国际呼吸杂志
國際呼吸雜誌
국제호흡잡지
INTERNATIONAL JOURNAL OF RESPIRATION
2011年
8期
571-575
,共5页
叶新民%钟南山%刘春丽%陈如冲%赵谨
葉新民%鐘南山%劉春麗%陳如遲%趙謹
협신민%종남산%류춘려%진여충%조근
呼吸道合胞病毒%咳嗽反射敏感性%气道反应性%辣椒素受体%蛋白基因产物9.5
呼吸道閤胞病毒%咳嗽反射敏感性%氣道反應性%辣椒素受體%蛋白基因產物9.5
호흡도합포병독%해수반사민감성%기도반응성%랄초소수체%단백기인산물9.5
Respiratory syncytial virus%Cough reflex sensitivity%Airway responsiveness%Vanilloid receptor%Protein gene products-9.5
目的 观察呼吸道合胞病毒RSV(感染)对豚鼠咳嗽相关的气道功能及神经递质的影响,探讨病毒感染后咳嗽的发病机制.方法 雄性SPF级豚鼠60只,按数字随机法随机分成正常对照组、病毒感染组和哮喘组,病毒感染组按病毒感染后天数分为6、12、28和42 d四个组,每组10只.通过滴鼻方法接种RSV.Buxco肺功能仪测定咳嗽反射敏感性(CRS)及气道反应性(AR).荧光定量PCR(Real-time PCR)方法检测辣椒素受体亚型1(VR1)的mRNA表达,免疫组织化学方法检测肺组织VR1及蛋白基因产物9.5(PGP-9.5)的蛋白表达.结果 病毒感染6、12、28、42 d组豚鼠CRS[(8.00±3.86)、(8.70±6.20)、(7.60±4.40)和(6.70±3.71)CCnt]均较正常对照组[(2.50±1.43)CCnt]升高(P值均＜0.05),并在12 d组达到最高峰(P＜0.01).感染后12 d组豚鼠AR对2个高浓度乙酰甲胆碱刺激结果为(1 069±156)%和(1 846±285)%,均高于正常对照组(P值分别＜0.05和0.01).感染后6、12和28 d组VR1的mRNA水平分别为1.57±0.43、1.61±0.47和1.68±0.56,均较正常对照组(1.00±0.34)升高(P值均＜0.05),而以28 d组为最高.与正常对照组相比,感染后28 d组VR1蛋白表达增强(P＜0.05);而感染后12 d组PGP-9.5表达增强(P＜0.05).结论 CRS增高伴随一定程度的AR增高是RSV引起咳嗽的特点,感染引起VR1和PGP-9.5的时空变化可能与病毒感染性咳嗽的发病机制有关.
目的 觀察呼吸道閤胞病毒RSV(感染)對豚鼠咳嗽相關的氣道功能及神經遞質的影響,探討病毒感染後咳嗽的髮病機製.方法 雄性SPF級豚鼠60隻,按數字隨機法隨機分成正常對照組、病毒感染組和哮喘組,病毒感染組按病毒感染後天數分為6、12、28和42 d四箇組,每組10隻.通過滴鼻方法接種RSV.Buxco肺功能儀測定咳嗽反射敏感性(CRS)及氣道反應性(AR).熒光定量PCR(Real-time PCR)方法檢測辣椒素受體亞型1(VR1)的mRNA錶達,免疫組織化學方法檢測肺組織VR1及蛋白基因產物9.5(PGP-9.5)的蛋白錶達.結果 病毒感染6、12、28、42 d組豚鼠CRS[(8.00±3.86)、(8.70±6.20)、(7.60±4.40)和(6.70±3.71)CCnt]均較正常對照組[(2.50±1.43)CCnt]升高(P值均＜0.05),併在12 d組達到最高峰(P＜0.01).感染後12 d組豚鼠AR對2箇高濃度乙酰甲膽堿刺激結果為(1 069±156)%和(1 846±285)%,均高于正常對照組(P值分彆＜0.05和0.01).感染後6、12和28 d組VR1的mRNA水平分彆為1.57±0.43、1.61±0.47和1.68±0.56,均較正常對照組(1.00±0.34)升高(P值均＜0.05),而以28 d組為最高.與正常對照組相比,感染後28 d組VR1蛋白錶達增彊(P＜0.05);而感染後12 d組PGP-9.5錶達增彊(P＜0.05).結論 CRS增高伴隨一定程度的AR增高是RSV引起咳嗽的特點,感染引起VR1和PGP-9.5的時空變化可能與病毒感染性咳嗽的髮病機製有關.
목적 관찰호흡도합포병독RSV(감염)대돈서해수상관적기도공능급신경체질적영향,탐토병독감염후해수적발병궤제.방법 웅성SPF급돈서60지,안수자수궤법수궤분성정상대조조、병독감염조화효천조,병독감염조안병독감염후천수분위6、12、28화42 d사개조,매조10지.통과적비방법접충RSV.Buxco폐공능의측정해수반사민감성(CRS)급기도반응성(AR).형광정량PCR(Real-time PCR)방법검측랄초소수체아형1(VR1)적mRNA표체,면역조직화학방법검측폐조직VR1급단백기인산물9.5(PGP-9.5)적단백표체.결과 병독감염6、12、28、42 d조돈서CRS[(8.00±3.86)、(8.70±6.20)、(7.60±4.40)화(6.70±3.71)CCnt]균교정상대조조[(2.50±1.43)CCnt]승고(P치균＜0.05),병재12 d조체도최고봉(P＜0.01).감염후12 d조돈서AR대2개고농도을선갑담감자격결과위(1 069±156)%화(1 846±285)%,균고우정상대조조(P치분별＜0.05화0.01).감염후6、12화28 d조VR1적mRNA수평분별위1.57±0.43、1.61±0.47화1.68±0.56,균교정상대조조(1.00±0.34)승고(P치균＜0.05),이이28 d조위최고.여정상대조조상비,감염후28 d조VR1단백표체증강(P＜0.05);이감염후12 d조PGP-9.5표체증강(P＜0.05).결론 CRS증고반수일정정도적AR증고시RSV인기해수적특점,감염인기VR1화PGP-9.5적시공변화가능여병독감염성해수적발병궤제유관.
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.
