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Human galectin-9 potently enhances SARS-CoV-2 replication and inflammation in airway epithelial cells

Journal of Molecular Cell Biology 2023年第4期15卷 46-59页

作者： Li Du Mohamed S.Bouzidi Akshay Gala Fred Deiter Jean-Noël Billaud Stephen T.Yeung Prerna Dabral Jing Jin Graham Simmons Zain Y.Dossani Toshiro Niki Lishomwa C.Ndhlovu John R.Greenland Satish K.Pillai Vitalant Research Institute San FranciscoCA 94105USA Department of Laboratory Medicine University of CaliforniaSan FranciscoCA 94143-0134USA Department of Medicine University of CaliforniaSan FranciscoCA 94143-0410USA Veterans Affairs Health Care System San FranciscoCA 94121USA QIAGEN Digital Insights Redwood CityCA 94063USA Division of Infectious Diseases Department of MedicineWeill Cornell MedicineNew YorkNY 10021USA Department of Immunology Kagawa UniversityKagawa 760-0016Japan

The severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) pandemic has caused a global economic and health crisis. Recently, plasma levels of galectin-9 (Gal-9), a β-galactoside-binding lectin involved in immune regulation and viral immunopathogenesis, were reported to be elevated in the setting of severe COVID-19 disease. However, the impact of Gal-9 on SARS-CoV-2 infection and immunopathology remained to be elucidated. In this study, we demonstrate that Gal-9 treatment potently enhances SARS-CoV-2 replication in human airway epithelial cells (AECs), including immortalized AECs and primary AECs cultured at the air–liquid interface. Gal-9–glycan interactions promote SARS-CoV-2 attachment and entry into AECs in an angiotensin-converting enzyme 2 (ACE2)-dependent manner, enhancing the binding of the viral spike protein to ACE2. Transcriptomic analysis revealed that Gal-9 and SARS-CoV-2 infection synergistically induced the expression of key pro-inflammatory programs in AECs, including the IL-6, IL-8, IL-17, EIF2, and TNFα signaling pathways. Our findings suggest that manipulation of Gal-9 should be explored as a therapeutic strategy for SARS-CoV-2 infection.

关键词： SARS-CoV-2 galectin-9 inflammation airway epithelial cells

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Inhibitory Effect of Dexamethasone on Expression of Cysteine-rich 61 Protein in airway epithelial cells of Allergic Mouse Models

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Journal of Huazhong University of Science and Technology(Medical Sciences) 2013年第5期33卷 628-631页

作者：曹勇陈辉龙程胜谢俊刚熊维宁徐永健方慧娟 Department of Respiratory and Critical Care Medicine Tongji Hospital Key Laboratory of Pulmonary Diseases of the Ministry of Health of China Tongji Medical College Huazhong University of Science and Technology

Summary： In order to study whether cysteine-rich 61 protein （cyr61） is involved in the pathogenesis of asthma and its relation to airway inflammation, the effect of dexamethasone （Dxm） on the expression of cyr61 in the lung tissues of asthmatic mice was investigated. Forty BALB/c mice were divided into asthma group （n=15）, control group （n=10） and Dxm group （n=15）. The asthma group was sensitized and challenged by ovalbumin （OVA）. The mice in Dxm group were intraperitoneally administered with Dxm after OVA challenge. The expression of cyr61 in the lung tissues was detected by using immuno- histochemistry, and that of eotaxin protein in the bronchoalveolar lavage fluid （BALF） by using en- zyme-linked immunosorbent assay （ELISA）. The number of inflammatory cells in BALF was also ana- lyzed. The results showed that the cyr61 expression was highest in asthma group （P〈0.05）, followed by Dxm group （P〈0.05） and control group. The cyr61 had a positive correlation with the total nucleated cells （r=0.867, P〈0.05）, especially eosinophils （r=0.856, P〈0.05）, and eotaxin level （r=0.983, P〈0.05） in the BALF. Our findings suggested that cyr61 is expressed in airway epithelial cells and has a positive correlation with eotaxin and number of airway infiltrating eosinophils.

