Nucleotide-binding oligomerization domain 1 is dispensable for host immune responses against pulmonary infection of Acinetobacter baumannii in mice.
10.5625/lar.2018.34.4.295
- Author:
Min Jung KANG
1
;
Jin A CHOI
;
Joo Hee CHOI
;
Ah Ra JANG
;
Ji Yeon PARK
;
Jae Hun AHN
;
Tae Sung LEE
;
Dong Yeon KIM
;
Jong Hwan PARK
Author Information
1. Laboratory Animal Medicine, College of Veterinary Medicine, Chonnam National University, Gwangju, Korea. jonpark@jnu.ac.kr
- Publication Type:Original Article
- Keywords:
Nucleotide-binding domain 1 (Nod1);
peptidoglycan;
Acinetobacter baumannii
- MeSH:
Acinetobacter baumannii*;
Acinetobacter*;
Animals;
Cytokines;
Cytosol;
Interleukin-6;
Lung;
Macrophages;
Mice*;
Pathology;
Peptidoglycan
- From:Laboratory Animal Research
2018;34(4):295-301
- CountryRepublic of Korea
- Language:English
-
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 3×107 CFU of A. baumannii and sacrificed at 1 and 3 days post-infection (dpi). Bacterial CFUs, cytokines production, histopathology, and mouse β-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-α, and IL-1β in the lung homogenates were comparable at days 1 and 3 between WT and Nod1-deficient mice, except the TNF-α 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-α, 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.
