Volume 301, August 2011
Kelleher ZT, Potts EN, Brahmajothi MV, Foster MW, Auten RL, Foster WM, Marshall HE.
NOS2 regulation of LPS-induced airway inflammation via S-nitrosylation of NF-κB p65. Am J Physiol Lung Cell Mol Physiol 301: L327–L333, 2011; doi: 10.1152/ajplung.00463.2010.
The cytokine data presented in Fig. 3 are not reliable due to concerns regarding the work product from the laboratory that performed these measurements. We have repeated the experiment and confirmed increased levels of IL-1β, KC, and MIP-1β in the bronchoalveolar lavage fluid (BALF) from NOS2−/− mice compared with wild-type controls. Differences in BALF levels of IL-6, TNFα, and GM-CSF were found not to be statistically significant (P > 0.05). Due to the discrepancy, we have corrected Fig. 3 and its legend.
While we acknowledge differences in the repeat BALF cytokine analysis, the changes do not alter the conclusion that NOS2 activity in the respiratory epithelium modulates airway inflammation via inhibitory S-nitrosylation of NF-κB. In addition to NF-κB, there are numerous other transcriptional regulators (e.g., histone deacetylases), cell processes (e.g., protein degradation, cell secretion), and other cell types (e.g., alveolar macrophages) that serve to regulate airway cytokine levels. As such, a uniform increase in inflammatory cytokines due to prolonged NF-κB activity in the NOS2−/− mice would not be expected.
All of the authors agree with the changes made to the publication. We regret any inconvenience caused to the journal and research community.
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