Title Nucleotide-Binding Oligomerization Domain 2 (Nod2) Is Dispensable for the Innate Immune Responses of Macrophages against Yersinia enterocolitica
Author Yu-Jin Jeong1, Chang-Hwan Kim2, Eun-Jung Song1,3, Min-Jung Kang1, Jee-Cheon Kim2, Sang-Muk Oh1, Kyung-Bok Lee1, and Jong-Hwan Park1*
Address 1Department of Biochemistry, College of Medicine, Konyang University, Daejeon 302-711, Republic of Korea, 2CBD 5th-4, Agency for Defense Development, Daejeon 305-152, Republic of Korea, 3Present address: Viral Infectious Disease Research Center, Korea Research Institute of Bioscience and Biotechnology, Daejeon 305-806, Republic of Korea
Bibliography Journal of Microbiology, 50(3),489-495, 2012,
Key Words Nod2, Yersinia, innate immunity, macrophages
Abstract Nucleotide-binding oligomerization domain 2 (Nod2) is a cytosolic sensor for muramyl dipeptide, a component of bacterial peptidoglycan. In this study, we have examined whether Nod2 mediates the immune response of macrophages against Yersinia enterocolitica. Bone-marrow-derived macrophages (BMDMs) were isolated from WT and Nod2-deficient mice and were infected with various strains of Y. enterocolitica. ELISA showed that the production of IL-6 and TNF-α in BMDMs infected with Y. enterocolitica was not affected by the Nod2 deficiency. iNOS mRNA expression was induced in both WT and Nod2-deficienct BMDMs in response to Y. enterocolitica, beginning 2 h after infection. Nitric oxide (NO) production by Y. enterocolitica did not differ between WT and Nod2-deficient BMDMs. Western blot analysis revealed that Y. enterocolitica induces activation of NF-κB, p38, and ERK MAPK through a Nod2-independent pathway. Neither LDH release by Y. enterocolitica nor the phagocytic activity of the macrophages was altered by Nod2 deficiency. An in vivo experiment showed that bacterial clearance ability and production of IL-6 and KC in serum were comparable in WT and Nod2-deficient mice infected with Y. enterocolitica. These findings suggest that Nod2 may not be critical for initiating the innate immune response of macrophages against Yersinia infection.