Jin, L., S. Batra, D. N. Douda, N. Palaniyar, and S. Jeyaseelan. 2014. CXCL1 contributes to host defense in polymicrobial sepsis via modulating T cell and neutrophil functions. J. Immunol. 193: 3549–3558.

In the original article, Fig. 3 had an inadvertently duplicated, misplaced GAPDH blot. The spleen 6 h GAPDH blot in panel (A) was used incorrectly as the lung 24 h GAPDH blot in panel (D). Because this article was published more than seven years ago, the authors no longer had access to the original blots or samples. Therefore, the authors repeated the experiment at least twice and ran all samples and controls together on one blot. A new version of Fig. 3 is shown below. The figure legend required minor changes and is also shown below for reference.

FIGURE 3.
FIGURE 3. Activation of NF-κB, MAPK, and NADPH oxidase, and expression of adhesion molecule ICAM-1 were impaired in cxcl1−/− mice after PMS. (A) CXCL1 is essential for the activation of NF-κB during PMS induction. Phosphorylation of NF-κB/p65(Ser536), and IκBα in the homogenates from liver, lung, and spleen from cxcl1−/− as compared with WT mice. (B) Attenuated activation of MAPKs in the organs of cxcl1−/− mice. Phosphorylated p38-MAPK, ERK, and JNK in the homogenates from different organs from cxcl1−/− and WT mice were probed with their respective Abs. (C) Expression of adhesion molecule ICAM-1, but not VCAM-1, is reduced in cxcl1−/− mice. The expression levels of ICAM-1 and VCAM-1 were determined in the organs of cxcl1−/− and WT control mice after PMS for time points 6 and 24 h. (D) The activation of NADPH oxidase is impaired in cxcl1−/− mice. The expression levels of Nox2, p22phox, p67phox, and p47phox were determined in the homogenates of organs of cxcl1−/− and WT control mice by immunoblotting at 6 and 24 h after PMS. GAPDH or total p38 MAPK expression levels were assessed in all samples as internal loading control, and the blots are representative of at least two independent experiments with similar results (A–D). n = 4–6/group.
View largeDownload slide

Activation of NF-κB, MAPK, and NADPH oxidase, and expression of adhesion molecule ICAM-1 were impaired in cxcl1−/− mice after PMS. (A) CXCL1 is essential for the activation of NF-κB during PMS induction. Phosphorylation of NF-κB/p65(Ser536), and IκBα in the homogenates from liver, lung, and spleen from cxcl1−/− as compared with WT mice. (B) Attenuated activation of MAPKs in the organs of cxcl1−/− mice. Phosphorylated p38-MAPK, ERK, and JNK in the homogenates from different organs from cxcl1−/− and WT mice were probed with their respective Abs. (C) Expression of adhesion molecule ICAM-1, but not VCAM-1, is reduced in cxcl1−/− mice. The expression levels of ICAM-1 and VCAM-1 were determined in the organs of cxcl1−/− and WT control mice after PMS for time points 6 and 24 h. (D) The activation of NADPH oxidase is impaired in cxcl1−/− mice. The expression levels of Nox2, p22phox, p67phox, and p47phox were determined in the homogenates of organs of cxcl1−/− and WT control mice by immunoblotting at 6 and 24 h after PMS. GAPDH or total p38 MAPK expression levels were assessed in all samples as internal loading control, and the blots are representative of at least two independent experiments with similar results (A–D). n = 4–6/group.

FIGURE 3.
FIGURE 3. Activation of NF-κB, MAPK, and NADPH oxidase, and expression of adhesion molecule ICAM-1 were impaired in cxcl1−/− mice after PMS. (A) CXCL1 is essential for the activation of NF-κB during PMS induction. Phosphorylation of NF-κB/p65(Ser536), and IκBα in the homogenates from liver, lung, and spleen from cxcl1−/− as compared with WT mice. (B) Attenuated activation of MAPKs in the organs of cxcl1−/− mice. Phosphorylated p38-MAPK, ERK, and JNK in the homogenates from different organs from cxcl1−/− and WT mice were probed with their respective Abs. (C) Expression of adhesion molecule ICAM-1, but not VCAM-1, is reduced in cxcl1−/− mice. The expression levels of ICAM-1 and VCAM-1 were determined in the organs of cxcl1−/− and WT control mice after PMS for time points 6 and 24 h. (D) The activation of NADPH oxidase is impaired in cxcl1−/− mice. The expression levels of Nox2, p22phox, p67phox, and p47phox were determined in the homogenates of organs of cxcl1−/− and WT control mice by immunoblotting at 6 and 24 h after PMS. GAPDH or total p38 MAPK expression levels were assessed in all samples as internal loading control, and the blots are representative of at least two independent experiments with similar results (A–D). n = 4–6/group.
View largeDownload slide

Activation of NF-κB, MAPK, and NADPH oxidase, and expression of adhesion molecule ICAM-1 were impaired in cxcl1−/− mice after PMS. (A) CXCL1 is essential for the activation of NF-κB during PMS induction. Phosphorylation of NF-κB/p65(Ser536), and IκBα in the homogenates from liver, lung, and spleen from cxcl1−/− as compared with WT mice. (B) Attenuated activation of MAPKs in the organs of cxcl1−/− mice. Phosphorylated p38-MAPK, ERK, and JNK in the homogenates from different organs from cxcl1−/− and WT mice were probed with their respective Abs. (C) Expression of adhesion molecule ICAM-1, but not VCAM-1, is reduced in cxcl1−/− mice. The expression levels of ICAM-1 and VCAM-1 were determined in the organs of cxcl1−/− and WT control mice after PMS for time points 6 and 24 h. (D) The activation of NADPH oxidase is impaired in cxcl1−/− mice. The expression levels of Nox2, p22phox, p67phox, and p47phox were determined in the homogenates of organs of cxcl1−/− and WT control mice by immunoblotting at 6 and 24 h after PMS. GAPDH or total p38 MAPK expression levels were assessed in all samples as internal loading control, and the blots are representative of at least two independent experiments with similar results (A–D). n = 4–6/group.

Close modal
View Original Article
Copyright © 2022 by The American Association of Immunologists, Inc.
2022
Copyright © 2022 by The American Association of Immunologists, Inc.