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SARS-CoV-2 treatment effects induced by ACE2-expressing microparticles are explained by the oxidized cholesterolincreased endosomal pH of alveolar macrophages

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Cellular & Molecular Immunology 2022年第2期19卷 210-221页

作者： Zhenfeng Wang Jiadi Lv Pin Yu Yajin Qu Yabo Zhou Li Zhou Qiangqiang Zhu Shunshun Li Jiangping Song Wei Deng Ran Gao Yuying Liu Jiangning Liu Wei-Min Tong Chuan Qin Bo Huang Department of Immunology&National Key Laboratory of Medical Molecular Biology Institute of Basic Medical SciencesChinese Academy of Medical Sciences(CAMS)&Peking Union Medical CollegeBeijing 100005China NHC Key Laboratory of Human Disease Comparative Medicine Beijing Key Laboratory for Animal Models of Emerging and Remerging Infectious DiseasesInstitute of Laboratory Animal ScienceCAMS and Comparative Medicine CenterPeking Union Medical CollegeBeijingChina State Key Laboratory of Cardiovascular Disease Fuwai HospitalNational Center for Cardiovascular DiseasesCAMS and Peking Union Medical CollegeBeijingChina Department of Pathology Institute of Basic Medical SciencesCAMS and Peking Union Medical CollegeBeijingChina Department of Biochemistry&Molecular Biology Tongji Medical CollegeHuazhong University of Science&TechnologyWuhan 430030China

Exploring the cross-talk between the immune system and advanced biomaterials to treat SARS-CoV-2 infection is a promising strategy.Here,we show that ACE2-overexpressing A549 cell-derived microparticles(AO-MPs)are a potential therapeutic agent against SARS-CoV-2 infection.Intranasally administered AO-MPs dexterously navigate the anatomical and biological features of the lungs to enter the alveoli and are taken up by alveolar macrophages(AMs).Then,AO-MPs increase the endosomal pH but decrease the lysosomal pH in AMs,thus escorting bound SARS-CoV-2 from phago-endosomes to lysosomes for degradation.This pH regulation is attributable to oxidized cholesterol,which is enriched in AO-MPs and translocated to endosomal membranes,thus interfering with proton pumps and impairing endosomal acidification.In addition to promoting viral degradation,AO-MPs also inhibit the proinflammatory phenotype of AMs,leading to increased treatment efficacy in a SARS-CoV-2-infected mouse model without side effects.These findings highlight the potential use of AO-MPs to treat SARS-CoV-2-infected patients and showcase the feasibility of MP therapies for combatting emerging respiratory viruses in the future.

关键词： SARS-CoV-2 microparticles alveolar macrophages Endosomes Lysosomes

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Dietary plant extracts modulate gene expression profiles in alveolar macrophages of pigs experimentally infected with porcine reproductive and respiratory syndrome virus

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Journal of Animal Science and Biotechnology 2021年第1期12卷 372-385页

作者： Kwangwook Kim Peng Ji Minho Song Tung M.Che David Bravo James E.Pettigrew Yanhong Liu Department of Animal Science University of CaliforniaDavisCAUSA. Department of Nutrition University of CaliforniaDavisCAUSA. Department of Animal Science and Biotechnology Chungnam National UniversityDaejeonSouth Korea Department of Animal Production Nong Lam UniversityHo Chi Minh CityVietnam Pancosma SA GenevaSwitzerland. Current address:Land O’Lakes Inc. Arden HillsMNUSA. Department of Animal Science University of IllinoisUrbanaILUSA.

Background: Our previous study showed that 3 plant extracts enhanced the immune responses and growth efficiency of weaned pigs infected with porcine reproductive and respiratory syndrome virus(PRRSV), which is one of the most economically important disease in swine industry. However, each plant extract differently effected on growth efficiency and immune responses. Therefore, the objective of this study was conducted to characterize the effects and investigate the potential underlying mechanisms of 3 plant extracts on gene expression of alveolar macrophages in weaned pigs experimentally infected with PRRSV.Results: PRRSV infection altered(P alveolar macrophages of PRRSV-infected pigs, respectively. PRRSV infection up-regulated(P alveolar macrophages of PRRSV-infected pigs, especially altering genes involved in immunity.

