International journal of clinical and experimental medicine · 2015
Up-regulation of Dectin-1 in airway epithelial cells promotes mice defense against invasive pulmonary aspergillosis.
СтатьяНазвание и аннотация: Перевод в очереди
Обработка статьи · этапы, ошибки и управление
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Liu Zhi-Cheng, Wang Min, Sun Wen-Kui, Xia Di, Tan Ming-Ming, Ding Yuan, Qian Qian, Su Xin, Shi Yi
Аннотация
INTRODUCTION: With the growing number of immunocompromised patients, the incidence of invasive pulmonary aspergillosis increases. Innate immunity plays a significant role in defensing against fungal infection. Airway epithelial cells induce immune responses like the production of cytokine and chemokine via Dectin-1 signaling pathway in response to Aspergillus fumigatus. Thus, we hypothesized that up-regulation of Dectin-1 on airway epithelium cells would promote the defense against A. fumigatus.
METHODS: We designed an adenoviral vector encoding full-length Dectin-1, and then transfected it into mice airway epithelial cells via intratracheal injection before the invasion of A. fumigatus. Transfect mice model was verified by using real-time PCR and immunohistochemistry. And also, we studied the effects of up-regulation of Dectin-1 on the production of proinflammatory cytokines, histological changes, fungal burden and survival rate during A. fumigatus infection.
RESULTS: The expression level of Dectin-1 in lungs of mice with Dectin-1 recombinant adenoviral vector significantly increased. And also, the mice had higher production of TNF-α, GM-CSF and IL-1β, lower fungal burden, more recruitment of neutrophils into lungs and higher survival rate in response to A. fumigatus infection.
CONCLUSIONS: The administration of Dectin-1 recombinant adenoviral vector through trachea can elevate the expression of Dectin-1 on airway epithelium, and also, its function during the course of A. fumigatus infection was demonstrated.
METHODS: We designed an adenoviral vector encoding full-length Dectin-1, and then transfected it into mice airway epithelial cells via intratracheal injection before the invasion of A. fumigatus. Transfect mice model was verified by using real-time PCR and immunohistochemistry. And also, we studied the effects of up-regulation of Dectin-1 on the production of proinflammatory cytokines, histological changes, fungal burden and survival rate during A. fumigatus infection.
RESULTS: The expression level of Dectin-1 in lungs of mice with Dectin-1 recombinant adenoviral vector significantly increased. And also, the mice had higher production of TNF-α, GM-CSF and IL-1β, lower fungal burden, more recruitment of neutrophils into lungs and higher survival rate in response to A. fumigatus infection.
CONCLUSIONS: The administration of Dectin-1 recombinant adenoviral vector through trachea can elevate the expression of Dectin-1 on airway epithelium, and also, its function during the course of A. fumigatus infection was demonstrated.