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Nucleotide-binding oligomerization domain 1 is dispensable for host immune responses against pulmonary infection of Acinetobacter baumannii in mice

  • Kang, Min-Jung (Laboratory Animal Medicine, College of Veterinary Medicine, Chonnam National University) ;
  • Choi, Jin-A (Laboratory Animal Medicine, College of Veterinary Medicine, Chonnam National University) ;
  • Choi, Joo-Hee (Laboratory Animal Medicine, College of Veterinary Medicine, Chonnam National University) ;
  • Jang, Ah-Ra (Laboratory Animal Medicine, College of Veterinary Medicine, Chonnam National University) ;
  • Park, Ji-Yeon (Laboratory Animal Medicine, College of Veterinary Medicine, Chonnam National University) ;
  • Ahn, Jae-Hun (Laboratory Animal Medicine, College of Veterinary Medicine, Chonnam National University) ;
  • Lee, Tae-Sung (Laboratory Animal Medicine, College of Veterinary Medicine, Chonnam National University) ;
  • Kim, Dong-Yeon (Laboratory Animal Medicine, College of Veterinary Medicine, Chonnam National University) ;
  • Park, Jong-Hwan (Laboratory Animal Medicine, College of Veterinary Medicine, Chonnam National University)
  • Received : 2018.11.22
  • Accepted : 2018.12.11
  • Published : 2018.12.31

Abstract

Nucleotide-binding domain 1 (Nod1) is a cytosolic receptor that is responsible for the recognition of a bacterial peptidoglycan motif containing meso-diaminophimelic acid. In this study, we sought to identify the role of Nod1 in host defense in vivo against pulmonary infection by multidrug resistant Acinetobacter baumannii. Wildtype (WT) and Nod1-deficient mice were intranasally infected with $3{\times}10^7CFU$ of A. baumannii and sacrificed at 1 and 3 days post-infection (dpi). Bacterial CFUs, cytokines production, histopathology, and mouse ${\beta}$-defensins (mBD) in the lungs of infected mice were evaluated. The production of cytokines in response to A. baumannii was also measured in WT and Nod1-deficient macrophages. The bacterial clearance in the lungs was not affected by Nod1 deficiency. Levels of IL-6, $TNF-{\alpha}$, and $IL-1{\beta}$ in the lung homogenates were comparable at days 1 and 3 between WT and Nod1-deficient mice, except the $TNF-{\alpha}$ level at day 3, which was higher in Nod1-deficient mice. There was no significant difference in lung pathology and expression of mBDs (mBD1, 2, 3, and 4) between WT and Nod1-deficient mice infected with A. baumannii. The production of IL-6, $TNF-{\alpha}$, and NO by macrophages in response to A. baumannii was also comparable in WT and Nod1-deficient mice. Our results indicated that Nod1 does not play an important role in host immune responses against A. baumannii infection.

Keywords

Acknowledgement

Supported by : National Research Foundation of Korea (NRF)

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