{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,4]],"date-time":"2026-10-04T06:39:36Z","timestamp":1791095976316,"version":"4.1.0"},"reference-count":42,"publisher":"Wiley","issue":"s3","license":[{"start":{"date-parts":[[2013,9,4]],"date-time":"2013-09-04T00:00:00Z","timestamp":1378252800000},"content-version":"vor","delay-in-days":3,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Diabetes Obesity Metabolism"],"published-print":{"date-parts":[[2013,9]]},"abstract":"<jats:p>\n                    Macrophages play a critical role in the pathogenesis of metabolic diseases including gout and type 2 diabetes. The Nod\u2010like receptor (\n                    <jats:styled-content style=\"fixed-case\">NLR<\/jats:styled-content>\n                    ) family, pyrin domain containing 3 (\n                    <jats:styled-content style=\"fixed-case\">NLRP3<\/jats:styled-content>\n                    ) forms the inflammasome with apoptosis\u2010associated speck\u2010like protein containing a\n                    <jats:styled-content style=\"fixed-case\">CARD<\/jats:styled-content>\n                    (\n                    <jats:styled-content style=\"fixed-case\">ASC<\/jats:styled-content>\n                    ), the adaptor protein, and mediates inflammatory responses by macrophages. By compound screening, we found that tubulin polymerization inhibitors suppress\n                    <jats:styled-content style=\"fixed-case\">NLRP3<\/jats:styled-content>\n                    inflammasome activation.\n                    <jats:styled-content style=\"fixed-case\">NLRP3<\/jats:styled-content>\n                    inflammasome inducers reduce the\n                    <jats:styled-content style=\"fixed-case\">NAD<\/jats:styled-content>\n                    <jats:sup>+<\/jats:sup>\n                    level to inactivate the \u03b1\u2010tubulin deacetylase Sirtuin 2, resulting in accumulation of acetylated \u03b1\u2010tubulin. Acetylated \u03b1\u2010tubulin mediates mitochondrial transport and subsequent proximity of\n                    <jats:styled-content style=\"fixed-case\">ASC<\/jats:styled-content>\n                    on mitochondria to\n                    <jats:styled-content style=\"fixed-case\">NLRP3<\/jats:styled-content>\n                    on the endoplasmic reticulum. Thus, microtubule\u2010driven transport of mitochondria is required for\n                    <jats:styled-content style=\"fixed-case\">NLRP3<\/jats:styled-content>\n                    inflammasome activation. Macrophages are comprised of two subsets,\n                    <jats:styled-content style=\"fixed-case\">M1<\/jats:styled-content>\n                    (inflammatory) and\n                    <jats:styled-content style=\"fixed-case\">M2<\/jats:styled-content>\n                    (anti\u2010inflammatory). Trib1 is an adaptor protein involved in protein degradation of immune\u2010related transcription factors. We found that Trib1 is critical for the differentiation of\n                    <jats:styled-content style=\"fixed-case\">F4<\/jats:styled-content>\n                    \/80\n                    <jats:sup>+<\/jats:sup>\n                    <jats:styled-content style=\"fixed-case\">MR<\/jats:styled-content>\n                    <jats:sup>+<\/jats:sup>\n                    tissue\u2010resident\n                    <jats:styled-content style=\"fixed-case\">M2<\/jats:styled-content>\n                    \u2010like macrophages. Mice lacking Trib1 in haematopoietic cells show severe lipodystrophy owing to increased lipolysis, even on a normal diet. In response to a high\u2010fat diet, the mice show hypertriglyceridaemia and insulin resistance, together with increased proinflammatory cytokine production. Thus, Trib1 is critical for adipose tissue maintenance and suppression of metabolic disorders by controlling the differentiation of tissue\u2010resident\n                    <jats:styled-content style=\"fixed-case\">M2<\/jats:styled-content>\n                    \u2010like macrophages.