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Inhibition of type I interferon signaling abrogates early Mycobacterium bovis infection

Authors
  • Wang, Jie1, 2
  • Hussain, Tariq1
  • Zhang, Kai3
  • Liao, Yi1
  • Yao, Jiao1
  • Song, Yinjuan1
  • Sabir, Naveed1
  • Cheng, Guangyu1
  • Dong, Haodi1
  • Li, Miaoxuan1
  • Ni, Jiamin1
  • Mangi, Mazhar Hussain1
  • Zhao, Deming1
  • Zhou, Xiangmei1
  • 1 China Agricultural University, Beijing, China , Beijing (China)
  • 2 Peking Union Medical College (PUMC), Beijing, China , Beijing (China)
  • 3 Ningxia University, Ningxia, China , Ningxia (China)
Type
Published Article
Journal
BMC Infectious Diseases
Publisher
Springer (Biomed Central Ltd.)
Publication Date
Dec 04, 2019
Volume
19
Issue
1
Identifiers
DOI: 10.1186/s12879-019-4654-3
Source
Springer Nature
Keywords
License
Green

Abstract

BackgroundMycobacterium bovis (M. bovis) is the principal causative agent of bovine tuberculosis; however, it may also cause serious infection in human being. Type I IFN is a key factor in reducing viral multiplication and modulating host immune response against viral infection. However, the regulatory pathways of Type I IFN signaling during M. bovis infection are not yet fully explored. Here, we investigate the role of Type I IFN signaling in the pathogenesis of M. bovis infection in mice.MethodsC57BL/6 mice were treated with IFNAR1-blocking antibody or Isotype control 24 h before M. bovis infection. After 21 and 84 days of infection, mice were sacrificed and the role of Type I IFN signaling in the pathogenesis of M. bovis was investigated. ELISA and qRT-PCR were performed to detect the expression of Type I IFNs and related genes. Lung lesions induced by M. bovis were assessed by histopathological examination. Viable bacterial count was determined by CFU assay.ResultsWe observed an abundant expression of Type I IFNs in the serum and lung tissues of M. bovis infected mice. In vivo blockade of Type I IFN signaling reduced the recruitment of neutrophils to the lung tissue, mediated the activation of macrophages leading to an increased pro-inflammatory profile and regulated the inflammatory cytokine production. However, no impact was observed on T cell activation and recruitment in the early acute phase of infection. Additionally, blocking of type I IFN signaling reduced bacterial burden in the infected mice as compared to untreated infected mice.ConclusionsAltogether, our results reveal that Type I IFN mediates a balance between M. bovis-mediated inflammatory reaction and host defense mechanism. Thus, modulating Type I IFN signaling could be exploited as a therapeutic strategy against a large repertoire of inflammatory disorders including tuberculosis.

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