• Jeanne Godon, Pierre-Emmanuel Charles, Sylvie Nguyen, de BarrosJean-Paul PaisJPLipidomic Analytic Platform, Dijon, France., Hélène Choubley, Marine Jacquier, Jennifer Tetu, QuenotJean-PierreJPDepartment of Intensive Care, Dijon-Bourgogne University Hospital, Dijon, France.Lipness Team, INSERM Research Centre LNC-UMR1231 and LabEx LipSTIC, University of Burgundy, Dijon, France.CHU Dijon-Bourgogne, INSERM, Université de Bourgo, Maxime Luu, Christine Binquet, David Masson, Lionel Piroth, Mathieu Blot, and Pneumotoxemia study group.
• Department of Infectious Diseases, Dijon-Bourgogne University Hospital, Dijon, France.
• Eur. J. Clin. Invest. 2024 Jan 1; 54 (1): e14077e14077.

BackgroundCirculating endotoxins could result from bacterial digestive translocation during sepsis, thus contributing to uncontrolled systemic inflammation, leading in turn to organ dysfunction. We addressed this issue in the setting of severe pneumococcal pneumonia.MethodsEndotoxemia was measured in a clinically relevant rabbit model of ventilated pneumococcal pneumonia and in 110 patients with bacteraemic pneumonia, using a patented mass spectrometry (LC-MS/MS) method for detection of 3-OH fatty acids (C10, C12, C14, C16 and C18), which are molecules bound to the lipid A motif of LPS.ResultsWhereas higher levels of systemic inflammation and organ dysfunctions were found, there was no significant difference in lipopolysaccharide concentrations when infected rabbits were compared to non-infected ones, or when patients were compared to healthy volunteers.ConclusionsSeemingly, endotoxins do not drive the overwhelming inflammation associated with severe forms of pneumococcal pneumonia.© 2023 Stichting European Society for Clinical Investigation Journal Foundation. Published by John Wiley & Sons Ltd.

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