| Summary: | 碩士 === 國立陽明大學 === 急重症醫學研究所 === 97 === NOD2, an intracellular sensor of bacteria, are linked to increased susceptibility to bacteria in Crohn’s disease (CD). The NOD2 protein is expressed mainly by macrophages and dendritic cells. This study is to examine the role of NOD2 in the innate response of macrophages to bacterial challenge. First, peritoneal macrophages and alveolar macrophages were harvested from WT, Nod22939iC, as well as TLR4-/- mice and incubated with E. coli or P. aeruginosa. Bacterial killing activity; IL-1b and TLR4 protein expression; NF-kB DNA binding activity assay; as well as IL-1b, TNFa, TLR2, TLR4 and TLR9 mRNA expression of macrophages were examined. We found that alveolar macrophages and peritoneal macrophages of Nod22939iC mice but not WT mice or TLR4-/- mice demonstrated a significant increase of E. coli killing activity. Bacterial challenge also induced a significant increase of pro-IL-1b protein expression; NF-kB DNA binding activity; as well as IL-1b and TNFa mRNA expression of the peritoneal macrophages in Nod22939iC mice. Colletively, the increase of bacterial killing activity, IL-1b expression, and NF-kB DNA binding activity of macrophages in Nod22939iC mice suggests that NOD2 is a positive regulator of NF-kB/IL-1b-mediated innate response to bacteria challenge in Crohn’s disease. Nod22939iC also cause increased bacterial killing activity in macrophage of mice.
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