title: Resveratrol-mediated gamma interferon reduction prevents airway inflammation and airway hyperresponsiveness in respiratory syncytial virus-infected immunocompromised mice.
abstract: Respiratory syncytial virus (RSV) is the most important cause of severe, lower respiratory tract infections in infants, and RSV infections have been associated with chronic wheezing and asthma during childhood. However, the mechanism of RSV-induced airway inflammation and airway hyperresponsiveness (AHR) is poorly understood. Furthermore, there are presently neither effective vaccines nor drugs available for the prevention or treatment of RSV infections. In this study, we investigated the effect of the plant extract resveratrol as a means of preventing airway inflammation and attenuating RSV-induced AHR. Our data showed that resveratrol reduced RSV lung titers and the number of infiltrating lymphocytes present in bronchoalveolar lavage fluid (BALF) and reduced inflammation. Furthermore, resveratrol attenuated airway responses to methacholine following RSV infection and significantly decreased gamma interferon (IFN-γ) levels in BALF of RSV-infected mice. Data presented in this report demonstrated that resveratrol controlled Toll-like receptor 3 (TLR3) expression, inhibited the TRIF signaling pathway, and induced M2 receptor expression following RSV infection. These data support a role for the use of resveratrol as a means of reducing IFN-γ levels associated with RSV-mediated airway inflammation and AHR, which may be mediated via TLR3 signaling.
authors.affiliation: Department of Respiratory Medicine, Children's Hospital of Chongqing Medical University, No. 136 Zhongshan 2nd Road, Yuzhong District, Chongqing 400014, China.  emliu186@hotmail.com.
authors.forename: Na
authors.initials: N
authors.lastname: Zang
authors.forename: Xiaohong
authors.initials: X
authors.lastname: Xie
authors.forename: Yu
authors.initials: Y
authors.lastname: Deng
authors.forename: Shengde
authors.initials: S
authors.lastname: Wu
authors.forename: Lijia
authors.initials: L
authors.lastname: Wang
authors.forename: Caijing
authors.initials: C
authors.lastname: Peng
authors.forename: Simin
authors.initials: S
authors.lastname: Li
authors.forename: Ke
authors.initials: K
authors.lastname: Ni
authors.forename: Yan
authors.initials: Y
authors.lastname: Luo
authors.forename: Enmei
authors.initials: E
authors.lastname: Liu
mesh_terms: D000818:Animals; D000894:Anti-Inflammatory Agents, Non-Steroidal / Q000008:administration & dosage*; D001992:Bronchoalveolar Lavage Fluid / Q000737:chemistry / Q000166:cytology; D005260:Female; D020869:Gene Expression Profiling; D007249:Inflammation / Q000473:pathology* / Q000517:prevention & control*; D007371:Interferon-gamma / Q000032:analysis / Q000037:antagonists & inhibitors*; D008168:Lung / Q000821:virology; D051379:Mice; D008807:Mice, Inbred BALB C; D018357:Respiratory Syncytial Virus Infections / Q000188:drug therapy* / Q000276:immunology / Q000473:pathology; D012136:Respiratory Syncytial Viruses / Q000276:immunology / Q000472:pathogenicity*; D000077185:Resveratrol; D015398:Signal Transduction / Q000187:drug effects; D013267:Stilbenes / Q000008:administration & dosage*; D051196:Toll-Like Receptor 3 / Q000096:biosynthesis; D019562:Viral Load
chemical_list: D000894:Anti-Inflammatory Agents, Non-Steroidal; D013267:Stilbenes; C519703:TLR3 protein, mouse; D051196:Toll-Like Receptor 3; D007371:Interferon-gamma; D000077185:Resveratrol