关键词： alveolar macrophages Gene expression Plant extracts PRRSV Weaned pigs

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Voltage-dependent K^+-channel Responses during Activation and Damage in alveolar macrophages Induced by Quartz Particles

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Journal of Huazhong University of Science and Technology(Medical Sciences) 2009年第4期29卷 404-408页

作者：孙敬智梅勇郭翔殷霄赵学彬王正伦杨磊 Department of Occupational and Environmental Health Ministry of Education Key Laboratory of Environment and Health School of Public Health Tongji Medical College Huazhong University of Science and Technology Wuhan 430030 China Department of Occupational and Environmental Health Medical College Wuhan University of Science and Technology Wuhan 430065 China

The roles of voltage-dependent K^＋ channels during activation and damage in alveolar macrophages （AMs） exposed to different silica particles were examined. Rat AMs were collected by means of bronchoalveolar lavage, and were adjusted to 5× 10^5/mL. After AMs were exposed to different concentrations （0, 25, 50, 100, 200 μg/mL） of quartz particles and 100 μg/mL amorphous silica particles for 24 h, the voltage-depended K^＋ current in AMs was measured by using patch clamp technique. Meanwhile the leakage of lactate dehydrogenase （LDH） and the viability of AMs were detected respectively. Patch clamp studies demonstrated that AMs possessed outward delayed and inward rectifying K^＋ current. Exposure to quartz particles increased the outward delayed K^＋ current but it had no effect on inward rectifier K^＋ current in AMs. Neither of the two K^＋ channels in AMs was affected by amorphous silica particles. Cytotoxicity test showed that both silica particles could damage AM membrane and result in significant leakage of LDH （P〈0.05）. MTT studies, however, showed that only quartz particles reduced viability of AMs （P〈0.05）. It is concluded that quartz parti- cles can activate the outward delayed K^＋ channel in AMs, which may act as an activating signal in AMs to initiate an inflammatory response during damage and necrosis in AMs induced by exposure to quartz particle. K^＋ channels do not contribute to the membrane damage of AMs.

关键词： quartz alveolar macrophages patch clamp voltage-dependent K^＋ channels

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Monocyte and macrophage function in respiratory viral infections

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Animal Diseases 2024年第1期4卷 40-47页

作者： Mohd Arish Jie Sun Beirne B.Carter Center for Immunology Research University of VirginiaCharlottesvilleVA 22908USA Division of Infectious Disease and International Health Department of MedicineUniversity of VirginiaCharlottesvilleVA 22908USA

Pulmonary macrophages,such as tissue-resident alveolar and interstitial macrophages and recruited monocyte-derived macrophages,are the major macrophages present in the lungs during homeostasis and diseased conditions.While tissue-resident macrophages act as sentinels of the alveolar space and play an important role in maintaining homeostasis and immune regulation,recruited macrophages accumulate in the respiratory tract after acute viral infections.Despite sharing similar anatomical niches,these macrophages are distinct in terms of their origins,surface marker expression,and transcriptional profiles,which impart macrophages with distinguished characteristics in physi-ological and pathophysiological conditions.In this review,we summarize the current view on these macrophage populations,their shared functions,and what makes them distinct from each other in the context of homeostasis andrespiratoryviral infections.

