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ACBP: a poor-prognosis biomarker in sepsis and a target for disease mitigation

ABSTRACT: Septic shock remains a major clinical challenge, with high mortality and long-term disability despite current interventions. Here, we identify the tissue hormone acyl-CoA–binding protein (ACBP), also known as diazepam-binding inhibitor (DBI), as a biomarker and driver of poor outcomes in sepsis. ACBP/DBI was elevated in the plasma of septic patients, correlating with organ dysfunction and mortality. In murine models of endotoxemia, Escherichia coli infection, and polymicrobial sepsis, genetic deletion or antibody-mediated neutralization of ACBP/DBI conferred robust protection by enhancing pathogen clearance, dampening cytokine storms, and preserving organ function. Notably, ACBP/DBI inhibition could be favorably combined with glucocorticoids, enhancing survival and reversing transcriptional and metabolic signatures of septic shock across spleen, liver, heart, and kidney. These findings position ACBP/DBI as a mechanistic amplifier of sepsis pathophysiology and propose its neutralization—alone or combined with corticosteroids—as a promising therapeutic strategy to interrupt the fatal trajectory of septic shock.

ORGANISM(S): Mus musculus

PROVIDER: GSE304860 | GEO | 2026/01/26

REPOSITORIES: GEO

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ACBP: a poor-prognosis biomarker in sepsis and a target for disease mitigation II

Project description:Septic shock remains a major clinical challenge, with high mortality and long-term disability despite current interventions. Here, we identify the tissue hormone acyl-CoA–binding protein (ACBP), also known as diazepam-binding inhibitor (DBI), as a biomarker and driver of poor outcomes in sepsis. ACBP/DBI was elevated in the plasma of septic patients, correlating with organ dysfunction and mortality. In murine models of endotoxemia, Escherichia coli infection, and polymicrobial sepsis, genetic deletion or antibody-mediated neutralization of ACBP/DBI conferred robust protection by enhancing pathogen clearance, dampening cytokine storms, and preserving organ function. Notably, ACBP/DBI inhibition could be favorably combined with glucocorticoids, enhancing survival and reversing transcriptional and metabolic signatures of septic shock across spleen, liver, heart, and kidney. These findings position ACBP/DBI as a mechanistic amplifier of sepsis pathophysiology and propose its neutralization—alone or combined with corticosteroids—as a promising therapeutic strategy to interrupt the fatal trajectory of septic shock.

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ACBP: a poor-prognosis biomarker in sepsis and a target for disease mitigation [Lung]

Project description:Sepsis remains a major clinical challenge, with high mortality and long-term disability despite current interventions. Here, we identify the tissue hormone acyl-CoA–binding protein (ACBP), also known as diazepam-binding inhibitor (DBI), as a biomarker and driver of poor outcome in sepsis. ACBP/DBI was elevated in the plasma of septic patients and associated with organ dysfunction and increased mortality. In murine models of endotoxemia, Escherichia coli infection, and polymicrobial sepsis, genetic deletion or antibody-mediated neutralization of ACBP/DBI conferred robust protection by enhancing pathogen clearance, dampening cytokine storm, and preserving organ function. Notably, ACBP/DBI inhibition could be favorably combined with glucocorticoids, enhancing survival and reversing histopathological, transcriptional, or metabolic signatures of septic shock across heart, kidney, liver, lung, spleen, and plasma. These findings position ACBP/DBI as a mechanistic amplifier of sepsis pathophysiology and propose its neutralization, alone or in combination with corticosteroids, as a promising therapeutic strategy to interrupt the fatal trajectory of septic shock.

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