Infection and sepsis 34 items
What CETP does during bacterial infection, and whether inhibiting it helps. A secondary thread with more evidence behind it than most readers expect: Mendelian randomisation finds genetically proxied CETP inhibition protects against sepsis, anacetrapib improves survival in pneumococcal sepsis in mice, and endotoxin has been known since the 1990s to suppress CETP. Not all of it agrees, which is why the thread is worth reading whole.
Studies
- Despite no direct LPS-binding activity, human CETP raises mortality in mouse models of endotoxemia and sepsis by impairing lipoprotein-mediated protection (J Lipid Res 2020)
- Landmark hypothesis proposes CETP as an immunological gatekeeper that could be repurposed to treat sepsis (Trends Endocrinol Metab 2020)
- Human CETP transgenic mice show higher survival and lower IL-6 after polymicrobial sepsis, linked to reduced macrophage TLR4 and NF-kB activation (Mediators Inflamm 2016)
- CETP discovered to protect mice against lethal bacterial endotoxin by dampening the inflammatory response (Shock 2008)
- Mendelian randomization finds genetically proxied CETP inhibition reduces sepsis-related critical care admission and death (World J Emerg Med 2025)
- Genetic evidence suggests the HDL cholesterol-sepsis association is not causally mediated through CETP (Clin Transl Sci 2023)
- A specific CETP isoform tracks disease severity and may help neutralize bacterial toxin in Gram-negative sepsis (Mol Med 2022)
- Genetic and drug-based CETP inhibition preserves HDL and improves survival in sepsis, in humans and humanized mice (Circulation 2021)
- A rare CETP variant lowers HDL cholesterol and predicts worse survival in sepsis, with Mendelian randomization suggesting causation (Am J Respir Crit Care Med 2019)
- Falling CETP levels during hospitalization predict mortality in patients with severe sepsis (Eur J Clin Invest 2010)
- Endotoxin cuts CETP levels below 20 percent of normal in hamsters, partly via TNF and interleukin-1 (J Clin Invest 1996)
- Mouse mechanism study: CETP inhibition raises HDL, which blocks IL-1beta activation via SR-B1 and cuts endotoxaemia mortality (J Lipid Res 2025)
- Anacetrapib reduces mortality from pneumococcal sepsis in mice by priming monocytes and speeding bacterial clearance (JCI Insight 2024)
- Mendelian randomisation finds genetically proxied CETP inhibitors protect against sepsis, an effect explained largely by ApoA-I (Front Cardiovasc Med 2023)
- Metabolic liver inflammation in obesity does not clearly lower CETP, unlike bacterial-endotoxin activation of Kupffer cells (Atherosclerosis 2018)
- Bacterial LPS lowers CETP by switching off resting Kupffer cells, an anti-inflammatory response that raises HDL during infection (J Am Heart Assoc 2018)
- Sirtori weighs the cancer and sepsis signals of torcetrapib against the dramatic 139% HDL rise seen with anacetrapib (Expert Opin Investig Drugs 2011)
- Brucella infection raises CETP activity and leaves an unresolved atherogenic lipid profile four months after treatment (J Lipid Res 2009)
- CETP-mediated cholesterol transfer cannot substitute for SR-BI in adrenal steroid production (J Lipid Res 2009)
- Chimeric fusions of CETP with the bacterial-binding protein BPI retain function from both parent proteins up to a threshold (Biochemistry 2006)
- Endotoxin suppresses CETP via adrenal corticosteroid release, raising HDL in transgenic mice (J Clin Invest 1995)
- Review highlights CETP inhibition improving survival in a mouse model of sepsis (Curr Opin Lipidol 2026)
- Bacterial iron-chelating pigments called ferroverdins turn out to be potent CETP inhibitors, with 43 new structural variants identified (Biomolecules 2022)
- CETP pushes macrophages toward the M2 phenotype and worsens elastase-induced emphysema in mice, an unexpected lung-disease link (Front Immunol 2021)
- Review argues patient stratification, and caution in sepsis, are needed before CETP can succeed as a drug target (Expert Opin Ther Targets 2015)
- The rodent-specific scavenger receptor MARCO drives the off-target lipid uptake seen with dalcetrapib in mouse macrophages (Toxicol In Vitro 2010)
- Torcetrapib does not block CETP or LPS-binding-protein interactions, ruling out a direct sepsis-mortality mechanism (J Lipid Res 2010)
- Review highlights a paradox, CETP protects against bacterial infection but promotes atherosclerosis (Atherosclerosis 2009)
- JTT-705, the dalcetrapib precursor compound, blocks LPS-triggered TNF-alpha production in mice by targeting a cysteine on MD-2 (J Biol Chem 2009)
- ALPS study finds CETP mass changes track LDL cholesterol, not HDL, with the probucol derivative AGI-1067 (J Clin Lipidol 2007)
- Review proposes CETP inhibition among potential HDL-directed treatments for sepsis (Int J Mol Sci 2022)
- A CETP isoform, CETPI, is highlighted as a newly described contributor to LPS inactivation in the gut-liver axis of sepsis (Biomed Pharmacother 2021)
- Unlike LBP, its structural relatives BPI, CETP and PLTP show no expression difference in necrotizing enterocolitis, isolating LBP as the disease-associated biomarker (J Pediatr Surg 2026)
- Single endotoxin dose triggers rapid LDL decline and slower CETP activity loss in healthy volunteers (J Lipid Res 2003)