Effects of Respiratory Syncytial Virus Infection on Dynamic Changes of Airway Hyperresponsiveness in Ovalbumin-Induced Asthma in Mice
Zhu Y
Abstract
Zhu Y
Abstract
Objective To investigate the effects of respiratory syncytial virus(RSV) infection on the dynamic changes of airway hyperresponsiveness(AHR) in ovalbumin(OVA)-induced asthma in mice.Methods 60 BALB/c female mice were randomly divided into PBS control group(A group,n=6),OVA group,OVA/RSV group,dexamethasone group(D group,n=6).Kinetics of AHR of OVA group mice was carried out on day 21,25,29 and 33(B1,B2,B3,B4 groups,n=6),and the same with the OVA/RSV group(C1,C2,C3,C4 groups,n=6).The mouse asthma model was established by OVA-sensitization of intraperitoneal injection and repeated inhalation of OVA while the mice in OVA/RSV group were treated with combined intranasal inoculation with RSV(1.0×106 pfu/mL in 50 μL).Airway resistance of expiring phase(RL) and compliance of throax and lung(CTL) with different doses of acetylcholine(Ach) were measured.Lung tissue sections were stained with hematoxylin and eosin(HE) and periodic acid-Schiff(PAS) for general morphology.Results Compared with B1 group,RL increased and CTL decreased in C1 group when Ach dose is above 5 g/L(P0.05,respectively),and the effects prolonged(6 d,10 d after challenge with OVA,respectively) much more than B1 group(2 d after challenge with OVA).Compared with C1 group,RL decreased and CTL increased in D group and the infiltration of inflammatory cells was obviously alleviated in C1 group after treatment with dexamethasone.Conclusions Airway hyperresponsiveness increases obviously in OVA-sensitized and RSV-infected mice.The prolonged increase in RL and decrease in CTL(6 d,10 d,respectively)may imply that RSV infection aggravates airway inflammation.The small airway inflammation may play a critical role in the persistence of airway hyperresponsiveness.
A significance statement is not available in the OpenAlex record.
A contribution statement is not available in the OpenAlex record.
Method details are not available in the OpenAlex metadata.
Findings are not separately available in the OpenAlex metadata.
Limitations are not available in the OpenAlex metadata.
Application details are not available in the OpenAlex metadata.
Objective To investigate the effects of respiratory syncytial virus(RSV) infection on the dynamic changes of airway hyperresponsiveness(AHR) in ovalbumin(OVA)-induced asthma in mice.Methods 60 BALB/c female mice were randomly divided into PBS control group(A group,n=6),OVA group,OVA/RSV group,dexamethasone group(D group,n=6).Kinetics of AHR of OVA group mice was carried out on day 21,25,29 and 33(B1,B2,B3,B4 groups,n=6),and the same with the OVA/RSV group(C1,C2,C3,C4 groups,n=6).The mouse asthma model was established by OVA-sensitization of intraperitoneal injection and repeated inhalation of OVA while the mice in OVA/RSV group were treated with combined intranasal inoculation with RSV(1.0×106 pfu/mL in 50 μL).Airway resistance of expiring phase(RL) and compliance of throax and lung(CTL) with different doses of acetylcholine(Ach) were measured.Lung tissue sections were stained with hematoxylin and eosin(HE) and periodic acid-Schiff(PAS) for general morphology.Results Compared with B1 group,RL increased and CTL decreased in C1 group when Ach dose is above 5 g/L(P0.05,respectively),and the effects prolonged(6 d,10 d after challenge with OVA,respectively) much more than B1 group(2 d after challenge with OVA).Compared with C1 group,RL decreased and CTL increased in D group and the infiltration of inflammatory cells was obviously alleviated in C1 group after treatment with dexamethasone.Conclusions Airway hyperresponsiveness increases obviously in OVA-sensitized and RSV-infected mice.The prolonged increase in RL and decrease in CTL(6 d,10 d,respectively)may imply that RSV infection aggravates airway inflammation.The small airway inflammation may play a critical role in the persistence of airway hyperresponsiveness.
Key concepts: Ovalbumin, Medicine, Dexamethasone, Intraperitoneal injection, Sensitization, Immunology, Airway resistance, CTL*