Inhibition of miR-497-3p Downregulates the Expression of Procalcitonin and Ameliorates Bacterial Pneumonia in Mice.

Abstract

Pneumonia is usually caused by a wide variety of pathogen infection. The underlying mechanism contributing to pneumonia remains elusive. Here, the role of microRNA-497-3p (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 (RT-PCR) 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 miR-497-3p 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 miR-497-3p 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 C-reactive 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.