{"title":"Effect of erythromycin on the ultrastructure of human macrophages exposed to cigarette smoke extract <i>in vitro</i>.","authors":"Shaoshuang Wang, Jianjun Huo, Yanlin Wei, Mei Huan, Zhouling Luo, Meihua Li, Mingzhi Wen, Xiaoning Zhong, Zhiyi He, Nan Ma, Jufeng Qiu, Xiaojuan Tang","doi":"10.1080/01913123.2022.2060395","DOIUrl":null,"url":null,"abstract":"<p><p>Macrophages serve an active role in the pathophysiology of chronic obstructive pulmonary disease (COPD). Erythromycin (EM) has been verified as an effective treatment for COPD. However, there are few studies on the effect of EM on the ultrastructure of macrophages exposed to cigarette smoke extract (CSE). In the present study, human macrophages were randomly divided into three groups: The control, CSE and the CSE+EM group, using electron microscopy, the effect of EM was evaluated by comparing the ultrastructural changes between these groups. The macrophages were additionally divided into a further four groups: The control, CSE, CSE+EM 24 h and CSE+EM 48 h groups. The generation of reactive oxygen species (ROS) in each group was evaluated by detecting fluorescence intensity. It was observed that the cellular ultrastructure of the CSE group exhibited abnormal changes, though this effect was reversed back to the level of the control in the CSE+EM group. Compared with the control group, the ROS expression level was significantly increased in the CSE group (P < .05); however, compared with the CSE group, the ROS concentration was decreased in the CSE+EM 24 h (P < .05) and CSE+EM 48 h groups (P < .05), though this was more apparent in the EM 48 h group. It was concluded that EM protects human macrophages against CSE. Moreover, it was hypothesized that EM may reduce the symptoms of patients with COPD by protecting the macrophage ultrastructure from the effects of CSE, resulting in the decreased generation of ROS, inhibiting autophagy and reducing endoplasmic reticulum stress.</p>","PeriodicalId":23430,"journal":{"name":"Ultrastructural Pathology","volume":"46 1","pages":"303-312"},"PeriodicalIF":1.1000,"publicationDate":"2022-07-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Ultrastructural Pathology","FirstCategoryId":"5","ListUrlMain":"https://doi.org/10.1080/01913123.2022.2060395","RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"2022/6/10 0:00:00","PubModel":"Epub","JCR":"Q4","JCRName":"MICROSCOPY","Score":null,"Total":0}
引用次数: 0
Abstract
Macrophages serve an active role in the pathophysiology of chronic obstructive pulmonary disease (COPD). Erythromycin (EM) has been verified as an effective treatment for COPD. However, there are few studies on the effect of EM on the ultrastructure of macrophages exposed to cigarette smoke extract (CSE). In the present study, human macrophages were randomly divided into three groups: The control, CSE and the CSE+EM group, using electron microscopy, the effect of EM was evaluated by comparing the ultrastructural changes between these groups. The macrophages were additionally divided into a further four groups: The control, CSE, CSE+EM 24 h and CSE+EM 48 h groups. The generation of reactive oxygen species (ROS) in each group was evaluated by detecting fluorescence intensity. It was observed that the cellular ultrastructure of the CSE group exhibited abnormal changes, though this effect was reversed back to the level of the control in the CSE+EM group. Compared with the control group, the ROS expression level was significantly increased in the CSE group (P < .05); however, compared with the CSE group, the ROS concentration was decreased in the CSE+EM 24 h (P < .05) and CSE+EM 48 h groups (P < .05), though this was more apparent in the EM 48 h group. It was concluded that EM protects human macrophages against CSE. Moreover, it was hypothesized that EM may reduce the symptoms of patients with COPD by protecting the macrophage ultrastructure from the effects of CSE, resulting in the decreased generation of ROS, inhibiting autophagy and reducing endoplasmic reticulum stress.
期刊介绍:
Ultrastructural Pathology is the official journal of the Society for Ultrastructural Pathology. Published bimonthly, we are the only journal to be devoted entirely to diagnostic ultrastructural pathology.
Ultrastructural Pathology is the ideal journal to publish high-quality research on the following topics:
Advances in the uses of electron microscopic and immunohistochemical techniques
Correlations of ultrastructural data with light microscopy, histochemistry, immunohistochemistry, biochemistry, cell and tissue culturing, and electron probe analysis
Important new, investigative, clinical, and diagnostic EM methods.