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Respiratory syncytial virus upregulates IL-33 expression in mouse model of virus-induced inflammation exacerbation in OVA-sensitized mice and in asthmatic subjects
被引:10
作者:
Nikonova, Alexandra
[1
,2
]
Shilovskiy, Igor
[1
]
Galitskaya, Mariola
[1
]
Sokolova, Alina
[1
]
Sundukova, Maria
[1
]
Dmitrieva-Posocco, Oksana
[1
]
Mitin, Aleksandr
[1
]
Komogorova, Viktoria
[1
]
Litvina, Marina
[1
]
Sharova, Nina
[1
]
Zhernov, Yury
[1
]
Kudlay, Dmitry
[1
]
Dvornikov, Anton
[3
]
Kurbacheva, Oksana
[1
]
Khaitov, Rakhim
[1
]
Khaitov, Musa
[1
]
机构:
[1] NRC Inst Immunol FMBA, Kashirskoe Shosse 24, Moscow 115478, Russia
[2] Mechnikov Res Inst Vaccines & Sera, M Kazenny Per 5A, Moscow 105064, Russia
[3] Pirogov Russian Natl Res Med Univ, Ostrovitianov Str 1, Moscow 117513, Russia
来源:
基金:
俄罗斯科学基金会;
关键词:
RSV;
IL-33;
siRNA;
Allergic asthma;
Respiratory viruses;
INNATE LYMPHOID-CELLS;
IFN-GAMMA PRODUCTION;
AIRWAY INFLAMMATION;
HUMAN BASOPHILS;
RECEPTOR ST2;
MURINE MODEL;
INTERLEUKIN-33;
HYPERREACTIVITY;
PREDISPOSES;
HEPATITIS;
D O I:
10.1016/j.cyto.2020.155349
中图分类号:
Q5 [生物化学];
Q7 [分子生物学];
学科分类号:
071010 ;
081704 ;
摘要:
Background: Bronchial asthma (BA) is a chronic disease of the airways. The great majority of BA exacerbations are associated with respiratory viral infections. Recent findings point out a possible role of proinflammatory cytokine interleukin-33 (IL-33) in the development of atopic diseases. Although, little is known about the role of IL-33 in virus-induced BA exacerbations. Methods: We used mouse models of RSV (respiratory syncytial virus)-induced inflammation exacerbation in OVA-sensitized mice and RSV infection alone in adult animals to characterize expression of il33 in the mouse lungs. Moreover, we studied the influence of il33 knockdown with intranasally administrated siRNA on the development of RSV-induced inflammation exacerbation. In addition, we evaluated the expression of IL33 in the ex vivo stimulated PBMCs from allergic asthma patients and healthy subjects with and without confirmed acute respiratory viral infection. Results: Using mouse models, we found that infection with RSV drives enhanced il33 mRNA expression in the mouse lung. Treatment with anti-il33 siRNA diminishes airway inflammation in the lungs (we found a decrease in the number of inflammatory cells in the lungs and in the severity of histopathological alterations) of mice with RSV-induced inflammation exacerbation, but do not influence viral load. Elevated level of the IL33 mRNA was detected in ex vivo stimulated blood lymphocytes of allergic asthmatics infected with respiratory viruses. RSV and rhinovirus were the most detected viruses in volunteers with symptoms of respiratory infection. Conclusion: The present study provides additional evidence of the crucial role of the IL-33 in pathogenesis of RSV infection and virus-induced allergic bronchial asthma exacerbations.
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页数:10
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