关键词： alveolar macrophages Interstitial macrophages Monocytes derived macrophages Viral infection IAV RSV SARS-COV-2

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Regulation of activity of nuclear factor-kB and activator protein-1 by nitric oxide, surfactant and glucocorticoids in alveolar macrophages from piglets with acute lung injury

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Acta Pharmacologica Sinica 2003年第12期 142-149页

作者： CAO Lei~(2,3). QIAN Li-Ling~2, ZHU You-Rong~2, GUO Chun-Bao~2, GONG Xiao-Hui~2, SUN Bo~(2,4) ~3Laboratory of Respiratory and Intensive Care, Children’s Hospital of Fudan University, Shanghai 200032 ~3Department of Pediatrics, Hebei Provincial People’s Hospital, Shijiazhuang, China

AIM: To investigate whether acute lung injury (ALl) in ventilated piglets with bacterial infection affects NF-κB and AP-1 expression in alveolar macrophages (AM) and whether nitric oxide (NO), surfactant (Surf), glucocorticoids (GC) affect NF-κB and AP-1 activation in AM in vivo and in vitro. METHODS: The animals were intraperitoneally injected Escherichia coli, which caused ALl. Nuclear extracts of AM were analyzed by electrophoretic mobility shift assay (EMSA) for the nuclear factor-kappa B (NF-κB) and activation protein-1 (AP-1) expression. Detection of IκB-α protein was from cytoplasmic extract by Western blotting. Immunocytochemistry staining was used for intracellular location of p65 subunits of NF-κB. RESULTS: In ex vivo experiments, strikingly higher expression of NF-κB and AP-1 by EMSA was found 6 h after bacterial injection in contrast to the Normal group. In the NO, SNO, and GC groups, markedly attenuated NF-κB and AP-1 activation was observed. The NF-κB and AP-1 activation in Surf g

关键词： acute lung injury alveolar macrophages NF-kappa B activator protein-1 nitric oxide surfaceactive agents glucocorticoids

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Surfactant protein D inhibits lipid-laden foamy macrophages and lung inflammation in chronic obstructive pulmonary disease

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Cellular & Molecular Immunology 2023年第1期20卷 38-50页

作者： Miao-Hsi Hsieh Pei-Chi Chen Han-Yin Hsu Jui-Chang Liu Yu-Sheng Ho Yuh Jyh Lin Chin-Wei Kuo Wen-Shuo Kuo Hui-Fang Kao Shulhn-Der Wang Zhi-Gang Liu Lawrence Shih-Hsin Wu Jiu-Yao Wang Center for Allergy Immunologyand Microbiome(A.I.M.)China Medical University HospitalTaichungTaiwanChina Graduate Institute of Basic Medical Sciences College of MedicineNational Cheng Kung UniversityTainanTaiwanChina Department of Nursing National Tainan Junior College of NursingTainanTaiwanChina Graduate Institute of Biochemistry and Molecular Biology College of MedicineNational Cheng Kung UniversityTainanTaiwanChina Department of Pediatrics National Cheng Kung University HospitalTainanTaiwanChina Division of Pulmonary Medicine Department of Internal MedicineNational Cheng Kung University HospitalCollege of MedicineNational Cheng Kung UniversityTainanTaiwanChina Institute of Clinical Medicine College of MedicineNational Cheng Kung UniversityTainanTaiwanChina School of Chemistry and Materials Science Nanjing University of Information Science and TechnologyNanjingChina School of Post-Baccalaureate Chinese Medicine China Medical UniversityTaichungTaiwanChina Department of Respirology and Allergy Third Affiliated Hospital of Shenzhen UniversityShenzhenChina Institute of Biomedical Sciences China Medical UniversityTaichungTaiwanChina Department of Allergy Immunologyand Rheumatology(AIR)China Medical University Children’s HospitalTaichungTaiwanChina

