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Interleukin-23 Facilitates Th1 and Th2 Cell Differentiation In Vitro Following Respiratory Syncytial Virus Infection
Chest Infections SESSION TITLE: Chest Infections SESSION TYPE: Original Investigation Poster PRESENTED ON: Saturday, April 16, 2016 at 11:45 AM - 12:45 PM
Interleukin-23 Facilitates Th1 and Th2 Cell Differentiation In Vitro Following Respiratory Syncytial Virus Infection Jingjing Feng*; and Zhijun Jie PhD The Fifth People’s Hospital of Shanghai, Fudan University, Shanghai, China PURPOSE: Respiratory syncytial virus (RSV) infection induces activation and imbalance of the immune system; however, the role of T helper 17 cells (Th17) in the response to RSV infection remains unclear. Interleukin-23 (IL-23) is a key cytokine in Th17 cell differentiation. The aim of this study was to explore the function of IL-23 in determining the distribution of Th lymphocyte subsets (Th1, Th2, and Th17) after RSV infection in vitro. METHODS: Human bronchial epithelial cell line BEAS-2B was infected with mock or RSV at various multiplicities of infection (MOI) and transcript expression of IL-6, IL-23p19, and transforming growth factor (TGF-b) was detected by real-time polymerase chain reaction; IL-6, IL-23, and TGF-b in the supernatant were measured by enzyme-linked immunosorbent assay. The Th subset distribution in lymphocytes was determined by flow cytometry after co-culture with supernatants from mock and 72-hr RSV infection cultures. The role of IL-23 in lymphocytes was assessed by specific receptor blockade (IL-23R) prior to co-culture with supernatants from RSV-infected BEAS-2B cells, followed by flow cytometry to analyze Th subset differentiation. RESULTS: Cytokine expression increased after RSV infection. IL-23R blockade suppressed the differentiation of Th1, Th2, and Th17 cells in the presence of supernatants from RSV-infected BEAS-2B cells. CONCLUSIONS: RSV infection may induce cytokine secretion, thus inducing Th1, Th2, and Th17 differentiation via an IL-23Rdependent process. CLINICAL IMPLICATIONS: Our results further clarified the pathogenic mechanism of RSV, and could provide a solid, novel basis for clinical treatment
No Product/Research Disclosure Information DOI:
http://dx.doi.org/10.1016/j.chest.2016.02.086
Copyright ª 2016 American College of Chest Physicians. Published by Elsevier Inc. All rights reserved.
journal.publications.chestnet.org
81A
CHEST INFECTIONS
DISCLOSURE: Jingjing feng: University grant monies: National Natural Science Foundation of China; Grant number: 81370131, University grant monies: Shanghai Committee of Science and Technology; Grant number: 134119b1200 Zhijun Jie: University grant monies: National Natural Science Foundation of China; Grant number: 81370131, University grant monies: Shanghai Committee of Science and Technology; Grant number: 134119b1200
Interleukin-23 Facilitates Th1 and Th2 Cell Differentiation In Vitro Following Respiratory Syncytial Virus Infection Jingjing Feng*; and Zhijun Jie PhD The Fifth People’s Hospital of Shanghai, Fudan University, Shanghai, China PURPOSE: Respiratory syncytial virus (RSV) infection induces activation and imbalance of the immune system; however, the role of T helper 17 cells (Th17) in the response to RSV infection remains unclear. Interleukin-23 (IL-23) is a key cytokine in Th17 cell differentiation. The aim of this study was to explore the function of IL-23 in determining the distribution of Th lymphocyte subsets (Th1, Th2, and Th17) after RSV infection in vitro. METHODS: Human bronchial epithelial cell line BEAS-2B was infected with mock or RSV at various multiplicities of infection (MOI) and transcript expression of IL-6, IL-23p19, and transforming growth factor (TGF-b) was detected by real-time polymerase chain reaction; IL-6, IL-23, and TGF-b in the supernatant were measured by enzyme-linked immunosorbent assay. The Th subset distribution in lymphocytes was determined by flow cytometry after co-culture with supernatants from mock and 72-hr RSV infection cultures. The role of IL-23 in lymphocytes was assessed by specific receptor blockade (IL-23R) prior to co-culture with supernatants from RSV-infected BEAS-2B cells, followed by flow cytometry to analyze Th subset differentiation. RESULTS: Cytokine expression increased after RSV infection. IL-23R blockade suppressed the differentiation of Th1, Th2, and Th17 cells in the presence of supernatants from RSV-infected BEAS-2B cells. CONCLUSIONS: RSV infection may induce cytokine secretion, thus inducing Th1, Th2, and Th17 differentiation via an IL-23Rdependent process. CLINICAL IMPLICATIONS: Our results further clarified the pathogenic mechanism of RSV, and could provide a solid, novel basis for clinical treatment
No Product/Research Disclosure Information DOI:
http://dx.doi.org/10.1016/j.chest.2016.02.086
Copyright ª 2016 American College of Chest Physicians. Published by Elsevier Inc. All rights reserved.
journal.publications.chestnet.org
81A
CHEST INFECTIONS
DISCLOSURE: Jingjing feng: University grant monies: National Natural Science Foundation of China; Grant number: 81370131, University grant monies: Shanghai Committee of Science and Technology; Grant number: 134119b1200 Zhijun Jie: University grant monies: National Natural Science Foundation of China; Grant number: 81370131, University grant monies: Shanghai Committee of Science and Technology; Grant number: 134119b1200