Enterotoxigenic Escherichia coli heat labile enterotoxin affects neutrophil effector functions via cAMP/PKA/ERK signaling.

IF 12.2 1区 医学 Q1 GASTROENTEROLOGY & HEPATOLOGY Gut Microbes Pub Date : 2024-09-16 DOI:10.1080/19490976.2024.2399215
Jinglin Ma,Leen Hermans,Matthias Dierick,Hans Van der Weken,Eric Cox,Bert Devriendt
{"title":"Enterotoxigenic Escherichia coli heat labile enterotoxin affects neutrophil effector functions via cAMP/PKA/ERK signaling.","authors":"Jinglin Ma,Leen Hermans,Matthias Dierick,Hans Van der Weken,Eric Cox,Bert Devriendt","doi":"10.1080/19490976.2024.2399215","DOIUrl":null,"url":null,"abstract":"Enterotoxigenic Escherichia coli (ETEC) are a major cause of diarrheal illness in humans and animals, induced by enterotoxins produced by these pathogens. Despite the crucial role of neutrophils in combatting bacterial infections, our understanding of how enterotoxins impact neutrophil function is limited. To address this knowledge gap, we used heat-labile enterotoxin (LT) and heat-stable enterotoxin a (STa) to investigate their impact on the effector functions of neutrophils. Our study reveals that pSTa does not exert any discernible effect on the function of neutrophils. In contrast, LT altered the migration and phagocytosis of neutrophils and induced the production of inflammatory factors via activation of cAMP/PKA and ERK1/2 signaling. LT also attenuated the release of neutrophil extracellular traps by neutrophils via the PKA signaling pathway. Our findings provide novel insights into the impact of LT on neutrophil function, shedding light on the underlying mechanisms that govern its immunoregulatory effects. This might help ETEC in subverting the immune system and establishing infection.","PeriodicalId":12909,"journal":{"name":"Gut Microbes","volume":"23 1","pages":"2399215"},"PeriodicalIF":12.2000,"publicationDate":"2024-09-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Gut Microbes","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.1080/19490976.2024.2399215","RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q1","JCRName":"GASTROENTEROLOGY & HEPATOLOGY","Score":null,"Total":0}
引用次数: 0

Abstract

Enterotoxigenic Escherichia coli (ETEC) are a major cause of diarrheal illness in humans and animals, induced by enterotoxins produced by these pathogens. Despite the crucial role of neutrophils in combatting bacterial infections, our understanding of how enterotoxins impact neutrophil function is limited. To address this knowledge gap, we used heat-labile enterotoxin (LT) and heat-stable enterotoxin a (STa) to investigate their impact on the effector functions of neutrophils. Our study reveals that pSTa does not exert any discernible effect on the function of neutrophils. In contrast, LT altered the migration and phagocytosis of neutrophils and induced the production of inflammatory factors via activation of cAMP/PKA and ERK1/2 signaling. LT also attenuated the release of neutrophil extracellular traps by neutrophils via the PKA signaling pathway. Our findings provide novel insights into the impact of LT on neutrophil function, shedding light on the underlying mechanisms that govern its immunoregulatory effects. This might help ETEC in subverting the immune system and establishing infection.
查看原文
分享 分享
微信好友 朋友圈 QQ好友 复制链接
本刊更多论文
肠毒性大肠埃希氏菌热溶性肠毒素通过 cAMP/PKA/ERK 信号转导影响中性粒细胞效应功能
肠毒性大肠杆菌(ETEC)是导致人类和动物腹泻的主要原因,这些病原体产生的肠毒素会诱发腹泻。尽管中性粒细胞在对抗细菌感染方面发挥着至关重要的作用,但我们对肠毒素如何影响中性粒细胞功能的了解却很有限。为了填补这一知识空白,我们使用热凋亡肠毒素(LT)和热稳定肠毒素 a(STa)来研究它们对中性粒细胞效应功能的影响。我们的研究发现,pSTa 对中性粒细胞的功能没有任何明显的影响。相反,LT 改变了中性粒细胞的迁移和吞噬功能,并通过激活 cAMP/PKA 和 ERK1/2 信号诱导炎症因子的产生。LT还能通过PKA信号通路减少中性粒细胞释放中性粒细胞胞外捕获物。我们的研究结果为了解 LT 对中性粒细胞功能的影响提供了新的视角,揭示了其免疫调节作用的潜在机制。这可能有助于 ETEC 破坏免疫系统并建立感染。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
求助全文
约1分钟内获得全文 去求助
来源期刊
Gut Microbes
Gut Microbes Medicine-Microbiology (medical)
CiteScore
18.20
自引率
3.30%
发文量
196
审稿时长
10 weeks
期刊介绍: The intestinal microbiota plays a crucial role in human physiology, influencing various aspects of health and disease such as nutrition, obesity, brain function, allergic responses, immunity, inflammatory bowel disease, irritable bowel syndrome, cancer development, cardiac disease, liver disease, and more. Gut Microbes serves as a platform for showcasing and discussing state-of-the-art research related to the microorganisms present in the intestine. The journal emphasizes mechanistic and cause-and-effect studies. Additionally, it has a counterpart, Gut Microbes Reports, which places a greater focus on emerging topics and comparative and incremental studies.
期刊最新文献
Genomic island-encoded LmiA regulates acid resistance and biofilm formation in enterohemorrhagic Escherichia coli O157:H7. Gut microbiota and microbial metabolites for osteoporosis. Non-stochastic reassembly of a metabolically cohesive gut consortium shaped by N-acetyl-lactosamine-enriched fibers. The regulatory effect of chitooligosaccharides on islet inflammation in T2D individuals after islet cell transplantation: the mechanism behind Candida albicans abundance and macrophage polarization. Systematically-designed mixtures outperform single fibers for gut microbiota support.
×
引用
GB/T 7714-2015
复制
MLA
复制
APA
复制
导出至
BibTeX EndNote RefMan NoteFirst NoteExpress
×
×
提示
您的信息不完整,为了账户安全,请先补充。
现在去补充
×
提示
您因"违规操作"
具体请查看互助需知
我知道了
×
提示
现在去查看 取消
×
提示
确定
0
微信
客服QQ
Book学术公众号 扫码关注我们
反馈
×
意见反馈
请填写您的意见或建议
请填写您的手机或邮箱
已复制链接
已复制链接
快去分享给好友吧!
我知道了
×
扫码分享
扫码分享
Book学术官方微信
Book学术文献互助
Book学术文献互助群
群 号:481959085
Book学术
文献互助 智能选刊 最新文献 互助须知 联系我们:info@booksci.cn
Book学术提供免费学术资源搜索服务,方便国内外学者检索中英文文献。致力于提供最便捷和优质的服务体验。
Copyright © 2023 Book学术 All rights reserved.
ghs 京公网安备 11010802042870号 京ICP备2023020795号-1