\n                  <\/jats:p>","DOI":"10.1111\/dom.12151","type":"journal-article","created":{"date-parts":[[2013,9,4]],"date-time":"2013-09-04T09:27:06Z","timestamp":1378286826000},"page":"10-18","source":"Crossref","is-referenced-by-count":54,"title":["Macrophages control innate inflammation"],"prefix":"10.1111","volume":"15","author":[{"given":"S.","family":"Akira","sequence":"first","affiliation":[{"name":"Laboratory of Host Defense WPI Immunology Frontier Research Center, Osaka University Osaka Japan"},{"name":"Department of Host Defense Research Institute for Microbial Diseases, Osaka University Osaka Japan"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"T.","family":"Misawa","sequence":"additional","affiliation":[{"name":"Laboratory of Host Defense WPI Immunology Frontier Research Center, Osaka University Osaka Japan"},{"name":"Department of Host Defense Research Institute for Microbial Diseases, Osaka University Osaka Japan"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"T.","family":"Satoh","sequence":"additional","affiliation":[{"name":"Laboratory of Host Defense WPI Immunology Frontier Research Center, Osaka University Osaka Japan"},{"name":"Department of Host Defense Research Institute for Microbial Diseases, Osaka University Osaka Japan"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"T.","family":"Saitoh","sequence":"additional","affiliation":[{"name":"Laboratory of Host Defense WPI Immunology Frontier Research Center, Osaka University Osaka Japan"},{"name":"Department of Host Defense Research Institute for Microbial Diseases, Osaka University Osaka Japan"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"311","published-online":{"date-parts":[[2013,9,4]]},"reference":[{"key":"e_1_2_6_2_1","doi-asserted-by":"publisher","DOI":"10.1016\/j.cell.2010.01.022"},{"key":"e_1_2_6_3_1","doi-asserted-by":"publisher","DOI":"10.1038\/ni.1863"},{"key":"e_1_2_6_4_1","doi-asserted-by":"publisher","DOI":"10.1038\/nature07201"},{"key":"e_1_2_6_5_1","doi-asserted-by":"publisher","DOI":"10.1146\/annurev.immunol.021908.132715"},{"key":"e_1_2_6_6_1","doi-asserted-by":"publisher","DOI":"10.1111\/j.1600-065X.2011.01058.x"},{"key":"e_1_2_6_7_1","doi-asserted-by":"publisher","DOI":"10.1038\/nature10759"},{"key":"e_1_2_6_8_1","doi-asserted-by":"publisher","DOI":"10.1111\/j.1600-065X.2011.01052.x"},{"key":"e_1_2_6_9_1","doi-asserted-by":"publisher","DOI":"10.1146\/annurev-immunol-031210-101352"},{"key":"e_1_2_6_10_1","doi-asserted-by":"publisher","DOI":"10.1038\/ni.2369"},{"key":"e_1_2_6_11_1","doi-asserted-by":"publisher","DOI":"10.1038\/nature04516"},{"key":"e_1_2_6_12_1","doi-asserted-by":"publisher","DOI":"10.1038\/nature08938"},{"key":"e_1_2_6_13_1","doi-asserted-by":"publisher","DOI":"10.1038\/ni.1935"},{"key":"e_1_2_6_14_1","doi-asserted-by":"publisher","DOI":"10.1038\/ni.2550"},{"key":"e_1_2_6_15_1","doi-asserted-by":"publisher","DOI":"10.1038\/nature01600"},{"key":"e_1_2_6_16_1","doi-asserted-by":"publisher","DOI":"10.1038\/nrm2804"},{"key":"e_1_2_6_17_1","doi-asserted-by":"publisher","DOI":"10.1038\/nature10936"},{"key":"e_1_2_6_18_1","doi-asserted-by":"publisher","DOI":"10.1242\/jcs.063727"},{"key":"e_1_2_6_19_1","doi-asserted-by":"publisher","DOI":"10.1038\/nature09324"},{"key":"e_1_2_6_20_1","doi-asserted-by":"publisher","DOI":"10.1016\/S1097-2765(03)00038-8"},{"key":"e_1_2_6_21_1","doi-asserted-by":"publisher","DOI":"10.1038\/417455a"},{"key":"e_1_2_6_22_1","doi-asserted-by":"publisher","DOI":"10.1126\/science.1217141"},{"key":"e_1_2_6_23_1","doi-asserted-by":"publisher","DOI":"10.1016\/j.cell.2012.02.035"},{"key":"e_1_2_6_24_1","doi-asserted-by":"publisher","DOI":"10.1083\/jcb.201002021"},{"key":"e_1_2_6_25_1","doi-asserted-by":"publisher","DOI":"10.1038\/nature11930"},{"key":"e_1_2_6_26_1","doi-asserted-by":"publisher","DOI":"10.1146\/annurev.immunol.021908.132532"},{"key":"e_1_2_6_27_1","doi-asserted-by":"publisher","DOI":"10.1038\/ni.1937"},{"key":"e_1_2_6_28_1","doi-asserted-by":"publisher","DOI":"10.1016\/j.coi.2010.01.009"},{"key":"e_1_2_6_29_1","doi-asserted-by":"publisher","DOI":"10.1016\/j.cellsig.2006.06.010"},{"key":"e_1_2_6_30_1","doi-asserted-by":"publisher","DOI":"10.1084\/jem.20070183"},{"key":"e_1_2_6_31_1","doi-asserted-by":"publisher","DOI":"10.1182\/blood-2009-10-246264"},{"key":"e_1_2_6_32_1","doi-asserted-by":"publisher","DOI":"10.1182\/blood-2006-08-041202"},{"key":"e_1_2_6_33_1","doi-asserted-by":"publisher","DOI":"10.1016\/j.ccr.2006.09.012"},{"key":"e_1_2_6_34_1","doi-asserted-by":"publisher","DOI":"10.1126\/science.1079817"},{"key":"e_1_2_6_35_1","doi-asserted-by":"publisher","DOI":"10.1161\/ATVBAHA.110.216333"},{"key":"e_1_2_6_36_1","doi-asserted-by":"crossref","first-page":"230","DOI":"10.1186\/1476-511X-10-230","article-title":"Association 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