关键词： asthma airway inflammation cysteine-rich 61 airway epithelial cells eosinophils

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Exposure to ephedrine attenuates Th1/Th2 imbalance underlying OVA-induced asthma through airway epithelial cell-derived exo-somal lnc-TRPM2-AS

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Chinese Journal of Natural Medicines 2024年第6期22卷 530-540页

作者： HU Yan WANG Mengqing XIE Jing JIAO Luojia DING Yi LUO Yinhe Department of Pediatrics The First Hospital of Hunan University of Chinese MedicineChangsha 410007China Hunan University of Chinese Medicine Changsha 410208China Department of Rehabilitation Medical CollegeChangsha Civil Affairs Vocational and Technical CollegeChangsha 410004Hunan ProvinceChina Teaching and Research Office of Chinese and Western Combination Hunan University of Chinese MedicineChangsha 410208China

Although various anti-inflammatory medications,such as ephedrine,are employed to manage cough-variant asthma,their underlying mechanisms are yet to be fully understood.Recent studies suggest that exosomes derived from airway epithelial cells(AECs)contain components like messenger RNAs(mRNAs),micro-RNAs(miRNAs),and long noncoding RNA(lncRNA),which play roles in the occurrence and progression of airway inflammation.This study investigates the influence of AEC-derived exosomes on the efficacy of ephedrine in treating cough-variant asthma.We established a mouse model of asthma and measured airway resist-ance and serum inflammatory cell levels.Real-time polymerase chain reaction(RT-qPCR),Western blotting,and enzyme-linked im-munosorbent assay(ELISA)analyses were used to assess gene and protein expression levels.Exosomes were isolated and character-ized.RNA immunoprecipitation(RIP)and RNA pull-down assays were conducted to examine the interaction between hnRNPA2B1 and lnc-TRPM2-AS1.In the ovalbumin(OVA)-challenged mouse model,ephedrine treatment reduced inflammatory responses,air-way resistance,and Th1/Th2 cell imbalance.Exosomes from OVA-treated AECs showed elevated levels of lnc-TRPM2-AS1,which were diminished following ephedrine treatment.The exosomal lnc-TRPM2-AS1 mediated the Th1/Th2 imbalance in CD4^(+)T cells,with its packaging into exosomes being facilitated by hnRNPA2B1.This study unveils a novel mechanism by which ephedrine ameli-orates OVA-induced CD4^(+)T cell imbalance by suppressing AEC-derived exosomal lnc-TRPM2-AS1.These findings could provide a theoretical framework for using ephedrine in asthma treatment.

关键词： Asthma Ephedrine Exosomal lnc-TRPM2-AS1 Th1/Th2 imbalance HnRNPA2B1 airway epithelial cells

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Activity of Matrix Metalloproteinase in airway epithelial cells of COPD Patients

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Journal of Huazhong University of Science and Technology(Medical Sciences) 2005年第2期25卷 151-154页

作者：李雯徐永健张珍祥 Department of Respiration Medicine Tongji Hospital Tongji Medical College Huazhong University of Science and Technology Wuhan 430030

Summary:To examine the mRNA expression of matrix metalloproteinase 9 (MMP-9) and the gelatinase activity of its inhibitor, tissue inhibitor of matrix metalloproteinase 1 (TIMP-1) in the primary epithelial cells of patients with COPD, airway epithelial cells were taken from 15 COPD patients and cultured in vitro. The patients were divided into three groups, COPD group, normal smoking control group and non-smoking control group, with 5 subjects in each group, on basis of the smoking history and lung function. The semi-qualitative RT-PCR was employed to determine the mRNA levels of MMP-9 and TIMP-1 and SDS PAGE was used for the determination of the gelatinase activity of MMP-9 and TIMP-1. Our result showed that the mRNA of MMP-9 and TIMP-1 in epithelial cells of the non-smoking subjects was at a low level. The mRNA of MMP-9 and TIMP-1 in COPD patients and smokers was significantly higher than that in non-smokers (Pepithelial cells between the COPD patients and smokers. The MMP-9/TIMP-1 ratios in COPD patients and smokers were significantly lower than that of non-smokers (Pepithelial cells of both COPD patients and normal smokers was increased (Pepithelial cells between COPD patients and normal smokers. It is concluded that the transcription of MMP-9 and TIMP-1 and the gelatinase activity of MMP-9 and MMP-2 in the epithelial cells in COPD patients were increased, which resulted in an imbalance of MMP-9/TIMP-1, thereby causing pulmonary fibrosis. These factors play important roles in the pathogenesis of COPD.

