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West Ashley Library
9 a.m. – 7 p.m.
Phone: (843) 766-6635
Folly Beach Library
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Phone: (843) 588-2001
Edgar Allan Poe/Sullivan's Island Library
Closed for renovations
Phone: (843) 883-3914
Wando Mount Pleasant Library
9 a.m. – 8 p.m.
Phone: (843) 805-6888
Village Library
9 a.m. – 6 p.m.
Phone: (843) 884-9741
St. Paul's/Hollywood Library
9 a.m. – 8 p.m.
Phone: (843) 889-3300
Otranto Road Library
9 a.m. – 8 p.m.
Phone: (843) 572-4094
Mt. Pleasant Library
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McClellanville Library
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Keith Summey North Charleston Library
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John's Island Library
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Hurd/St. Andrews Library
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Miss Jane's Building (Edisto Library Temporary Location)
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Dorchester Road Library
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John L. Dart Library
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Phone: (843) 722-7550
Baxter-Patrick James Island
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Phone: (843) 795-6679
Main Library
9 a.m. – 8 p.m.
Phone: (843) 805-6930
Bees Ferry West Ashley Library
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Phone: (843) 805-6892
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Phone: (843) 805-6909
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IL-10 Counteracts IFN-γ to Alleviate Acute Lung Injury in a Viral-Bacterial Superinfection Model.
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- Author(s): McKelvey, Michael; Uddin, Md Bashir; Palani, Sunil; Shao, Shengjun; Sun, Keer
- Source:
American Journal of Respiratory Cell & Molecular Biology; July2024, Vol. 71 Issue 1, p110-120, 11p- Subject Terms:
- Source:
- Additional Information
- Abstract: Immune activation is essential for lung control of viral and bacterial infection, but an overwhelming inflammatory response often leads to the onset of acute respiratory distress syndrome. IL-10 plays a crucial role in regulating the balance between antimicrobial immunity and immunopathology. In the present study, we investigated the role of IL-10 in acute lung injury induced by influenza A virus and methicillin-resistant Staphylococcus aureus coinfection. This unique coinfection model resembles patients with acute pneumonia undergoing appropriate antibiotic therapies. Using global IL-10 and IL-10 receptor gene-deficient mice, as well as in vivo neutralizing antibodies, we show that IL-10 deficiency promotes IFN-γ–dominant cytokine responses and triggers acute animal death. Interestingly, this extreme susceptibility is fully preventable by IFN-γ neutralization during coinfection. Further studies using mice with Il10ra deletion in selective myeloid subsets reveal that IL-10 primarily acts on mononuclear phagocytes to prevent IFN-γ/TNF-α hyperproduction and acute mortality. Importantly, this antiinflammatory IL-10 signaling is independent of its inhibitory effect on antiviral and antibacterial defense. Collectively, our results demonstrate a key mechanism of IL-10 in preventing hypercytokinemia and acute respiratory distress syndrome pathogenesis by counteracting the IFN-γ response. [ABSTRACT FROM AUTHOR]
- Abstract: Copyright of American Journal of Respiratory Cell & Molecular Biology is the property of American Thoracic Society and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)
- Abstract:
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