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Correction to: CCL3 contributes to secondary damage after spinal cord injury

The Original Article was published on 27 November 2020

Correction to: J Neuroinflammation 17, 362 (2020)

Following publication of the original article [1], the authors noticed that there was a covered up area which seems to be hiding something found in Fig. 7a. The original article has been corrected.

Fig. 7
figure 1

Inflammatory response in CCL3−/− mice is reduced after SCI. a Representative images of Ly-6B.2-positive neutrophils in wild-type and CCL3–/– SCI tissue at the lesion epicenter at day 1 after injury. Scale bar = 100 μm. Arrows indicate Ly-6B.2-positive profiles. b Quantitative analysis of neutrophil recruitment shows a significant reduction of neutrophils at the lesion epicenter of CCL3–/– mice. n = 3/group. * = p value < 0.05. c Expression levels of the pro-inflammatory cytokines il-1bil-6tnfinos, and the apoptotic marker bax were significantly increased at different time points in wild-type mice compared to laminectomy controls. CCL3–/– mice, however, showed significantly lower expression levels compared to wild-type. Arginase-1 and TGFb, which can indicate anti-inflammatory properties, were significantly upregulated in CCL3–/– mice in relation to wild-type mice. IL-10 was upregulated compared to the laminectomy control but did not differ between genotypes. n = 6 wild-type, 5 CCL3–/– mice. + = p value < 0.05, ++ = p value < 0.01, +++ = p value < 0.001 (wild-type compared to laminectomy control), * < p value 0.05, *** < p value 0.0001 (CCL3–/– compared to wild-type, same day)


  1. Pelisch N, Rosas Almanza J, Stehlik KE, et al. CCL3 contributes to secondary damage after spinal cord injury. J Neuroinflammation. 2020;17:362

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Correspondence to Antje Kroner.

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Pelisch, N., Almanza, J.R., Stehlik, K.E. et al. Correction to: CCL3 contributes to secondary damage after spinal cord injury. J Neuroinflammation 18, 87 (2021).

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