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Correction to Int. J. Mol. Sci. 2019, 20(10), 2395.
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Correction

Correction: Fisher, Aron B., et al. A Peptide Inhibitor of NADPH Oxidase (NOX2) Activation Markedly Decreases Mouse Lung Injury and Mortality Following Administration of Lipopolysaccharide (LPS). Int. J. Mol. Sci. 2019, 20, 2395

by
Aron B. Fisher
*,
Chandra Dodia
,
Shampa Chatterjee
and
Sheldon I. Feinstein
Institute for Environmental Medicine and Department of Physiology, University of Pennsylvania Perelman School of Medicine, Philadelphia, PA 19104, USA
*
Author to whom correspondence should be addressed.
Int. J. Mol. Sci. 2020, 21(2), 398; https://doi.org/10.3390/ijms21020398
Submission received: 12 September 2019 / Accepted: 18 November 2019 / Published: 8 January 2020
(This article belongs to the Special Issue Acute Lung Injury – New Insights into the Mechanisms and Emerging Therapies)
Browse Figures
Versions Notes
The authors wish to make the following corrections to our previously published paper [1].
Because of partially incorrect data plotted by error, replace old Figure 2
with new Figure 2.
Because of publication of the incorrect figure, replace old Figure 5
with new Figure 5.

Conflicts of Interest

The authors declare no conflict of interest.

Reference

  1. Fisher, A.B.; Dodia, C.; Chatterjee, S.; Feinstein, S.I. A Peptide Inhibitor of NADPH Oxidase (NOX2) Activation Markedly Decreases Mouse Lung Injury and Mortality Following Administration of Lipopolysaccharide (LPS). Int. J. Mol. Sci. 2019, 20, 2395. [Google Scholar] [CrossRef] [PubMed] [Green Version]
Ijms 21 00398 i002 550
Figure 2. PIP-2 inhibits the increased lung aiPLA2 activity and increased ROS generation after LPS administration. LPS (5 µg/g body weight) was administered by intratracheal (IT) instillation along with liposomes alone (labeled as LPS) or with PIP-2 in liposomes (labeled as +PIP-2). Control was liposomes alone without LPS (labeled as control). Mice were sacrificed at 6, 12, or 24 h after LPS and lungs were perfused in situ for 15 min with saline solution containing the fluorophore difluorofluoroscein diacetate (DFF-DA). Lungs were then homogenized and assayed for (A) aiPLA2 activity; and (B) fluorescence of the lung homogenate as an index of ROS production. Results are mean ± SE for n = 3 for (A) and n = 4 for (B). * p < 0.05 vs. corresponding control and corresponding +PIP-2 values at the same time point; Δ p < 0.05 vs. the corresponding value at 6 h.
Figure 2. PIP-2 inhibits the increased lung aiPLA2 activity and increased ROS generation after LPS administration. LPS (5 µg/g body weight) was administered by intratracheal (IT) instillation along with liposomes alone (labeled as LPS) or with PIP-2 in liposomes (labeled as +PIP-2). Control was liposomes alone without LPS (labeled as control). Mice were sacrificed at 6, 12, or 24 h after LPS and lungs were perfused in situ for 15 min with saline solution containing the fluorophore difluorofluoroscein diacetate (DFF-DA). Lungs were then homogenized and assayed for (A) aiPLA2 activity; and (B) fluorescence of the lung homogenate as an index of ROS production. Results are mean ± SE for n = 3 for (A) and n = 4 for (B). * p < 0.05 vs. corresponding control and corresponding +PIP-2 values at the same time point; Δ p < 0.05 vs. the corresponding value at 6 h.
Ijms 21 00398 i002
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Figure 2. PIP-2 inhibits the increased lung aiPLA2 activity and increased ROS generation that follows LPS administration. LPS (5 µg/g body weight) was administered by intratracheal (IT) instillation along with liposomes alone (labeled as LPS) or with PIP-2 in liposomes (labeled as +PIP-2). Control was liposomes alone without LPS (labeled as control). Mice were sacrificed at 6, 12, or 24 h after LPS and some lungs were perfused in situ for 15 min with saline solution (A) while others were perfused in situ for 15 min with saline solution containing the fluorophore difluorofluoroscein diacetate (DFF-DA) (B). Lungs were then homogenized and assayed for aiPLA2 activity (A), or fluorescence of the lung homogenate as an index of ROS production (B). Results are mean ± SE for n = 3 for (A) and n = 4 for (B). * p < 0.05 vs. both the corresponding control and the corresponding LPS+PIP-2 values at the same time point; § p < 0.05 vs. 12 h and 24 h LPS values; Δ p < 0.05 vs. corresponding control value.
Figure 2. PIP-2 inhibits the increased lung aiPLA2 activity and increased ROS generation that follows LPS administration. LPS (5 µg/g body weight) was administered by intratracheal (IT) instillation along with liposomes alone (labeled as LPS) or with PIP-2 in liposomes (labeled as +PIP-2). Control was liposomes alone without LPS (labeled as control). Mice were sacrificed at 6, 12, or 24 h after LPS and some lungs were perfused in situ for 15 min with saline solution (A) while others were perfused in situ for 15 min with saline solution containing the fluorophore difluorofluoroscein diacetate (DFF-DA) (B). Lungs were then homogenized and assayed for aiPLA2 activity (A), or fluorescence of the lung homogenate as an index of ROS production (B). Results are mean ± SE for n = 3 for (A) and n = 4 for (B). * p < 0.05 vs. both the corresponding control and the corresponding LPS+PIP-2 values at the same time point; § p < 0.05 vs. 12 h and 24 h LPS values; Δ p < 0.05 vs. corresponding control value.
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Ijms 21 00398 i005 550
Figure 5. PIP-2 prevents mouse mortality with high dose LPS. Mice were administered LPS (15 µg/g body weight) by intratracheal instillation and divided into two groups. At 12 h after LPS, one group was given PIP-2 in liposomes by intravenous injection (IV) while the other group (placebo) was given liposomes alone. The time of the treatment initiation (12 h after LPS) is plotted as zero time. Treatment was repeated at 12, 36, 60, and 84 h after the initial dose of PIP-2,co-incident with the plotted points. Surviving mice were sacrificed at 108 h. n = 12 for placebo and n = 11 for PIP-2.
Figure 5. PIP-2 prevents mouse mortality with high dose LPS. Mice were administered LPS (15 µg/g body weight) by intratracheal instillation and divided into two groups. At 12 h after LPS, one group was given PIP-2 in liposomes by intravenous injection (IV) while the other group (placebo) was given liposomes alone. The time of the treatment initiation (12 h after LPS) is plotted as zero time. Treatment was repeated at 12, 36, 60, and 84 h after the initial dose of PIP-2,co-incident with the plotted points. Surviving mice were sacrificed at 108 h. n = 12 for placebo and n = 11 for PIP-2.
Ijms 21 00398 i005
Ijms 21 00398 g005 550
Figure 5. PIP-2 prevents mouse mortality with high dose LPS. Mice were administered LPS (15 µg/g body weight) by intratracheal instillation and divided into two groups. At 12 h after LPS, one group was given PIP-2 (2 µg/g body weight) in liposomes by intravenous injection (IV) while the other group (placebo) was given liposomes alone. The time of treatment initiation (12 h after LPS) is plotted as zero time. Treatment was repeated at 12, 36, 60, and 84 h after the initial dose of PIP-2, as indicated by the arrows. Surviving mice were sacrificed at 108 h after start of PIP-2 (120 h after LPS). n = 12 for placebo and n = 11 for PIP-2.
Figure 5. PIP-2 prevents mouse mortality with high dose LPS. Mice were administered LPS (15 µg/g body weight) by intratracheal instillation and divided into two groups. At 12 h after LPS, one group was given PIP-2 (2 µg/g body weight) in liposomes by intravenous injection (IV) while the other group (placebo) was given liposomes alone. The time of treatment initiation (12 h after LPS) is plotted as zero time. Treatment was repeated at 12, 36, 60, and 84 h after the initial dose of PIP-2, as indicated by the arrows. Surviving mice were sacrificed at 108 h after start of PIP-2 (120 h after LPS). n = 12 for placebo and n = 11 for PIP-2.
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MDPI and ACS Style

