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Thiamine is a central water\u2010soluble vitamin involved in cellular energy metabolism, and its deficiency has been reported in IBD patients. However, whether thiamine deficiency is a cause or consequence of IBD pathogenesis remains unclear. The current study aimed to reveal the immunometabolic regulation of macrophages and underlying mechanism of thiamine deficiency in colitis development.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Experimental Approach<\/jats:title>\n                    <jats:p>Thiamine deficiency was induced in C57BL\/6 mice and bone marrow\u2010derived macrophages (BMDMs), by administering a thiamine\u2010deficient diet\/medium together with pyrithiamine hydrobromide. The frequency of macrophage phenotypes and their intracellular metabolism were detected using flow cytometry and non\u2010targeted metabolomics, respectively.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Key Results<\/jats:title>\n                    <jats:p>Thiamine deficiency aggravated ulcerative colitis in mice and promoted the infiltration of proinflammatory M1 macrophages in colonic lamina propria. Our mechanistic study revealed that thiamine deficiency impaired pyruvate dehydrogenase (PDH) activity, thereby reprogramming cellular glucose metabolism to enhance glycolysis and lactic acid accumulation in M1 macrophages. Using a well\u2010established PDH inhibitor (CPI\u2010613) and lactic acid dehydrogenase inhibitor (galloflavin), we further demonstrated that PDH inhibition mimics, while lactate dehydrogenase inhibition partially rescues, thiamine deficiency\u2010induced proinflammatory macrophage infiltration and experimental colitis in mice.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusion and Implications<\/jats:title>\n                    <jats:p>Our study provides evidence linking thiamine deficiency with proinflammatory macrophage activation and colitis aggravation, suggesting that monitoring thiamine status and adjusting thiamine intake is necessary to protect against colitis.<\/jats:p>\n                  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