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1
Diabetic sepsis patients show elevated inflammatory cytokines and impaired antigen presentation, leading to higher mortality rates compared to non-diabetics.
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2
Lactate levels rise significantly during sepsis, activating GPR81 receptors and inducing histone lactylation, which affects immune responses.
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3
Histone lactylation at H3K18 selectively activates inflammatory genes while suppressing antigen-presentation pathways in diabetic sepsis.
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4
Preliminary studies indicate a correlation between H3K18la levels and disease severity, with poor lactate clearance linked to worse prognosis.
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5
Potential therapeutic targets include metabolic regulation to reduce lactate, intervention in the GPR81-H3K18la axis, and personalized immune phenotype therapy.