关键词： chronic obitrucitve pulmonary disease matrix metalloproteinase airway epithelial cells

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A MyD88-dependent TLR signaling pathway plays a key role in sheep airway epithelial cells in response to Mycoplasma Ovipneumoniae infection

A MyD88-dependent TLR signaling pathway plays a key role in ...

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第九届全国免疫学学术大会

作者： Di Xue Min Li Yan Ma Yanan Li Haixia Luo Xiaoming Liu Yujiong Wang Key Lab of Ministry of Education for Protection and Utilization of Special Biological Resources in Western China Ningxia University School of Life Science Ningxia University

Mycoplasma ovipneumoniae(M.ovipneumoniae)is a species of Mycoplasma bacteria that specifically infects sheep and goat,which is the cause of ovine infectious pleuropneumonia.In an effort to understand the pathogen-host interaction between the M.ovipneumoniae and airway epithelial cells,we investigated the host cell apoptosis in a primary air-liquid interface(ALI)epithelial culture model generated from bronchial epithelial cells of Ningxia Tan sheep(ovis aries).We found that M.ovipneumoniae initially bound to ciliated epithelial cells of the sheep bronchial epithelial cell ALI cultures.Furthermore,an exposure of M.ovipneumoniae to the ALI cultures led to an increased number of TUNEL positive apoptotic cells;and the flow cytometric analysis using dual staining with annexin-V-FITC and propidium iodide(PI)further showed that M.ovipneumoniae could induce a time-dependent apoptosis in ALI cultures.Mechanistically,the M.ovipneumoniae could evoke the epithelial cells to produce superoxide anion and nitric oxide(NO),and activate caspase-3activity in ALI culture model.Of interest,the increased apoptotic rate and caspase-3 activation could be reduced by an addition of NOS inhibitor or antioxidant.These results suggest that increased productions of NO and superoxide anion production,and caspase-3 activation may play a crucial role in the apoptosis for sheep airway epithelial cells in response to M.ovipneumoniae infection,which also indicate that the ALI culture system may be a reliable model for investigating the pathogen-host interaction of M.ovipneumoniae and airway epithelial cells.

关键词： M.ovipneumoniae air-liquid interface culture sheep airway epithelial cells Apoptosis Nitric oxide Caspase-3

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Dexamethasone protects airway epithelial cell line NCI-H292 against lipopolysaccharide induced endoplasmic reticulum stress and apoptosis

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Chinese Medical Journal 2011年第1期124卷 38-44页

作者： SHANG Yan WANG Fang BAI Chong HUANG Yi ZHAO Li-jun YAO Xiao-peng LI Qiang SUN Shu-han Department of Respiratory Medicine Changhai Hospital Second Military Medical University Shanghai 200433 China Department of Medical Genetics Second Military Medical University Shanghai 200433 China

Background Endoplasmic reticulum （ER） stress and ER stress-mediated apoptosis were reported to be involved in the pathogenesis of several diseases. In a recent study, it was reported that the ER stress pathway was activated in the lungs of lipopolysaccharide （LPS）-treated mice. It was also found that the C/EBP homologous protein （CHOP）, an apoptosis-related molecule, played a key role in LPS-induced lung damage. The aim of this study was to verify whether LPS could activate the ER stress response in airway epithelial cells and which molecule was involved in the pathway. This study was also aimed at finding new reagents to protect the airway epithelial cells during LPS injury. Methods ER stress markers were observed in LPS-incubated NCI-H292 cells. SiRNA-MUC5AC was transfected into NCI-H292 cells. The effects of dexamethasone and erythromycin were observed in LPS-induced NCI-H292 cells. Results LPS incubation increased the expression of ER stress markers at the protein and mRNA levels. The knockout of MUC5AC in cells attenuated the increase in ER stress markers after incubation with LPS. Dexamethasone and erythromycin decreased caspase-3 activity in LPS-induced NCI-H292 cells. Conclusions LPS may activate ER stress through the overexpression of MUC5AC. Dexamethasone may protect human airway epithelial cells against ER stress-related apoptosis by attenuating the overload of MUC5AC.

