[Transcription factors in spinal dorsal root ganglion in rats recurrently infected with respiratory syncytial virus].
OBJECTIVE
To elucidate intracellular transcription factor activation of C(7) approximately T(5) dorsal root ganglia in rats recurrently infected with respiratory syncytial virus (RSV).


METHODS
Eighty 1 approximately 2 weeks old Sprague-Dawley rats were randomly divided into 2 groups: a control group and a RSV-infection group. The rats in the RSV-infection group were infected with 5 x 10(5) U/mL RSV once a week and the rats in the control group were treated with culture medium without RSV. Airway response was measured after 8 weeks. Lung tissue was submitted for HE staining and in situ hybridization. The C(7) approximately T(5) dorsal root ganglia were obtained for the preliminary screening of the intracellular transcription factors by TranSignal protein/DNA combo array. Nuclear protein of C(7) approximately T(5) dorsal root ganglia were extracted and submitted to Western blot.


RESULTS
Airway response in the RSV-infection group was higher than that in the control group (P<0.05). HE staining showed inflammatory cell infiltration, and in situ hybridization demonstrated positive RSV RNA in the RSV-infection rat lung which was not present in the control group, thus validating the efficacy of our model. TranSignal protein/DNA combo array screening showed that 55 transcription factors increased by at least 2 folds in the C(7) approximately T(5) DRG cells of the RSV-infection group. The transcription factors Smad and interferon regulatory factor (1 or 2) were the 2 most upregulated transcription factors identified by combo array screening (59 and 43 fold increase compared with the control, respectively). Western blot confirmed Smad(1/2/3) and IRF-1 upregulate while IRF-2 remained unchanged.


CONCLUSIONS
Respiratory syncytial virus infection results in airway hyperresponsiveness and transcription factor activation in C(7) approximately T(5) spinal adorsal root ganglia in rats, which may contribute to airway nerve network dysfunction and airway hyperresponsiveness.
Tan
Hongyi
H
Department of Respiratory Diseases, Xiangya Hospital, Central South University, Changsha 410008, China.
Pan
Pinhua
P
Zhao
Ranran
R
Qin
Qingwu
Q
Wang
Hui
H
Hu
Chengping
C
D000818:Animals; D000831:Animals, Newborn; D005727:Ganglia, Spinal / Q000378:metabolism*; D009687:Nuclear Proteins / Q000378:metabolism; D011897:Random Allocation; D051381:Rats; D017207:Rats, Sprague-Dawley; D012008:Recurrence; D012130:Respiratory Hypersensitivity / Q000209:etiology* / Q000378:metabolism; D018357:Respiratory Syncytial Virus Infections / Q000150:complications* / Q000378:metabolism*; D013116:Spinal Cord / Q000378:metabolism; D014157:Transcription Factors / Q000378:metabolism*
D009687:Nuclear Proteins; D014157:Transcription Factors