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Oral vancomycin treatment does not alter markers of postprandial inflammation in lean and obese subjects

Journal article
Authors G. J. Bakker
J. G. Schnitzler
S. Bekkering
N. C. Clercq
A. M. Koopen
A. V. Hartstra
E. C. E. Meessen
T. P. Scheithauers
M. Winkelmeijer
G. M. Dallinga-Thie
P. D. Cani
E. M. Kemper
M. R. Soeters
J. Kroon
A. K. Groen
D. H. van Raalte
H. Herrema
Max Nieuwdorp
Published in Physiological Reports
Volume 7
Issue 16
ISSN 2051-817X
Publication year 2019
Published at Wallenberg Laboratory
Institute of Medicine, Department of Molecular and Clinical Medicine
Language en
Keywords Bacterial endotoxins, bacterial translocation, inflammation, obesity, lipopolysaccharide-binding protein, augments monocyte responses, gut, microbiota, systemic inflammation, circulating monocytes, inhibitory-activity, severe sepsis, endotoxemia, fat, lps, Physiology
Subject categories Physiology


Intake of a high-fat meal induces a systemic inflammatory response in the postprandial which is augmented in obese subjects. However, the underlying mechanisms of this response have not been fully elucidated. We aimed to assess the effect of gut microbiota modulation on postprandial inflammatory response in lean and obese subjects. Ten lean and ten obese subjects with metabolic syndrome received oral vancomycin 500 mg four times per day for 7 days. Oral high-fat meal tests (50 g fat/m(2) body surface area) were performed before and after vancomycin intervention. Gut microbiota composition, leukocyte counts, plasma lipopolysaccharides (LPS), LPS-binding protein (LBP), IL-6 and MCP-1 concentrations and monocyte CCR2 and cytokine expression were determined before and after the high-fat meal. Oral vancomycin treatment resulted in profound changes in gut microbiota composition and significantly decreased bacterial diversity in both groups (phylogenetic diversity pre- versus post-intervention: lean, 56.9 +/- 7.8 vs. 21.4 +/- 6.6, P < 0.001; obese, 53.9 +/- 7.8 vs. 21.0 +/- 5.9, P < 0.001). After intervention, fasting plasma LPS significantly increased (lean, median [IQR] 0.81 [0.63-1.45] EU/mL vs. 2.23 [1.33-3.83] EU/mL, P = 0.017; obese, median [IQR] 0.76 [0.45-1.03] EU/mL vs. 1.44 [1.11-4.24], P = 0.014). However, postprandial increases in leukocytes and plasma LPS were unaffected by vancomycin in both groups. Moreover, we found no changes in plasma LBP, IL-6 and MCP-1 or in monocyte CCR2 expression. Despite major vancomycin-induced disruption of the gut microbiota and increased fasting plasma LPS, the postprandial inflammatory phenotype in lean and obese subjects was unaffected in this study.

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