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    TLR5 participates in the TLR4 receptor complex and promotes MyD88- dependent signaling in environmental lung injury

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    Author
    Hussain, Salik; Johnson, Collin G; Sciurba, Joseph; Meng, Xianglin; Stober, Vandy P; Liu, Caini; Cyphert-Daly, Jaime M; Bulek, Katarzyna; Qian, Wen; Solis, Alma; Sakamachi, Yosuke; Trempus, Carol S; Aloor, Jim J; Gowdy, Kym M; Foster, W Michael; Hollingsworth, John W; Tighe, Robert M; Li, Xiaoxia; Fessler, Michael B; Garantziotis, Stavros
    Abstract
    Lung disease causes significant morbidity and mortality, and is exacerbated by environmental injury, for example through lipopolysaccharide (LPS) or ozone (O3). Toll-like receptors (TLRs) orchestrate immune responses to injury by recognizing pathogen- or danger-associated molecular patterns. TLR4, the prototypic receptor for LPS, also mediates inflammation after O3, triggered by endogenous hyaluronan. Regulation of TLR4 signaling is incompletely understood. TLR5, the flagellin receptor, is expressed in alveolar macrophages, and regulates immune responses to environmental injury. Using in vivo animal models of TLR4-mediated inflammations (LPS, O3, hyaluronan), we show that TLR5 impacts the in vivo response to LPS, hyaluronan and O3. We demonstrate that immune cells of human carriers of a dominant negative TLR5 allele have decreased inflammatory response to O3 exposure ex vivo and LPS exposure in vitro. Using primary murine macrophages, we find that TLR5 physically associates with TLR4 and biases TLR4 signaling towards the MyD88 pathway. Our results suggest an updated paradigm for TLR4/TLR5 signaling.
    URI
    http://hdl.handle.net/10342/7837
    Date
    2020-01-28
    Citation:
    APA:
    Hussain, Salik, & Johnson, Collin G, & Sciurba, Joseph, & Meng, Xianglin, & Stober, Vandy P, & Liu, Caini, & Cyphert-Daly, Jaime M, & Bulek, Katarzyna, & Qian, Wen, & Solis, Alma, & Sakamachi, Yosuke, & Trempus, Carol S, & Aloor, Jim J, & Gowdy, Kym M, & Foster, W Michael, & Hollingsworth, John W, & Tighe, Robert M, & Li, Xiaoxia, & Fessler, Michael B, & Garantziotis, Stavros. (January 2020). TLR5 participates in the TLR4 receptor complex and promotes MyD88- dependent signaling in environmental lung injury. eLife, (. Retrieved from http://hdl.handle.net/10342/7837

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    MLA:
    Hussain, Salik, and Johnson, Collin G, and Sciurba, Joseph, and Meng, Xianglin, and Stober, Vandy P, and Liu, Caini, and Cyphert-Daly, Jaime M, and Bulek, Katarzyna, and Qian, Wen, and Solis, Alma, and Sakamachi, Yosuke, and Trempus, Carol S, and Aloor, Jim J, and Gowdy, Kym M, and Foster, W Michael, and Hollingsworth, John W, and Tighe, Robert M, and Li, Xiaoxia, and Fessler, Michael B, and Garantziotis, Stavros. "TLR5 participates in the TLR4 receptor complex and promotes MyD88- dependent signaling in environmental lung injury". eLife. . (.), January 2020. February 27, 2021. http://hdl.handle.net/10342/7837.
    Chicago:
    Hussain, Salik and Johnson, Collin G and Sciurba, Joseph and Meng, Xianglin and Stober, Vandy P and Liu, Caini and Cyphert-Daly, Jaime M and Bulek, Katarzyna and Qian, Wen and Solis, Alma and Sakamachi, Yosuke and Trempus, Carol S and Aloor, Jim J and Gowdy, Kym M and Foster, W Michael and Hollingsworth, John W and Tighe, Robert M and Li, Xiaoxia and Fessler, Michael B and Garantziotis, Stavros, "TLR5 participates in the TLR4 receptor complex and promotes MyD88- dependent signaling in environmental lung injury," eLife 9, no. (January 2020), http://hdl.handle.net/10342/7837 (accessed February 27, 2021).
    AMA:
    Hussain, Salik, Johnson, Collin G, Sciurba, Joseph, Meng, Xianglin, Stober, Vandy P, Liu, Caini, Cyphert-Daly, Jaime M, Bulek, Katarzyna, Qian, Wen, Solis, Alma, Sakamachi, Yosuke, Trempus, Carol S, Aloor, Jim J, Gowdy, Kym M, Foster, W Michael, Hollingsworth, John W, Tighe, Robert M, Li, Xiaoxia, Fessler, Michael B, Garantziotis, Stavros. TLR5 participates in the TLR4 receptor complex and promotes MyD88- dependent signaling in environmental lung injury. eLife. January 2020; 9() . http://hdl.handle.net/10342/7837. Accessed February 27, 2021.
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