{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,4]],"date-time":"2026-10-04T11:36:39Z","timestamp":1791113799942,"version":"4.1.0"},"reference-count":57,"publisher":"Oxford University Press (OUP)","issue":"9","license":[{"start":{"date-parts":[[2002,5,1]],"date-time":"2002-05-01T00:00:00Z","timestamp":1020211200000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/academic.oup.com\/pages\/standard-publication-reuse-rights"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"published-print":{"date-parts":[[2002,5,1]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:p>Mitogen-activated protein kinase-activated protein kinase 2 (MK2) is one of several kinases activated through direct phosphorylation by p38 mitogen-activated protein kinase. MK2 regulates LPS-induced TNF mRNA translation, and targeted mutation of the MK2 gene renders mice more resistant to d-galactosamine plus LPS-induced liver damage. In the present study, we investigated the role of MK2 in immune defense against Listeria monocytogenes infection. MK2-deficient mice displayed diminished resistance to L. monocytogenes due to impaired control of bacterial growth. The increase in bacterial load in MK2\u2212\/\u2212 mice was associated with normal levels of IL-1\u03b2, IL-6, and IFN-\u03b3, whereas TNF production was strongly attenuated. In line, MK2-deficient bone marrow-derived macrophages showed impaired release of TNF, but not of IL-1\u03b2, in response to various bacterial stimuli in addition to decreased phagocytosis of fluorescence-labeled bacteria. Furthermore, spleen cells from MK2\u2212\/\u2212 mice displayed diminished IFN-\u03b3 synthesis after stimulation with L. monocytogenes. In contrast, MK2 deficiency had no effect on macrophage generation of NO or on oxidative burst activity in response to L. moocytogenes. These results indicate an essential role of MK2 in host defense against intracellular bacteria probably via regulation of TNF and IFN-\u03b3 production required for activation of antibacterial effector mechanisms.<\/jats:p>","DOI":"10.4049\/jimmunol.168.9.4667","type":"journal-article","created":{"date-parts":[[2014,4,20]],"date-time":"2014-04-20T19:46:54Z","timestamp":1398023214000},"page":"4667-4673","source":"Crossref","is-referenced-by-count":70,"title":["Mitogen-Activated Protein Kinase-Activated Protein Kinase 2-Deficient Mice Show Increased Susceptibility to\n                    <i>Listeria monocytogenes<\/i>\n                    Infection"],"prefix":"10.1093","volume":"168","author":[{"given":"Martin D","family":"Lehner","sequence":"first","affiliation":[{"name":"Department of Biochemical Pharmacology, University of Konstanz , Konstanz ,","place":["Germany"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Frank","family":"Schwoebel","sequence":"additional","affiliation":[{"name":"Department of Molecular Toxicology, University of Konstanz , Konstanz ,","place":["Germany"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Alexey","family":"Kotlyarov","sequence":"additional","affiliation":[{"name":"Department of Medical School Hannover, Institute of Biochemistry , Hannover ,","place":["Germany"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Marcel","family":"Leist","sequence":"additional","affiliation":[{"name":"Department of Neurobiology, H. 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