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Nucleotide oligomerization domain 2 (NOD2) is an intracellular receptor of innate immunity for muramyldipeptide (MDP). Mutations of the NOD2 gene followed by decreased recognition of MDP are associated with chronic intestinal inflammation and pulmonary complications of patients with allogenic stem cell transplant and sepsis. Our study provides evidence that NOD2, toll\u2010like receptor 4 (TLR4) and the adapter protein receptor\u2010interacting protein 2 (RIP2) are induced by tumor\u2010necrosis factor\u2010\u03b1 (TNF\u2010\u03b1) and interferon\u2010\u03b3 (IFN\u2010\u03b3) in the bronchial epithelial cell line BEAS\u20102B. We also demonstrate that lipopolysaccharide (LPS) can further increase NOD2 transcription in a TNF\u2010\u03b1 and IFN\u2010\u03b3\u2010induced activation state. In addition, we show that, while MDP fails to enhance CXCL\u20108 release from otherwise unstimulated BEAS\u20102B cells, a 12\u2003h prestimulation period with TNF\u2010\u03b1 and IFN\u2010\u03b3 primes the cells for an additional increase of CXCL\u20108 secretion via induction of NOD2 and RIP2. LPS itself significantly augments CXCL\u20108 production and co\u2010administration of MDP further increases cytokine secretion. Finally, overexpression of an SNP13 mutant decreased MDP\u2010induced chemokine production in BEAS\u20102B cells compared with NOD2 wild type overexpression. Taken together, our work indicates that MDP and NOD2 play an important role for CXCL\u20108 release of BEAS\u20102B cells following LPS\u2010challenge via synergistic interactions between MDP and LPS.<\/jats:p>","DOI":"10.1111\/j.1365-3083.2008.02145.x","type":"journal-article","created":{"date-parts":[[2008,7,21]],"date-time":"2008-07-21T12:50:19Z","timestamp":1216644619000},"page":"315-322","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":13,"title":["Muramyldipeptide Modulates CXCL\u20108 Release of BEAS\u20102B Cells via 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