{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,16]],"date-time":"2026-10-16T19:25:32Z","timestamp":1792178732165,"version":"4.4.0"},"reference-count":23,"publisher":"Oxford University Press (OUP)","issue":"5","license":[{"start":{"date-parts":[[2003,3,1]],"date-time":"2003-03-01T00:00:00Z","timestamp":1046476800000},"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":[[2003,3,1]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:p>The phagolysosomal compartment is crucial for the defense against infection with intracellular pathogens. Within this compartment, the TNF- and IFN-\u03b3-responsive acid sphingomyelinase (ASMase) generates the signaling molecule ceramide, resulting in the activation of proteases like cathepsin D. To investigate the possible role of ASMase as a mediator of the antibacterial effects of TNF and IFN-\u03b3, ASMase\u2212\/\u2212 mice were infected with Listeria monocytogenes. ASMase\u2212\/\u2212 mice showed a dramatically increased susceptibility to L. monocytogenes (LD50 \u223c100 CFU) when compared with syngeneic wild-type mice (LD50 \u223c10,000 CFU). In L. monocytogenes-challenged ASMase\u2212\/\u2212 mice, IFN-\u03b3 serum levels as well as IL-1\u03b2 and IL-6 secretion by macrophages were similar to those observed in wild-type C57BL\/6 mice. Although macrophages and granulocytes from ASMase\u2212\/\u2212 mice showed intact production of reactive nitrogen intermediates and oxidative burst, ASMase\u2212\/\u2212 macrophages proved completely incapable of restricting the growth of L. monocytogenes in vitro. The results of this study suggest that ASMase is crucially required for the intracellular control of L. monocytogenes in macrophages and granulocytes by nonoxidative mechanisms.<\/jats:p>","DOI":"10.4049\/jimmunol.170.5.2621","type":"journal-article","created":{"date-parts":[[2014,4,20]],"date-time":"2014-04-20T21:32:44Z","timestamp":1398029564000},"page":"2621-2628","source":"Crossref","is-referenced-by-count":77,"title":["Severe Impairment in Early Host Defense Against\n                    <i>Listeria monocytogenes<\/i>\n                    in Mice Deficient in Acid Sphingomyelinase"],"prefix":"10.1093","volume":"170","author":[{"given":"Olaf","family":"Utermo\u0308hlen","sequence":"first","affiliation":[{"name":"Institute for Medical Microbiology, Immunology and Hygiene, Medical Center of the University of Cologne , Cologne ,","place":["Germany"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ulrike","family":"Karow","sequence":"additional","affiliation":[{"name":"Institute for Medical Microbiology, Immunology and Hygiene, Medical Center of the University of Cologne , Cologne ,","place":["Germany"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ju\u0308rgen","family":"Lo\u0308hler","sequence":"additional","affiliation":[{"name":"Heinrich-Pette-Institute for Experimental Virology and Immunology, University of Hamburg , Hamburg ,","place":["Germany"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Martin","family":"Kro\u0308nke","sequence":"additional","affiliation":[{"name":"Institute for Medical Microbiology, Immunology and Hygiene, Medical Center of the University of Cologne , Cologne ,","place":["Germany"]}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"286","published-online":{"date-parts":[[2003,3,1]]},"reference":[{"key":"2026020210081697300_R1","first-page":"11","volume-title":"Immunol. 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