关键词： airway epithelial cells endoplasmic reticulum stress apoptosis lipopolysaccharide dexamethasone

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Plasmacytoid dendritic cell deficiency in neonates enhances allergic airway inflammation via reduced production of IFN-α

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Cellular & Molecular Immunology 2020年第5期17卷 519-532页

作者： Min Wu Liuchuang Gao Miao He Hangyu Liu Han Jiang Ketai Shi Runshi Shang Bing Liu Shan Gao Hebin Chen Feili Gong Erwin WGelfand Yafei Huang Junyan Han Department of Immunology School of Basic MedicineTongji Medical CollegeHuazhong University of Science and TechnologyWuhanChina Department of Respiratory Medicine Zhongnan Hospital of Wuhan UniversityWuhanChina Department of Respiratory Diseases Wuhan Central HospitalTongji Medical CollegeHuazhong University of Science and TechnologyWuhanChina Department of Pulmonary Medicine Wuhan Children’s HospitalTongji Medical CollegeHuazhong University of Science and TechnologyWuhanChina Division of Cell Biology Department of PediatricsNational Jewish HealthDenverCOUSA Department of Pathogen Biology School of Basic MedicineTongji Medical CollegeHuazhong University of Science and TechnologyWuhanChina

Allergic asthma,a chronic inflammatory airway disease associated with type 2 cytokines,often originates in early life.Immune responses at an early age exhibit a Th2 cell bias,but the precise mechanisms remain elusive.Plasmacytoid dendritic cells(pDCs),which play a regulatory role in allergic asthma,were shown to be deficient in neonatal mice.We report here that this pDC deficiency renders neonatal mice more susceptible to severe allergic airway inflammation than adult mice in an OVA-induced experimental asthma model.Adoptive transfer of pDCs or administration of IFN-αto neonatal mice prevented the development of allergic inflammation in wild type but not in IFNAR1−/−mice.Similarly,adult mice developed more severe allergic inflammation when pDCs were depleted.The protective effects of pDCs were mediated by the pDC-/IFN-α-mediated negative regulation of the secretion of epithelial cell-derived CCL20,GM-CSF,and IL-33,which in turn impaired the recruitment of cDC2 and ILC2 cells to the airway.In asthmatic patients,the percentage of pDCs and the level of IFN-αwere lower in children than in adults.These results indicate that impairment of pDC-epithelial cell crosstalk in neonates is a susceptibility factor for the development of allergeninduced allergic airway inflammation.

关键词： Neonate Plasmacytoid Dendritic cells Allergic airway inflammation IFN-α airway epithelial cells

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airway epithelial Cell Function and Respiratory Host Defense in Chronic Obstructive Pulmonary Disease

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Chinese Medical Journal 2018年第9期131卷 1099-1107页

作者： Gimano D.Amatngalim Pieter S.Hiemstra Department of Pulmonology Leiden University Medical Center Leiden The Netherlands Department of Pediatrics Wilhelmina Children's Hospital Regenerative Medicine Center Utrecht University Medical Center Utrecht Utrecht The Netherlands

INTRODUCTIONOur lungs have a vital role in mediating the exchange of oxygen and carbon dioxide between the air we breathe and the body.This function is under constant pressure as inhaled air contains numerous particles,gasses,and microorganisms that may cause injury and infection to the lungs.Removal and neutralization of potential harmful substances from inhaled air is a main function of the airway epithelium.

关键词： airway epithelial cells Cell Culture Chronic Obstructive Pulmonary Disease Respiratory Infections

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