Additional file 1 of DPP4 inhibition curbs systemic inflammation

Supplementary Material 1: Figure 1. A: Postoperative DPP4 enzyme activity 6h after cardiac surgery measured in human serum in the DPP4i-group compared to the control-group (n=7 patients/group; mean ± SEM; unpaired t- test). Asterisk indicates difference vs. control group (*p<0.05). Figure 2. A: Percentage of recent thymic emigrant-cells (RTE-cells) among total lymphocytes. B: T-distributed stochastic neighbor embedding (t-SNE) map and mean fluorescence intensity of T-cell immunoglobulin mucin-3 (TIM-3) positive monocytes. C: Mean fluorescence intensity (MFI) of C-X3-C Motif Chemokine Receptor 1 (CX3CR1) positive monocytes. D: t-SNE map and mean fluorescence intensity of CX3CR1 positive non-classical monocytes. E: Mean fluorescence intensity of C-C chemokine receptor type 7 (CCR7), CD163 and CD206 positive monocytes. F: t-SNE map and mean fluorescence intensity of Programmed cell death protein 1 (PD-1) positive monocytes. G: Myeloid dendritic cells (mDCs) among total PBMCs.H: Quantity of natural killer group 2 member D+ (NKG2D+) NK cells. All figures: Diabetic patients vs. diabetic patients with DPP4 inhibitor treatment 18h after surgery; n=7 patients/group; mean ± SEM; unpaired t- test. Asterisks indicate differences vs. control (*p<0.05), ns=not significant vs. control, or p- value=as indicated vs. control group. Figure 3. A: Quantitative summary of changes in cytokine and chemokine levels in diabetic control vs. diabetic patients with DPP4 inhibitor treatment 18h after cardiac surgery (Granulocyte-macrophage colony-stimulating factor (GM-CSF), interferon (IFN), interleukin (IL), interferon gamma-induced protein-10 (IP-10), monocyte chemoattractant protein-1 (MCP-1), Macrophage inflammatory protein-1 (MIP-1), tumor necrosis factor (TNF), interferon (IFN)). All figures: n=7 patients/group; mean ± SEM; unpaired t- test. Asterisk indicates difference vs. control group (*p<0.05) or p-value=as indicated vs. control group. Figure 4. A: Pulmonary edema visualized by hematoxylin and eosin-stained micrographs of murine lungs 18h after sepsis induction and injection of vehicle or DPP4 inhibitor K579. B: Quantitative summary of ventilated pulmonary area 18h after sepsis induction following administration of the DPP4 inhibitor sitagliptin after cecal ligation and puncture (CLP)/sham surgery (n=6-9 mice/group; mean ± SEM; one-way ANOVA/Bonferroni). Asterisks indicate difference vs. sham-operated mice (**p<0.01). Hashtags indicate difference vs. septic mice (###p<0.001).

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Figshare
Published
2025-01-01
DOI
https://doi.org/10.6084/m9.figshare.29926684
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Theoretical and Computational Physics
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Additional file 1 of DPP4 inhibition curbs systemic inflammation

Figshare
Theoretical and Computational Physics
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Additional file 1 of DPP4 inhibition curbs systemic inflammation

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Abstract

Supplementary Material 1: Figure 1. A: Postoperative DPP4 enzyme activity 6h after cardiac surgery measured in human serum in the DPP4i-group compared to the control-group (n=7 patients/group; mean ± SEM; unpaired t- test). Asterisk indicates difference vs. control group (*p<0.05). Figure 2. A: Percentage of recent thymic emigrant-cells (RTE-cells) among total lymphocytes. B: T-distributed stochastic neighbor embedding (t-SNE) map and mean fluorescence intensity of T-cell immunoglobulin mucin-3 (TIM-3) positive monocytes. C: Mean fluorescence intensity (MFI) of C-X3-C Motif Chemokine Receptor 1 (CX3CR1) positive monocytes. D: t-SNE map and mean fluorescence intensity of CX3CR1 positive non-classical monocytes. E: Mean fluorescence intensity of C-C chemokine receptor type 7 (CCR7), CD163 and CD206 positive monocytes. F: t-SNE map and mean fluorescence intensity of Programmed cell death protein 1 (PD-1) positive monocytes. G: Myeloid dendritic cells (mDCs) among total PBMCs.H: Quantity of natural killer group 2 member D+ (NKG2D+) NK cells. All figures: Diabetic patients vs. diabetic patients with DPP4 inhibitor treatment 18h after surgery; n=7 patients/group; mean ± SEM; unpaired t- test. Asterisks indicate differences vs. control (*p<0.05), ns=not significant vs. control, or p- value=as indicated vs. control group. Figure 3. A: Quantitative summary of changes in cytokine and chemokine levels in diabetic control vs. diabetic patients with DPP4 inhibitor treatment 18h after cardiac surgery (Granulocyte-macrophage colony-stimulating factor (GM-CSF), interferon (IFN), interleukin (IL), interferon gamma-induced protein-10 (IP-10), monocyte chemoattractant protein-1 (MCP-1), Macrophage inflammatory protein-1 (MIP-1), tumor necrosis factor (TNF), interferon (IFN)). All figures: n=7 patients/group; mean ± SEM; unpaired t- test. Asterisk indicates difference vs. control group (*p<0.05) or p-value=as indicated vs. control group. Figure 4. A: Pulmonary edema visualized by hematoxylin and eosin-stained micrographs of murine lungs 18h after sepsis induction and injection of vehicle or DPP4 inhibitor K579. B: Quantitative summary of ventilated pulmonary area 18h after sepsis induction following administration of the DPP4 inhibitor sitagliptin after cecal ligation and puncture (CLP)/sham surgery (n=6-9 mice/group; mean ± SEM; one-way ANOVA/Bonferroni). Asterisks indicate difference vs. sham-operated mice (**p<0.01). Hashtags indicate difference vs. septic mice (###p<0.001).

Figshare
University of Tennessee Health Science Center (US), University of Münster (DE), Karolinska Institutet (SE), University Hospital Münster (DE), Universitätsklinikum Würzburg (DE)
Good health and well-being
Openalex Percentile: Top 59%
Theoretical and Computational Physics
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