Inhibition of miR-497-3p Downregulates the Expression of Procalcitonin and Ameliorates Bacterial Pneumonia in Mice
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ORIGINAL ARTICLE
Inhibition of miR-497-3p Downregulates the Expression of Procalcitonin and Ameliorates Bacterial Pneumonia in Mice Wenlong Wang ,1,5 Yitang Zhu,1 Linlin Yin,1 Yaoyao Deng,2 Guoxian Chu,3 and Supin Liu4
Pneumonia is usually caused by a wide variety of pathogen infection. The underlying mechanism contributing to pneumonia remains elusive. Here, the role of microRNA-4973p (miR-497-3p) was explored in bacterial pneumonia. The expression levels of miR-497-3p and procalcitonin (PCT) in patient serum were detected by real-time polymerase chain reaction (RTPCR) and enzyme-linked immunosorbent assay (ELISA), respectively. The interaction between miR-497-3p and PCT was further verified in A549 cell line. To further explore the role of miR497-3p in pneumonia, mouse model of bacterial pneumonia was established via Sp TIGR4 strain (SpT4) infection. Subsequently, LV-miR-497-3p sponge was administrated in mice with bacterial pneumonia. The severity of pneumonia and inflammatory response were evaluated. Serum miR497-3p and PCT levels increased in patients with bacterial pneumonia and miR-497-3p level positively corrected with the PCT level. The functional assay demonstrated that CALCA is the target of miR-497-3p in the A549 cell line. In mice with bacterial pneumonia, both miR-497-3p and PCT levels were upregulated after SpT4 infection. LV-miR-497-3p sponge administration attenuated pneumonia, accompanied with increasing gain of bodyweight and blood oxygen levels, as well as uninjured lungs. miR-497-3p inhibition attenuates the expression of Creactive protein (CRP) and inflammatory cytokines in lung tissues of SpT4-infected mice, including nterleukin-6 (IL-6) and tumor necrosis factor-α (TNF-α). In conclusion, inhibition of miR-497-3p downregulates the expression of procalcitonin and ameliorates bacterial pneumonia in mice.
Abstract—
KEY WORDS: miR-497; PCT; Bacterial pneumonia.
1
Department of Clinical Laboratory, Cangzhou Central Hospital, No.16 Xinhua West Road, Cangzhou, 061001, Hebei, China 2 Clinical Laboratory, Mengcun Hui Autonomous County Hospital, Chaoyang Dajie, Mengcun Hui Autonomous County, Cangzhou, 061400, Hebei, China 3 Clinical Laboratory, People’s Hospital of Qingxian, Nanhuanxi Road, Qingxian, Cangzhou, 062650, Hebei, China 4 Department of Blood Collection Center, Cangzhou Central Hospital, No.16 Xinhua West Road, Cangzhou, 061001, Hebei, China 5 To whom correspondence should be addressed at Department of Clinical Laboratory, Cangzhou Central Hospital, No.16 Xinhua West Road, Cangzhou, 061001, Hebei, China. E-mail: [email protected]
INTRODUCTION Pneumonia is the infectious disease of the lower respiratory tract, and serves as one of the most common reasons for severe morbidity [1, 2]. Patients with pneumonia always have a long recovery, and have the increased chance to die [3]. The pathobiological characters of pneumonia are enhanced host immune responses, which finally leads to lung injury [4–6]. Following flu infection-induced
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