AI Article Synopsis
- Miscommunication between antiviral and antibacterial signals during respiratory infections can worsen illness and increase death rates.
- Extracellular vesicles (EVs), released from epithelial cells during antiviral responses, hinder the ability of macrophages to fight bacterial infections in the airway.
- This study highlights how these EVs disrupt communication between epithelial cells and macrophages, leading to impaired immune responses and offering new insights into the challenges of immune dysfunction in respiratory coinfections.
Article Abstract
Miscommunication of antiviral and antibacterial immune signals drives worsened morbidity and mortality during respiratory viral-bacterial coinfections. Extracellular vesicles (EVs) are a form of intercellular communication with broad implications during infection, and here we show that epithelium-derived EVs released during the antiviral response impair the antibacterial activity of macrophages, an innate immune cell crucial for bacterial control in the airway. Macrophages exposed to antiviral EVs display reduced clearance of as well as altered inflammatory signaling and anti-inflammatory metabolic reprogramming, thus revealing EVs as a source of dysregulated epithelium-macrophage crosstalk during coinfection. As effective epithelium-macrophage communication is critical in mounting an appropriate immune response, this novel observation of epithelium-macrophage crosstalk shaping macrophage metabolism and antimicrobial function provides exciting new insight and improves our understanding of immune dysfunction during respiratory coinfections.
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| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC10653878 | PMC |
| http://dx.doi.org/10.1128/mbio.00863-23 | DOI Listing |
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Article Synopsis
- Miscommunication between antiviral and antibacterial signals during respiratory infections can worsen illness and increase death rates.
- Extracellular vesicles (EVs), released from epithelial cells during antiviral responses, hinder the ability of macrophages to fight bacterial infections in the airway.
- This study highlights how these EVs disrupt communication between epithelial cells and macrophages, leading to impaired immune responses and offering new insights into the challenges of immune dysfunction in respiratory coinfections.
Naringenin suppresses BEAS-2B-derived extracellular vesicular cargoes disorder caused by cigarette smoke extract thereby inhibiting M1 macrophage polarization.
Front Immunol
August 2022
Guangdong Engineering and Technology Research Center for Quality and Efficacy Re-evaluation of Post-marketed Traditional Chinese Medicine (TCM), State Key Laboratory of Biocontrol, Guangdong Provincial Key Laboratory of Plant Resources, School of Life Sciences, Sun Yat-sen University, Guangzhou, China.
Extracellular vesicles (EVs)-mediated epithelium-macrophage crosstalk has been proved to maintain lung homeostasis in cigarette smoke-induced lung diseases such as chronic obstructive pulmonary disease (COPD). In our previous study, we found that EVs derived from cigarette smoke extract (CSE) treated BEAS-2B promoted M1 macrophage polarization, which probably accelerated the development of inflammatory responses. Naringenin has been proved to suppress M1 macrophage polarization, but whether naringenin regulates macrophage polarization mediated by EVs has not been reported.
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