might also be suitable for other lethal respiratory viruses. | Zhenfeng Wang Shunshun Li Bo Huang | 2022 | Signal Transduction and Targeted Therapy2022，7，8： | 1 |
| 3 | Mucins produced by type Ⅱ pneumocyte: culprits in SARS-CoV-2 pathogenesis显示文摘The pandemic of severe acute respiratory syndrome coronavirus 2(SARS-CoV-2)is sweeping across the world and has caused the loss of more than 3.3 million lives.Before clearance by virus-specific T and B cell-mediated adaptive immunity,excessive inflammation by innate immune cells might cause severe lung and even multiorganic pathologies,thus interfering with antiviral immunity.To curb infection and subsequent organic damage,a deep understanding of the pathogenetic process is highly desirable.Recently,we found that IFN-driven mucin expression in type Ⅱ alveolar epithelial cells is crucial in initiating hypoxia and early lung pathology1,and SARS-CoV-2 is disposed of by M1 and M2 alveolar macrophages(AMs)in distinct manners2.In this correspondence,we propose that(1)following the invasion of the alveoli and uptake by local alveolar macrophages,SARS-CoV-2 may stimulate macrophages to produce proinflammatory cytokines,including type Ⅰ interferon;(2)type I interferon acts on neighboring alveolar type Ⅱ pneumocytes and activates the cytoplasmic transcription factor aryl hydrocarbon receptor(AhR);(3)subsequently,AhR is translocated to the nucleus,where it promotes the expression of mucin genes,leading to mucus production;and(4)mucus begins to accumulate in the alveoli and gradually impairs the exchange of O2 and CO2,initially causing hypoxia and then dampening CO2 exhalation,leading to a critical illness.Here,we dissect these early pathogenic events,which might provide clues to interfering with SARS-CoV-2 infection at an early stage. | Bo Huang | 2021 | Cellular & Molecular Immunology2021，18，7： | 1 |
| 4 | 不同病原感染肺炎患儿发生气道黏液高分泌状态的危险因素分析显示文摘目的探讨不同病原感染的肺炎患儿发生气道黏液高分泌状态的危险因素。方法回顾性队列研究。收集2019年1月至2021年12月在重庆医科大学附属儿童医院呼吸科因肺炎支原体肺炎(MPP)、呼吸道合胞病毒(RSV)肺炎、腺病毒肺炎住院并行支气管镜检查的968例患儿临床资料。对支气管镜下黏液分泌情况进行评分,并分为气道黏液高分泌组和非高分泌组,分别比较3种病原感染肺炎患儿两组的人口学特征、临床特征、实验室检查、疾病严重度,分析其发生气道黏液高分泌状态的危险因素。应用χ2检验、Mann-Whithey U检验、Fisher确切概率法分析组间差异,多因素Logistic回归分析影响因素。结果968例患儿中男559例、女409例,就诊年龄4.0(1.4,6.0)岁。642例MPP患儿中高分泌组185例、非高分泌组457例;201例RSV肺炎患儿中高分泌组41例、非高分泌组160例;125例腺病毒肺炎患儿中高分泌组39例、非高分泌组86例。MPP、RSV、腺病毒3种病原感染的肺炎患儿高分泌组就诊年龄均大于非高分泌组[6.0(4.0,7.0)比5.0(3.0,7.0)岁、1.5(0.5,3.6)比0.8(0.4,1.6)岁、2.0(1.2,4.5)比1.3(0.8,2.0)岁,U=35295.00、2492.00、1101.00,均P<0.05]。多因素Logistic回归分析显示,外周血白细胞计数升高(OR=3.30,95%CI 1.51~7.93,P=0.004)、中性粒细胞比例升高(OR=2.24,95%CI 1.16~4.33,P=0.016)、淋巴细胞计数降低(OR=3.22,95%CI 1.66~6.31,P<0.001)、血清白蛋白降低(OR=2.00,95%CI 1.01~3.98,P=0.047)的MPP患儿发生气道黏液高分泌的风险增加;外周血嗜酸粒细胞升高(OR=3.04,95%CI 1.02~8.93,P=0.043)的RSV肺炎患儿发生气道黏液高分泌的风险增加,气道黏液高分泌与重症肺炎相关(OR=2.46,95%CI 1.03~6.15,P=0.047);年龄较大(OR=1.02,95%CI 1.00~1.04,P=0.026)、肺部听诊闻及啰音、哮鸣音或痰鸣音(OR=3.65,95%CI 1.22~12.64,P=0.028)的腺病毒肺炎患儿发生气道黏液高分泌的风险均增加。MPP患儿中高分泌组支气管肺泡灌洗液(BALF)中性粒细胞比例高于非高分泌组[0.65(0.43,0.81)比0.59(0.34,0.76),U=24507.00,P<0.01],BALF巨噬细胞比例低于非高分泌组[0.10(0.05,0.20)比0.12(0.06,0.24),U=33043.00,P<0.05];RSV肺炎患儿高分泌组BALF有核细胞计数及中性粒细胞比例均高于非高分泌组[1210(442,2100)×10^(6)比490(210,1510)×10^(6)/L、0.43(0.26,0.62)比0.30(0.13,0.52),U=2043.00、2064.00,均P<0.05]。结论MPP患儿的外周血白细胞计数升高、中性粒细胞比例升高、淋巴细胞计数降低以及白蛋白降低均与气道黏液高分泌有关,RSV肺炎患儿外周血嗜酸粒细胞异常升高与气道黏液高分泌相关,腺病毒肺炎患儿肺部啰音、哮鸣音、痰鸣音的出现与气道黏液高分泌相关。呼吸道局部中性粒细胞浸润与肺炎支原体和RSV感染的气道黏液高分泌的发生密切相关。 | 蔡江瑜 晏春愉 王晓晴 罗征秀 罗健 李渠北 刘恩梅 邓昱 | 2023 | 中华儿科杂志2023，61，8： | 0 |
| 5 | GSDME with a moonlighting function in pancreatic ductal adenocarcinoma: a narrative review显示文摘Pancreatic ductal adenocarcinoma(PDAC)originates in the exocrine pancreas and accounts for 95%of pancreatic cancers,with 5-year survival rates of approximately 10%.Multiple factors are involved in PDAC pathogenesis,including internal genetic alterations and external inflammation-related stimuli.Overflow of exocrine pancreatic enzymes caused by PDAC obstruction inevitably results in autolysis of surrounding normal cells and extracellular matrix,generating tissue damage-related inflammation;however,this process does not cause autolysis of PDAC cells.How tumor cells acquire resistance to pancreatic enzymatic digestion has been ignored for a long time.In this review,we discuss how PDAC cells mobilize gasdermin E,a pore-forming protein,to achieve resistance to autolysis by pancreatic digestive enzymes. | Bo Huang | 2022 | Journal of Pancreatology2022，5，3： | 0 |
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