title: Respiratory syncytial virus infection differentiates airway dysfunction in the central and peripheral airways in OVA-sensitized mice.
abstract: Much evidence suggests that respiratory syncytial virus (RSV) infection prolongs airway hyperresponsiveness (AHR) and exacerbates asthma by enhancing airway inflammation. However, the characteristic of airway inflammation and kinetics of airway dysfunction occurred in the central and peripheral airways were not fully delineated. The objective of this study was to investigate the effect of RSV on the allergic airway inflammation in different size airways and to elucidate its possible mechanism. Using a murine model of prior ovalbumin (OVA) sensitization and subsequent RSV challenge, lung resistance (R(L)), and dynamic compliance (Cdyn) was conducted by barometric whole-body plethysmography. Histological examinations were carried out. Differential cells count in bronchoalveolar lavage (BAL) fluid, serum anti-OVA IgE, and IgG1 were measured. Cytokine mRNA expression in lung tissue were determined. RSV triggered a significant increase in R(L) and reduction in Cdyn, as well as greatly prolonged the recovery of Cdyn more than that of R(L) in OVA-sensitized mice. Also, RSV resulted in more severe peripheral airway inflammation which exhibit as globe cell hyperplasia and CD8+ T cell infiltration. Furthermore, the number of lymphocytes, neutrophils and macrophages in BAL fluid, serum anti-OVA IgE and IgG1 were remarkably increased. Additionally, mice increased relative expression of cytokines IL-4, IL-13, and IFN-γ, but not IL-5, IL-17, and IL-17F. These findings demonstrated that RSV could selectively affect pathologic processes that contribute to altered airway function in the central and peripheral airways in OVA-sensitized mice. These processes may be involved in goblet cell hyperplasia and CD8+ T cell infiltration in peripheral airways.
authors.affiliation: Department of Respiratory Disease, the First Affiliated Hospital of Nanjing Medical University, Nanjing, P.R. China. xiongbinjiang@126.com
authors.forename: Xiong-Bin
authors.initials: XB
authors.lastname: Jiang
authors.forename: Mao
authors.initials: M
authors.lastname: Huang
authors.forename: Xue-Fan
authors.initials: XF
authors.lastname: Cui
authors.forename: Yi
authors.initials: Y
authors.lastname: Zhu
authors.forename: Kai-Sheng
authors.initials: KS
authors.lastname: Yin
authors.forename: Kun
authors.initials: K
authors.lastname: Yao
mesh_terms: D000109:Acetylcholine; D000818:Animals; D001249:Asthma / Q000150:complications* / Q000503:physiopathology*; D001980:Bronchi / Q000503:physiopathology*; D045744:Cell Line, Tumor; D005260:Female; D006801:Humans; D007073:Immunoglobulin E / Q000097:blood; D007074:Immunoglobulin G / Q000097:blood; D007371:Interferon-gamma / Q000378:metabolism; D007378:Interleukins / Q000378:metabolism; D008168:Lung / Q000378:metabolism; D008170:Lung Compliance; D051379:Mice; D008807:Mice, Inbred BALB C; D010047:Ovalbumin / Q000276:immunology; D010503:Periodic Acid-Schiff Reaction; D012333:RNA, Messenger / Q000378:metabolism; D018357:Respiratory Syncytial Virus Infections / Q000150:complications* / Q000503:physiopathology*
chemical_list: D007074:Immunoglobulin G; D007378:Interleukins; D012333:RNA, Messenger; D007073:Immunoglobulin E; D007371:Interferon-gamma; D010047:Ovalbumin; D000109:Acetylcholine