@article{javkhlan2015expression,
  title = {Expression and LPS-Induced Elevation of Nod2 and Calprotectin in the Submandibular Gland of Wild-Type and TLR4-Knockout Male Mice},
  author = {Purevjav Javkhlan and Guangfei Xu and Gang Chen and Chenjuan Yao and Yuka Hiroshima and Hiroshi Yoshimura and Toshihiko Nagata and Kazuo Hosoi},
  year = 2015,
  url = {https://ibimapublishing.com/articles/DENT/2015/290259/},
  journal = {Journal of Research and Practice in Dentistry},
  volume = 2015 (2015),
  pages = 16,
  doi = 10.5171/2015.290259,
  abstract = {The salivary gland produces a number of inflammation-related cytokines and at least some of them including S100A8 and S100A9 (calprotectin subunits) in the gland are induced by endotoxins. The signaling pathway to induce these cytokines is complex and has not been thoroughly elucidated. Thus, we examined effects of lipopolysaccharide (LPS) on the level of salivary gland S100A8/A9 and investigated whether any signaling molecule is participated in elevation of these cytokines in this tissue. Toll-like receptor-4 (TLR4)-knockout C57BL/6 (TLR4-/-) mice and their wild-type (WT), C57BL/6, counterpart (TLR4+/+) were used in the experiment. Quantitative real-time RT-PCR, RT-PCR, and Western blotting were employed for analyses of mRNA and protein levels of S100A8/A9, nucleotide-binding oligomerization domain-containing protein (Nod) 1, and Nod2. Following the injection of E. coli LPS, the mRNA levels of S100A8/A9 were strongly elevated in the submandibular gland (SMG) of WT mice and at small degree but clearly so even in the same tissue of TLR4-knockout counterparts; this suggests the existence of a signaling pathway other than TLR4 to induce S100A8/A9. In the SMG of WT mice but not TLR4-knockout counterparts, both mRNA and protein levels of Nod2 were elevated by LPS, these increases were completely blocked by cycloheximide (CHX). CHX simultaneously suppressed LPS-induced elevation of S100A8/A9 mRNAs. These results, although more experiment using Nod2 specific inhibitors is required, imply the possibility that S100A8/A9 mRNA levels were increased by LPS via both TLR4 and Nod2 signaling pathways in the mouse SMG.},
  keywords = {Nod2, calprotectin, S100A8/A9, LPS, submandibular gland},
  note = Article ID: 290259
}