Yak IFNβ-3 enhances macrophage activity and attenuates Klebsiella pneumoniae infection.

Interferon-β (IFNβ) is an important member of the type I interferon family and plays key roles in antiviral response and treatment of autoimmune disease. However, the immunomodulation and antimicrobial potential of yak IFNβ3 protein are still unclear. In the current study, the 558 bp long cDNA sequence of the yak IFNβ3 gene was amplified and successfully expressed in a prokaryotic system. The mRNA expression level of IFNβ3 in yak spleen was higher than in heart, liver, lung and kidney. The minimum inhibitory concentration of recombinant IFNβ3 protein against Klebsiella pneumoniae was determined to be 64 μg/mL. The activity, phagocytosis, and nucleic acid intensity of yak macrophages were significantly increased by IFNβ3 protein (P < 0.05). In addition, the vitality of macrophages infected with Klebsiella pneumoniae was significantly increased by IFNβ3 protein (P < 0.05). The IFNβ3 protein significantly reduced the release of nitric oxide (NO) from macrophages infected with Klebsiella pneumoniae (P < 0.05). The mRNA levels of Capg, Man2b1, Mrc-1, γ-actin and Marco in macrophages were upregulated by IFNβ3 protein (P < 0.05). The contents of aspartate aminotransferase (AST) and lactate dehydrogenase (LDH) in the serum of mice after Klebsiella pneumoniae infection were reduced by IFNβ3 protein (P < 0.05). The lung and kidney injuries in mice induced by Klebsiella pneumoniae infection were alleviated by IFNβ3 protein. In summary, the yak IFNβ3 protein enhanced macrophage activity and reduced the damage caused by Klebsiella pneumoniae infection in mice.