{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,7,22]],"date-time":"2026-07-22T02:14:37Z","timestamp":1784686477420,"version":"3.55.0"},"reference-count":41,"publisher":"Wiley","issue":"11","license":[{"start":{"date-parts":[[2019,4,10]],"date-time":"2019-04-10T00:00:00Z","timestamp":1554854400000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"},{"start":{"date-parts":[[2019,4,10]],"date-time":"2019-04-10T00:00:00Z","timestamp":1554854400000},"content-version":"tdm","delay-in-days":0,"URL":"http:\/\/doi.wiley.com\/10.1002\/tdm_license_1.1"}],"funder":[{"name":"National Natural Science Foundation for Key Program of China","award":["31730024"],"award-info":[{"award-number":["31730024"]}]},{"name":"National Natural Science Foundation for General Programs of China","award":["31671524"],"award-info":[{"award-number":["31671524"]}]},{"name":"National Natural Science Foundation for General Programs of China","award":["81273201"],"award-info":[{"award-number":["81273201"]}]}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Journal Cellular Physiology"],"published-print":{"date-parts":[[2019,11]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:p>\n                    The metabolism of immune cells reprograms inflammatory responses to protect against infection by pathogenic microorganisms, but the immune effects of glycolysis and the oxidative phosphorylation (OXPHOS) metabolic pathway remain unclear. Herein, the effects of glycolysis or OXPHOS on the neutrophils and T cells were investigated using a pharmacological approach in mice. 2\u2010Deoxy\u2010\n                    <jats:sc>d<\/jats:sc>\n                    \u2010glucose (2\u2010DG), which blocks the key enzyme hexokinase of glycolysis, and dimethyl malonate (DMM), which blocks the key element succinate of OXPHOS, both efficiently expanded the population of neutrophils, but significantly inhibited tumor necrosis factor a secretion and reactive oxygen species (ROS) production. These compounds also effectively inhibited the differentiation of type 1 T helper cells (Th1) but had no effects on the differentiation of type 2 T helper cells (Th2) and regulatory T cells. A study of the underlying mechanism showed that hypoxia\u2010inducible factor 1\u2010alpha (HIF1\u03b1) was an upstream signal in the regulation of glycolysis, but not OXPHOS. In thioglycolate broth\u2010induced neutrophil peritonitis, blockade of glycolysis or OXPHOS efficiently expanded the population of neutrophils, but diminished their abilities to secrete proinflammatory factors, produce ROS, and phagocytose bacteria. In\n                    <jats:italic>Listeria monocytogenes<\/jats:italic>\n                    bacteria\u2010infected mice, 2\u2010DG or DMM treatment consistently inhibited antibacterial activity and Th1 function. Thus, our results provide a basis for comprehensively understanding the role of glycolysis and OXPHOS in anti\u2010infectious immunity.\n                  <\/jats:p>","DOI":"10.1002\/jcp.28630","type":"journal-article","created":{"date-parts":[[2019,4,11]],"date-time":"2019-04-11T17:52:52Z","timestamp":1555005172000},"page":"20298-20309","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":52,"title":["Immune effects of glycolysis or oxidative phosphorylation metabolic pathway in protecting against bacterial infection"],"prefix":"10.1002","volume":"234","author":[{"given":"Yan","family":"Li","sequence":"first","affiliation":[{"name":"Department of Immunology, School of Basic Medical Sciences Fudan University Shanghai China"},{"name":"Key Laboratory of Cell Proliferation and Regulation Biology, Ministry of Education, Institute of Cell Biology, College of Life Sciences Beijing Normal University Beijing 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