ArticleBMC microbiology2026
cAMP-response element binding protein (CREB)-mediated glycolysis enhancement promotes apoptosis of RAW264.7 macrophages infected with BCG under high glucose conditions.
Article in BMC microbiology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
backgroundMacrophages serve as the primary host defense against Mycobacterium tuberculosis (M.tb). Cellular glycolysis plays a critical role in macrophage-mediated resistance to mycobacterial infection. A hyperglycemic microenvironment impairs host defense and exacerbates mycobacterial infection. However, the role of cAMP response element-binding protein (CREB), a key transcription factor regulating metabolism and apoptosis, in macrophages' anti-mycobacterial response under high glucose (HG) conditions remains unclear. Here, we used the attenuated M.tb strain Bacillus Calmette‑Guérin (BCG) to investigate the role of CREB in HG‑modulated glycolysis and apoptosis in infected macrophages.
resultsIn the present study, we found that BCG infection significantly induced apoptosis and upregulated the expression of key glycolytic enzymes in RAW264.7 macrophages in vitro, and these effects were further amplified under HG conditions. In vivo, C57BL/6J mice fed a high-fat high-sugar (HFHS) diet and infected with BCG showed more pronounced lung tissue inflammatory cell infiltration and bacterial burden, along with upregulated p-CREB, GLUT4 and Cleaved-Caspase 9, compared with infected mice fed normal chow. siRNA-mediated CREB knockdown significantly reduced apoptosis-related proteins and glycolytic enzymes, decreased intracellular ROS accumulation, and improved cell survival in BCG-infected RAW264.7 cells under HG conditions. The glycolysis inhibitor 2-deoxy-D-glucose (2-DG) suppressed glycolytic enzyme expression and apoptosis, with further enhanced protection when combined with CREB siRNA.
conclusionBCG infection upregulated CREB expression in a time-dependent manner, and this effect was further potentiated under HG conditions. CREB upregulation was accompanied by enhanced glycolysis, increased ROS accumulation, and elevated macrophage apoptosis, and these changes were associated with exacerbated BCG infection under HG conditions. These findings suggest a mechanistic link between hyperglycemia and impaired antimycobacterial defense, and point to CREB as a candidate for further investigation under HG metabolic stress.
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