The aminoglycoside modifying enzyme Eis2 represents a new potential<i>in vivo</i>target for reducing antimicrobial drug resistance in<i>Mycobacterium abscessus</i>complex

脓肿分枝杆菌 支气管扩张 囊性纤维化 医学 非结核分枝杆菌 重症监护医学 分枝杆菌 内科学 病理 肺结核 肺
作者
Nicola Ivan Lorè,Fabio Saliu,Andrea Spitaleri,Daniel Schäfle,Francesca Nicola,Daniela Maria Cirillo,Peter Sander
出处
期刊:The European respiratory journal [European Respiratory Society]
卷期号:: 2201541-2201541
标识
DOI:10.1183/13993003.01541-2022
摘要

Mycobacterium abscessus complex (MABSC) is an emerging opportunistic pathogen complex responsible for lung infections after lung colonisation in people with pulmonary disorders, like bronchiectasis or cystic fibrosis [1, 2]. It is becoming one of the most clinically relevant nontuberculous mycobacteria for severity of infections and poor response to antibiotic treatment. The MABSC includes three subspecies abscessus , bolletii and massiliense [3–5]. MABSC pulmonary disease is characterized by the presence of specific microbiological, clinical, and radiological features described in the ATS/ESCMID/ERS/IDSA consensus statement [1]. Infections are difficult to treat due to the high-level of antibiotic resistance conferred by an almost impermeable cell wall, drug efflux pumps, or drug-modifying enzymes [2, 6]. Footnotes This manuscript has recently been accepted for publication in the European Respiratory Journal . It is published here in its accepted form prior to copyediting and typesetting by our production team. After these production processes are complete and the authors have approved the resulting proofs, the article will move to the latest issue of the ERJ online. Please open or download the PDF to view this article. Conflict of Interest: Nicola Lorè reports grants from US Cystic Fibrosis Foundation, Italian Cystic Fibrosis; outside the submitted work. Conflict of Interest: Peter Sander reports support from Swiss National Science Foundation, Cystic Fibrosis Switzerland, Federal Office of Public Health for the present manuscript. He also reports grants from InnoSuisse, Stiftung wissenschaftliche Forschung; outside the submitted work. Conflict of Interest: All other authors have nothing to disclose.

科研通智能强力驱动
Strongly Powered by AbleSci AI
科研通是完全免费的文献互助平台,具备全网最快的应助速度,最高的求助完成率。 对每一个文献求助,科研通都将尽心尽力,给求助人一个满意的交代。
实时播报
11发布了新的文献求助10
刚刚
追寻的问玉完成签到 ,获得积分10
1秒前
逊哥完成签到 ,获得积分10
2秒前
Ellalala完成签到 ,获得积分10
3秒前
orixero的应助被涵宇采纳,获得10
3秒前
Sun完成签到,获得积分20
4秒前
vampv举报北遇的求助涉嫌违规
4秒前
清新发布了新的文献求助10
5秒前
6秒前
xiaowang完成签到,获得积分10
7秒前
隐形曼青的应助被lagom采纳,获得10
7秒前
7秒前
Leon完成签到,获得积分10
7秒前
11秒前
追寻天菱完成签到,获得积分10
11秒前
Sun发布了新的文献求助10
11秒前
司空晓山发布了新的文献求助10
12秒前
深情安青的应助被内向的乐安采纳,获得10
12秒前
12秒前
零负一的应助被GENQINGE采纳,获得30
12秒前
小鲸鱼完成签到,获得积分10
12秒前
12秒前
YANGZIX发布了新的文献求助10
13秒前
eena完成签到,获得积分10
13秒前
13秒前
传奇3的应助被明理的又柔采纳,获得10
15秒前
luocan完成签到,获得积分10
18秒前
lagom发布了新的文献求助10
19秒前
黑默丁格发布了新的文献求助10
19秒前
20秒前
王星辰完成签到,获得积分10
20秒前
隐形萃完成签到 ,获得积分10
21秒前
王豆豆发布了新的文献求助10
24秒前
25秒前
25秒前
26秒前
科研通AI2S的应助被nike胡咧咧采纳,获得10
26秒前
内向的乐安完成签到,获得积分10
29秒前
隐形曼青的应助被11采纳,获得10
30秒前
外向烨磊完成签到,获得积分10
31秒前
高分求助中
(应助此贴封号)【重要!!请各用户(尤其是新用户)详细阅读】【科研通的精品贴汇总】 10000
Rosenblum, Global Change Biology 800
自動車の空力技術 800
Organizational Behavior 510
Management and the Arts 510
Issues in Task-Based Language Teaching 500
Wafer Surface Defect 420
热门求助领域 (近24小时)
化学 材料科学 医学 生物 纳米技术 计算机科学 化学工程 工程类 有机化学 物理 复合材料 生物化学 内科学 细胞生物学 基因 遗传学 免疫学 冶金 光电子学 癌症研究
热门帖子
关注 科研通微信公众号,转发送积分 7784635
求助须知:如何正确求助?哪些是违规求助? 9323917
关于积分的说明 20395985
捐赠科研通 7373351
什么是DOI,文献DOI怎么找? 3321092
关于科研通互助平台的介绍 2469015
邀请新用户注册赠送积分活动 2337355