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. 2016 Dec 6;6:38532. doi: 10.1038/srep38532

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Copyright © 2016, The Author(s)

This work is licensed under a Creative Commons Attribution 4.0 International License. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in the credit line; if the material is not included under the Creative Commons license, users will need to obtain permission from the license holder to reproduce the material. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/

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Both the in vitro and clinical studies indicated IP-10 is associated with mixed viral/bacterial infection in pediatric community-acquired pneumonia. In vitro, miR-200a-3p was synergistically induced following mixed IAV/SP infection of human MDMs and found to indirectly regulate CXCL10 (IP-10) expression by targeting the suppressor of cytokine signaling-6 gene (SOCS6), a well-known repressor of the JAK-STAT signaling pathway. In vivo, IP-10 was significantly elevated in the serum samples of pediatric patients with mixed viral/bacterial severe pneumonia compared to patients with single detection (P = 0.03) and non-severe pneumonia (P < 0.01).