Abstract

Objective To investigate the effects of respiratory syncytial virus (RSV) infection on cough-related airway function and neurotransmitter in guinea pigs and to explore the pathogenesis of cough after RSV infection. Methods Sixty SPF male guinea pigs were randomly divided into control group,asthma group and four RSV-infected groups (6,12,28 and 42 d group), ten in each group. Infected animals were inoculated by intranasal instillation of RSV suspension, Plethysmography was used to assess cough reflex sensitivity (CRS) and airway responsiveness (AR). Vanilloid receptor-1 (VR1) mRNA level was detected by real-time PCR. The protein expressions of VR1 and protein gene product-9.5 (PGP-9.5)were measured by immunohistochemistry. Results CRS in 6, 12, 28 and 42 d RSV-infected group [ (8. 00 ± 3. 86), (8. 70± 6.20 ), ( 7.60 ±4.40 ) and ( 6.70 ± 3. 71 ) CCnt] was higher than that in control group [(2. 50±1.43) CCnt,all P <0.05] and reached a peak in 12 d RSV-infected group ( P <0.01). AR to two high concentrations of methylocholine in 12 d RSV-infected group [( 1 069 ± 156 )%,( 1 846±285) %] was higher than that in control group (all P <0.05). VR1 mRNA level in 6,12,28 and 42 d RSV-infected group (1.57 ± 0.43,1.61 ±0. 47 and 1.68 ± 0. 56) was higher than that in control group (1.00±0.34, P <0.05), and remained at highest level in 28 d RSV-infected group. Compared with control group, VR1 protein expression in 28 d RSV-infected group and PGP-9.5 in 12 d RSV-infected group increased (all P <0. 05). Conclusions The increased CRS with increased AR in a certain degree is the feature of cough caused by RSV. The temporal and spatial variation of VR1 and PGP-9. 5 may be related to the pathogenesis of cough caused by RSV. Key words: Respiratory syncytial virus; Cough reflex sensitivity; Airway responsiveness; Vanilloid receptor; Protein gene products-9.5

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