title: Neural-endocrine  mechanisms of respiratory syncytial virus-associated asthma in a rat model.
abstract: We  examined the underlying neural-endocrine mechanisms of asthma associated with  respiratory syncytial virus infection. Thirty Sprague-Dawley rats were randomly  divided into control group, respiratory syncytial virus (RSV) group, and  anti-nerve growth factor (NGF) IgG group. An RSV infection model was  established by nasal drip once a week. In the anti-NGF antibody intervention  group, each rat was given an intraperitoneal injection of anti-NGF IgG 3 h  before RSV infection. Optical microscopy and transmission electron microscopy  were used to observe the structural changes in adrenal medulla cells. Changes  in adrenaline and norepinephrine in serum were detected by ELISA. NGF  expression was assayed by immunohistochemistry. Expression differences in  synaptophysin mRNA were detected by RT-PCR. Transmission electron microscopy  displayed widened adrenal medulla intercellular spaces, reduced chromaffin  particle concentration, and increased mitochondria in the RSV infection group.  At the same time, NGF expression was increased in the RSV infection group  significantly. In addition, the adrenaline concentration was significantly decreased  compared with the control and anti-NGF antibody groups. Synaptophysin mRNA  expression was significantly increased in the RSV infection and anti-NGF  antibody groups. However, compared with the RSV infection group, synaptophysin  mRNA expression was significantly decreased in the anti-NGF antibody group. We  conclude that RSV infection could induce adrenal medulla cell differentiation  to nerve cells by over-expression of NGF, resulting in the decreased endocrine  function found in asthma progression.
authors.affiliation: Second Department of Respiratory Disease, Jiangxi Provincial People's Hospital, Nanchang, P.R. China.
authors.forename: Q G
authors.initials: QG
authors.lastname: Li
authors.forename: X R
authors.initials: XR
authors.lastname: Wu
authors.forename: X Z
authors.initials: XZ
authors.lastname: Li
authors.forename: J
authors.initials: J
authors.lastname: Yu
authors.forename: Y
authors.initials: Y
authors.lastname: Xia
authors.forename: A P
authors.initials: AP
authors.lastname: Wang
authors.forename: J
authors.initials: J
authors.lastname: Wang
mesh_terms: D000313:Adrenal Medulla / Q000473:pathology / Q000648:ultrastructure; D000818:Animals; D001249:Asthma / Q000150:complications* / Q000503:physiopathology / Q000821:virology*; D016535:Bronchial Hyperreactivity / Q000150:complications / Q000503:physiopathology / Q000821:virology; D004195:Disease Models, Animal; D004703:Endocrine System / Q000378:metabolism*; D004837:Epinephrine / Q000378:metabolism; D005786:Gene Expression Regulation; D006367:HeLa Cells; D006801:Humans; D007150:Immunohistochemistry; D017403:In Situ Hybridization; D008168:Lung / Q000378:metabolism / Q000473:pathology / Q000821:virology; D020932:Nerve Growth Factor / Q000378:metabolism; D009420:Nervous System / Q000378:metabolism*; D009638:Norepinephrine / Q000378:metabolism; D012333:RNA, Messenger / Q000235:genetics / Q000378:metabolism; D051381:Rats; D017207:Rats, Sprague-Dawley; D018357:Respiratory Syncytial Virus Infections / Q000150:complications* / Q000503:physiopathology / Q000821:virology*; D012136:Respiratory Syncytial Viruses / Q000502:physiology*; D020133:Reverse Transcriptase Polymerase Chain Reaction; D016708:Synaptophysin / Q000235:genetics / Q000378:metabolism
chemical_list: D012333:RNA, Messenger; D016708:Synaptophysin; D020932:Nerve Growth Factor; D009638:Norepinephrine; D004837:Epinephrine