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Here, we confirm that TNF signaling hampers physical activity, food intake, and energy expenditure while enhancing glucose uptake by the liver and spleen as well as controlling parasitemia in\n                  <jats:italic>P. chabaudi<\/jats:italic>\n                  (\n                  <jats:italic>Pc<\/jats:italic>\n                  )-infected mice. We also report that TNF is required for expression of inducible nitric oxide synthase (iNOS), stabilization of HIF-1\u03b1, expression of glucose transporter GLUT1 and enhanced glycolysis in monocytic cells from\n                  <jats:italic>Pc<\/jats:italic>\n                  -infected mice. Importantly,\n                  <jats:italic>Pc<\/jats:italic>\n                  -infected iNOS\n                  <jats:sup>-\/-<\/jats:sup>\n                  , TNFR\n                  <jats:sup>\u0394Lyz2<\/jats:sup>\n                  and\n                  <jats:italic>HIF-1\u03b1<\/jats:italic>\n                  <jats:sup>\u0394Lyz2<\/jats:sup>\n                  mice show impaired release of TNF and glycolysis in monocytes, along with increased parasitemia and disease tolerance. Altogether, our results indicate that TNF-iNOS-HIF-1\u03b1-induced glycolysis in monocytes plays a critical role in host defense and sickness behavior in\n                  <jats:italic>Pc<\/jats:italic>\n                  -infected mice.\n                <\/jats:p>\n                <jats:sec>\n                  <jats:title>Tease<\/jats:title>\n                  <jats:p>\n                    The role of host energy metabolism and glycolysis in monocytes as determinant of host resistance to\n                    <jats:italic>Plasmodium<\/jats:italic>\n                    infection and tolerance to disease.\n                  <\/jats:p>\n                <\/jats:sec>","DOI":"10.1101\/2024.03.26.586751","type":"posted-content","created":{"date-parts":[[2024,3,29]],"date-time":"2024-03-29T15:20:22Z","timestamp":1711725622000},"source":"Crossref","is-referenced-by-count":1,"title":["Reprogramming of host energy metabolism mediated by the TNF-iNOS-HIF-1\u03b1 axis plays a key role in host resistance to\n                  <i>Plasmodium<\/i>\n                  infection"],"prefix":"10.64898","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-2474-1837","authenticated-orcid":false,"given":"Kely C.","family":"Matteucci","sequence":"first","affiliation":[{"name":"Translational Medicine Platform Oswaldo Cruz Foundation, Ribeir\u00e3o Preto Medical School, University of Sao Paulo, Brazil"},{"name":"Department of Biochemistry and Immunology, Ribeir\u00e3o Preto Medical School, University of Sao Paulo, Brazil"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-0275-2949","authenticated-orcid":false,"given":"Nathalia P. 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