Fisher, A.B.; Dodia, C.; Chatterjee, S.; Feinstein, S.I. Correction: Fisher, Aron B., et al. A Peptide Inhibitor of NADPH Oxidase (NOX2) Activation Markedly Decreases Mouse Lung Injury and Mortality Following Administration of Lipopolysaccharide (LPS). Int. J. Mol. Sci. 2019, 20, 2395. Int. J. Mol. Sci. 2020, 21, 398. https://doi.org/10.3390/ijms21020398

AMA Style

Fisher AB, Dodia C, Chatterjee S, Feinstein SI. Correction: Fisher, Aron B., et al. A Peptide Inhibitor of NADPH Oxidase (NOX2) Activation Markedly Decreases Mouse Lung Injury and Mortality Following Administration of Lipopolysaccharide (LPS). Int. J. Mol. Sci. 2019, 20, 2395. International Journal of Molecular Sciences. 2020; 21(2):398. https://doi.org/10.3390/ijms21020398

Chicago/Turabian Style

Fisher, Aron B., Chandra Dodia, Shampa Chatterjee, and Sheldon I. Feinstein. 2020. "Correction: Fisher, Aron B., et al. A Peptide Inhibitor of NADPH Oxidase (NOX2) Activation Markedly Decreases Mouse Lung Injury and Mortality Following Administration of Lipopolysaccharide (LPS). Int. J. Mol. Sci. 2019, 20, 2395" International Journal of Molecular Sciences 21, no. 2: 398. https://doi.org/10.3390/ijms21020398

APA Style

Fisher, A. B., Dodia, C., Chatterjee, S., & Feinstein, S. I. (2020). Correction: Fisher, Aron B., et al. A Peptide Inhibitor of NADPH Oxidase (NOX2) Activation Markedly Decreases Mouse Lung Injury and Mortality Following Administration of Lipopolysaccharide (LPS). Int. J. Mol. Sci. 2019, 20, 2395. International Journal of Molecular Sciences, 21(2), 398. https://doi.org/10.3390/ijms21020398

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