Increased levels of surfactant protein D (SP-D) and lipid-laden foamy macrophages (FMs) are frequently found under oxidative stress conditions and/or in patients with chronic obstructive pulmonary disease (COPD) who are also chronically exposed to cigarette smoke (CS). However, the roles and molecular mechanisms of SP-D and FMs in COPD have not yet been determined. In this study, increased levels of SP-D were found in the bronchoalveolar lavage fluid (BALF) and sera of ozone- and CS-exposed mice. Furthermore, SP-D-knockout mice showed increased lipid-laden FMs and airway inflammation caused by ozone and CS exposure, similar to that exhibited by our study cohort of chronic smokers and COPD patients. We also showed that an exogenous recombinant fragment of human SP-D (rfhSP-D) prevented the formation of oxidized low-density lipoprotein (oxLDL)-induced FMs in vitro and reversed the airway inflammation and emphysematous changes caused by oxidative stress and CS exposure in vivo. SP-D upregulated bone marrow-derived macrophage (BMDM) expression of genes involved in countering the oxidative stress and lipid metabolism perturbations induced by CS and oxLDL. Our study demonstrates the crucial roles of SP-D in the lipid homeostasis of dysfunctional alveolar macrophages caused by ozone and CS exposure in experimental mouse emphysema, which may provide a novel opportunity for the clinical application of SP-D in patients with COPD.

关键词： alveolar macrophages Chronic obstructive pulmonary diseases Surfactant protein D Lipid metabolism Ozone Cigarettes

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AdMSC-derived exosomes alleviate acute lung injury through transferring mitochondrial respiratory component to improve bioenergetics and immune homeostasis of alveolar macrophages

AdMSC-derived exosomes alleviate acute lung injury through t...

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第十四届全国免疫学学术大会

作者： Liangjun Xia Nianyin Lv Zihao Liang Tonghui Ma Haibo Cheng Youbing Xia Liyun Shi Nanjing University of Chinese Medicine Affiliated Hospital of Nanjing University of Chinese Medicine Affiliated Hospital of Xuzhou Medical University Zhejiang Shuren University

Currently,acute lung injury(ALI) and acute respiratory distress syndrome(ARDS) featured with severe hypoxemia,airway dysfunction,and extensive inflammation lack effective treatment.Aberrant activation of macrophages with mitochondria dismiss was proved to be associated with pathogenesis of ALI.Exosomes from adipose-derived mesenchymal stem cells(AdMSC-Exos) have been distinguished by their low immunogenicity,lack of tumorigenicity,and high clinical safety,but their role in treating ALI and the mechanism involved need to be defined.In this study,we showed that AdMSC-Exos provided profound protection against LPS-induced ALI in mice,accompanied by macrophages shifting from M1 proinflammatory to M2 anti-inflammatory type.Importantly,our data indicated that AdMSC-Exos deliver mitochondrial component to recipient macrophages,which were metabolically disturbed during the development of ALI.Consequently,transfering of AdMSC-Exos significantly improved macrophages mitochondrial integrity,mitochondrial membrane potential(MMP) and oxidative phosphorylation level,leading to the resumption of metabolic and immune homeostasis of airway macrophages and mitigating lung inflammatory pathology.Collectively,our study reveals the potential role for AdMSC-Exos in protecting ALI,and suggests that macrophage-centered and mitochondria-targeted strategy might become a promising treatment for certain inflammatory lung diseases.

关键词： stem cells exosomes acute lung injury alveolar macrophages mitochondrial function

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Distinct uptake, amplification, and release of SARS-CoV-2 by M1 and M2 alveolar macrophages

Distinct uptake, amplification, and release of SARS-CoV-2 by...

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第十四届全国免疫学学术大会

作者： Jiadi Lv Haoran Chen Yishen Jiang Bo Huang 中国医学科学院基础医学研究所

Severe acute respiratory syndrome coronavirus 2(SARS-CoV-2) invades the alveoli, where abundant alveolar macrophages(AMs) reside. How AMs respond to SARS-CoV-2 invasion remains elusive. Here, we show that classically activated M1 AMs facilitate viral spread;however, alternatively activated M2 AMs limit the spread. M1 AMs utilize cellular softness to efficiently take up SARS-CoV-2. Subsequently, the invaded viruses take over the endo-lysosomal system to escape. M1 AMs have a lower endosomal pH, favoring membrane fusion and allowing the entry of viral RNA from the endosomes into the cytoplasm, where the virus achieves replication and is packaged to be released. In contrast, M2 AMs have a higher endosomal pH but a lower lysosomal pH, thus delivering the virus to lysosomes for degradation. In hACE2 transgenic mouse model, M1 AMs are found to facilitate SARS-CoV-2 infection of the lungs. These findings provide insights into the complex roles of AMs during SARS-CoV-2 infection, along with potential therapeutic targets.

