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CORRECTION article

Front. Immunol., 27 November 2020
Sec. Microbial Immunology

Corrigendum: Concurrent Immune Suppression and Hyperinflammation in Patients With Community-Acquired Pneumonia

Xanthe Brands*Xanthe Brands1*Bastiaan W. HaakBastiaan W. Haak1Augustijn M. KlarenbeekAugustijn M. Klarenbeek1Natasja A. OttoNatasja A. Otto1Daniël R. FaberDaniël R. Faber2Ren LutterRené Lutter3Brendon P. Scicluna,Brendon P. Scicluna1,4W. Joost Wiersinga,W. Joost Wiersinga1,5Tom van der Poll,Tom van der Poll1,5
  • 1Center for Experimental and Molecular Medicine (CEMM), Amsterdam University Medical Centers - Location AMC, University of Amsterdam, Amsterdam, Netherlands
  • 2Department of Internal Medicine, BovenIJ Hospital, Amsterdam, Netherlands
  • 3Respiratory Medicine and Experimental Immunology, Amsterdam University Medical Centers - Location AMC, University of Amsterdam, Amsterdam, Netherlands
  • 4Department of Clinical Epidemiology, Biostatistics and Bioinformatics, Amsterdam University Medical Centers - Location AMC, University of Amsterdam, Amsterdam, Netherlands
  • 5Division of Infectious Diseases, Amsterdam University Medical Centers - Location AMC, University of Amsterdam, Amsterdam, Netherlands

A Corrigendum on
Concurrent Immune Suppression and Hyperinflammation in Patients With Community-Acquired Pneumonia

By Brands X, Haak BW, Klarenbeek AM, Otto NA, Faber DR, Lutter R, Scicluna BP, Wiersinga WJ and van der Poll T (2020). Front. Immunol. 11:796. doi: 10.3389/fimmu.2020.00796

In the original article, there was a mistake in Figures 13 as published. The colors in the legend mistakenly mislabeled the conditions. The corrected figures appear below, along with the figure legends, which remain unchanged.

FIGURE 1
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Figure 1 Blood leukocytes of patients with community-acquired pneumonia show an altered cytokine production profile upon ex vivo stimulation. Whole blood leukocytes were obtained from CAP patients at admission (n=79) and one month following admission (n=55), and from non-infected age and sex-matched controls (n=42), and stimulated for 24 hours with lipolysaccharide (LPS; 100 ng/mL) or heat-killed Klebsiella pneumoniae (Kpneu; equivalent of 12.5 * 106 CFU/mL). Cytokines were measured in supernatants. Individual data points are displayed with the horizontal line depicting the median. Dotted lines indicate the median concentrations in medium control samples (i.e., blood leukocytes incubated without stimulus), which were all significantly altered compared to LPS and Kpneu stimulation. Asterisks indicate differences between groups as indicated (*P < 0.05, **P < 0.01, ***P < 0.001). IL, interleukin; TNF, tumor necrosis factor; RA, receptor antagonist.

FIGURE 2
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Figure 2 Cytokine production of blood leukocytes from patients with community-acquired pneumonia stratified according to TNF-α production capacity. Patients were stratified into those with the lowest 25% blood leukocyte TNF-α production (low TNF-α producers, n=20) and those with the highest 25% blood leukocyte TNF-α production (high TNF-α producers, n=20) following LPS stimulation. Cytokines were measured in supernatants of whole blood leukocytes stimulated for 24 hours with lipolysaccharide (LPS; 100 ng/mL) or heat-killed Klebsiella pneumoniae (Kpneu; equivalent of 12.5 * 106 CFU/mL). Individual data points are displayed with the horizontal line depicting the median. Dotted lines indicate median concentrations in medium control samples (i.e., blood leukocytes incubated without stimulus), which were all significantly altered compared to LPS and Kpneu stimulation. Asterisks indicate differences between patients with the lowest and the highest TNF-production following LPS stimulation (*P < 0.05, **P < 0.01, ***P < 0.001). IL, interleukin; TNF, tumor necrosis factor; RA, receptor antagonist.

FIGURE 3
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Figure 3 Host response plasma biomarker levels in patients with community-acquired pneumonia with the lowest and highest blood leukocyte TNF-α production following LPS stimulation. Patients were stratified into those with the lowest 25% blood leukocyte TNF-α production (low TNF-α producers, n=20) and those with the highest 25% blood leukocyte TNF-α production (high TNF-α producers, n=20) following LPS stimulation. Plasma biomarkers were measured upon hospital admission. Individual data points are displayed with the horizontal line depicting the median. Dotted lines indicate median values obtained in 42 healthy age- and sex-matched subjects. Values in patients were all significantly different from those in healthy control subjects. Asterisks indicate differences between patients with the lowest 25% and the highest 25% TNF-production following LPS stimulation (Benjamini-Hochberg corrected, *P < 0.05, **P < 0.01). CRP, C-reactive protein; MPO, myeloperoxidase; NGAL, neutrophil gelatinase-associated lipocalin; sE-Selectin, soluble E-selectin; sTREM−1, soluble triggering receptor expressed on myeloid cells 1; sVCAM-1, soluble vascular cell adhesion protein 1; TFF3, trefoil factor 3.

The authors apologize for this error and state that this does not change the scientific conclusions of the article in any way. The original article has been updated.

Keywords: community-acquired pneumonia, immune suppression, systemic inflammation, sepsis, lipopolysaccharide

Citation: Brands X, Haak BW, Klarenbeek AM, Otto NA, Faber DR, Lutter R, Scicluna BP, Wiersinga WJ and van der Poll T (2020) Corrigendum: Concurrent Immune Suppression and Hyperinflammation in Patients With Community-Acquired Pneumonia. Front. Immunol. 11:626667. doi: 10.3389/fimmu.2020.626667

Received: 06 November 2020; Accepted: 09 November 2020;
Published: 27 November 2020.

Approved by: Frontiers Editorial Office, Frontiers Media SA, Switzerland

Copyright © 2020 Brands, Haak, Klarenbeek, Otto, Faber, Lutter, Scicluna, Wiersinga and van der Poll. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

*Correspondence: Xanthe Brands, x.brands@amsterdamumc.nl

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