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Although amelioration of infection by \u03b1-GalCer involves invariant natural killer T (iNKT)-cell activation, it remains to be determined whether macrophages (M\u03c6) participate in the control of microbial pathogens. In the present study, we examined the participation of M\u03c6 in immune intervention in infection by \u03b1-GalCer using a murine model of listeriosis. Phagocytic and bactericidal activities of peritoneal M\u03c6 from C57BL\/6 mice, but not iNKT cell-deficient mice, were enhanced after intraperitoneal injection of \u03b1-GalCer despite the absence of iNKT cells in the peritoneal cavity. High levels of gamma interferon (IFN-\u03b3) and nitric oxide (NO) were detected in the peritoneal cavities of mice treated with \u03b1-GalCer and in culture supernatants of peritoneal M\u03c6 from mice treated with \u03b1-GalCer, respectively. Although enhanced bactericidal activity of peritoneal M\u03c6 by \u03b1-GalCer was abrogated by endogenous IFN-\u03b3 neutralization, this was only marginally affected by NO inhibition. Similar results were obtained by using a listeriolysin O-deficient strain of<jats:italic>Listeria monocytogenes<\/jats:italic>. Moreover, respiratory burst in M\u03c6 was increased after \u03b1-GalCer treatment. Our results suggest that amelioration of listeriosis by \u03b1-GalCer is, in part, caused by enhanced killing of<jats:italic>L. monocytogenes<\/jats:italic>within phagosomes of M\u03c6 activated by IFN-\u03b3 from iNKT cells residing in an organ(s) other than the peritoneal cavity.<\/jats:p>","DOI":"10.1128\/iai.01441-09","type":"journal-article","created":{"date-parts":[[2010,3,30]],"date-time":"2010-03-30T03:28:48Z","timestamp":1269919728000},"page":"2667-2676","update-policy":"https:\/\/doi.org\/10.1128\/asmj-crossmark-policy-page","source":"Crossref","is-referenced-by-count":17,"title":["\u03b1-Galactosylceramide Promotes Killing of<i>Listeria monocytogenes<\/i>within the Macrophage Phagosome through Invariant NKT-Cell Activation"],"prefix":"10.1128","volume":"78","author":[{"given":"Masashi","family":"Emoto","sequence":"first","affiliation":[{"name":"Laboratory of Immunology, Department of Laboratory Sciences, Gunma University School of Health Sciences, Gunma 371-8511, Japan"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Tomomi","family":"Yoshida","sequence":"additional","affiliation":[{"name":"Laboratory of Pathology and Diagnostic Cytology, Department of Laboratory Sciences, Gunma University School of Health Sciences, Gunma 371-8511, Japan"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Toshio","family":"Fukuda","sequence":"additional","affiliation":[{"name":"Laboratory of Pathology and Diagnostic Cytology, Department of Laboratory Sciences, Gunma University School of Health Sciences, Gunma 371-8511, Japan"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ikuo","family":"Kawamura","sequence":"additional","affiliation":[{"name":"Department of Microbiology, Kyoto University Graduate School of Medicine, Kyoto 606-8501, Japan"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Masao","family":"Mitsuyama","sequence":"additional","affiliation":[{"name":"Department of Microbiology, Kyoto University Graduate School of Medicine, Kyoto 606-8501, Japan"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Eiji","family":"Kita","sequence":"additional","affiliation":[{"name":"Department of Bacteriology, Nara Medical University, Nara 634-8521, Japan"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Robert","family":"Hurwitz","sequence":"additional","affiliation":[{"name":"Core Facilities Biochemistry, Max Planck Institute for Infection Biology, Berlin 10117, Germany"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Stefan H. 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