关键词： SARS-CoV-2 alveolar macrophages ACE2 endosome

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Oxidized cholesterol-enriched microparticles target alveolar macrophages for SARS-CoV-2 treatment

Oxidized cholesterol-enriched microparticles target alveolar...

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第十四届全国免疫学学术大会

作者： Ruiyang Pang Haoran Chen Dilizhatai Saimi Zhenfeng Wang Peking Union Medical College

Exploring the cross of immune system and advanced biomaterials to treat SARS-CoV-2 infection is a promising strategy.Here,we show that ACE2-overexpressing A549 cell-derived microparticles(AO-MPs) are a potential therapeutic agent against SARS-CoV-2 infection.Intranasally administered AO-MPs dexterously navigate the anatomical and biological features of the lung to enter the alveoli and are taken up by alveolar macrophages(AMs).In turn,AO-MPs increase the endosomal pH but decrease lysosomal pH of AMs,thus escorting the bound SARS-CoV-2 from phago-endosomes to lysosomes for degradation.This pH regulation is attributable to oxidized cholesterol which is enriched in AO-MPs and translocated to endosomal membranes,thus interfering with proton pump and impairing endosomal acidification.In addition to promoting viral degradation,AO-MPs also inhibit AMs’ pro-inflammatory phenotype,leading to increased treatment efficacy in a SARS-CoV-2-infected mouse model without side effects.These findings highlight the potential use of AO-MPs to treat SARS-CoV-2 infected patients and showcases in the feasibility of MP therapies to combat emerging respiratory viruses in the future.

关键词： SARS-CoV-2 Microparticles alveolar macrophages

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Role of Endoplasmic Reticulum Stress in Silica-induced Apoptosis in RAW264.7 Cells＊

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Biomedical and Environmental Sciences 2017年第8期30卷 591-600页

作者： HU Yong Bin WU Xia QIN Xiao Feng WANG Lei PAN Pin Hua Department of Pathology Xiangya Basic Medical School Central South University Changsha 410013 Hunan China Department of Pathology Xiangya Hospital Central South University Changsha 410008 Hunan China Department of Pathology The Second Xiangya Hospital Central South University Changsha 410011 Hunan China Department of Respiratory Medicine Xiangya Hospital Central South University Changsha 410008 Hunan China

Objective We investigated the role of endoplasmic reticulum stress （ERS） in silica-induced apoptosis in alveolar macrophages in vitro. Methods RAW264.7 cells were incubated with 200 μm/mL silica for different time periods. Cell viability was assayed by the MTT assay. Cell apoptosis was evaluated by DAPI staining, flow cytometry analysis, and Western blot analysis of caspase-3. Morphological changes in the endoplasmic reticulum were observed by transmission electron microscopy. The expression of ERS markers binding protein （BiP） and CCAAT-enhancer-binding protein homologous protein （CHOP） was examined by Western blotting and real-time PCR. As an inhibitor of ERS, 4-phenylbutyric acid （4-PBA） was used in the experiments. Results Silica exposure induced nuclear condensation and caspase-3 expression in RAW264.7 cells. The number of apoptotic cells increased after silica exposure in a time-dependent manner. Silica treatment induced expansion of the endoplasmic reticulum. In addition, the expression of BiP and CHOP increased in silica-stimulated cells. Furthermore, 4-PBA treatment inhibited silica-induced endoplasmic reticulum expansion and the expression of BiP and CHOP. Moreover, 4-PBA treatment attenuated nuclear condensation, reduced apoptotic cells, and downregulated caspase-3 expression in silica-stimulated cells. Conclusion Silica-induced ERS is involved in the apoptosis of alveolar macrophages

关键词： Silica alveolar macrophages Endoplasmic reticulum stress Apoptosis

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