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The early phase of sepsis features dramatic changes in host metabolism and inflammation. While examining the effects of metabolic pathways on inflammation, we discovered that the highly reactive glycolytic metabolite, methylglyoxal (MG), accumulates intracellularly during classical activation of macrophages. Herein, we explored the role of glycolysis and the master regulator of glycolysis, Hypoxia-Inducing Factor-1\u03b1 (HIF-1\u03b1), in inflammation and MG accumulation in mouse and human macrophages. To determine how HIF-1\u03b1 regulates the inflammatory response of macrophages, we correlated HIF-1\u03b1 stabilization with proinflammatory gene expression and MG-adduct accumulation in WT vs HIF1a-deficient macrophages treated with LPS or LPS + IFN-\u03b3. A nearly complete loss of HIF-1\u03b1 protein expression in response to the hypoxia mimetic, cobalt chloride, confirmed the phenotype of the HIF1a-deficient macrophages. Moreover, absence of HIF-1\u03b1 was also associated with decreased MG accumulation. Increasing the glucose concentration in cultured macrophages was sufficient to cause accumulation of endogenous MG-adducts which correlated with increased Tnf and Il1b expression during classical activation. The use of the MG antagonist, aminoguanidine, led to a significant decrease in Tnf and Il1b expression in both mouse macrophages and the THP-1 human macrophage cell line. Although off-target effects cannot be ruled out, these results are consistent with the possibility that MG regulates cytokine expression in classically activated macrophages. Collectively, this work suggests that HIF-1\u03b1 stabilization is upstream of MG accumulation and that targeting the activity of HIF-1\u03b1 in macrophages may be therapeutic during sepsis by limiting endogenous MG accumulation.<\/jats:p>","DOI":"10.1093\/jleuko\/qiae215","type":"journal-article","created":{"date-parts":[[2024,10,3]],"date-time":"2024-10-03T14:30:43Z","timestamp":1727965843000},"source":"Crossref","is-referenced-by-count":7,"title":["Intracellular methylglyoxal accumulation in classically activated mouse macrophages is mediated by HIF-1\u03b1"],"prefix":"10.1093","volume":"117","author":[{"ORCID":"https:\/\/orcid.org\/0000-0003-2180-043X","authenticated-orcid":false,"given":"Daniel","family":"Prantner","sequence":"first","affiliation":[{"name":"Department of Microbiology and Immunology, University of Maryland School of Medicine , 685 West Baltimore St., Suite 380, Baltimore, MD 21201, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Stefanie N","family":"Vogel","sequence":"additional","affiliation":[{"name":"Department of Microbiology and Immunology, University of Maryland School of Medicine , 685 West Baltimore St., Suite 380, Baltimore, MD 21201, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"286","published-online":{"date-parts":[[2024,10,3]]},"reference":[{"issue":"8","key":"2025033004023903100_qiae215-B1","doi-asserted-by":"publisher","first-page":"801","DOI":"10.1001\/jama.2016.0287","article-title":"The third international consensus definitions for sepsis and septic shock (sepsis-3)","volume":"315","author":"Singer","year":"2016","journal-title":"JAMA"},{"issue":"11","key":"2025033004023903100_qiae215-B2","doi-asserted-by":"publisher","first-page":"2450","DOI":"10.1016\/j.immuni.2021.10.012","article-title":"The immunology of sepsis","volume":"54","author":"van der 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