Correction: Ozone Inhalation Promotes CX3CR1-Dependent Maturation of Resident Lung Macrophages That Limit Oxidative Stress and Inflammation

Abstract

Following an inquiry at Duke University, we have been informed that FlexiVent data provided to us by the animal pulmonary physiology laboratory may have been unreliable. The data in Figs. 1-4 are not affected. We have replicated the studies in Fig. 5A-F, and the new data support the originally published findings. We were unable to repeat the experiments in Fig. 5G; therefore, to maintain the accuracy of the scientific record, a corrected Fig. 5 and figure legend, representing the new data, are shown below. www.jimmunol.org/cgi/doi/10.4049/jimmunol.1600002 FIGURE 5. Ozone exposure in CX3CR1-null mice. C57BL/6 (WT) and CX3CR1 GFP/GFP (CX3CR1-null) mice were exposed to filtered air or 2 ppm of ozone for 3 h and then underwent analysis 12-24 h after exposure. A, Flow cytometric analysis of Gr-1 Macs in WT (open box) and CX3CR1-null mice (closed box) as a percentage of total cells at 24 h after exposure to filtered air (FA) or ozone. B, CX3CL1 protein expression was analyzed by ELISA in BAL from WT and CX3CR1-null mice 24 h after filtered air (open box) or ozone (closed box) exposure. C, AHR after increasing doses of methacholine in WT and CX3CR1-null mice 24 h after filtered air or ozone exposure. D, Total cells and neutrophils (PMNs) from BAL cell count differentials in WT (open box) and CX3CR1-null mice (closed box) 24 h after filtered air or ozone exposure. E, Analysis of total protein in BAL from WT (open box) and CX3CR1-null mice (closed box) 24 h after filtered air or ozone exposure. F, Analysis of cytokines by multiplex from concentrated BAL fluid in WT (open box) and CX3CR1-null mice (closed box) 12 h after filtered air or ozone exposure. Data for AHR are from n 5 7 WT FA, n 5 7 CX3CR1-null FA, n 5 12 WT O3, and n 5 14 CX3CR1-null O3 (# p , 0.05 for WT or CX3CR1-null O3 versus FA control, *p , 0.05 for WT versus CX3CR1-null O3 exposed, & p , 0.05 for WT versus CX3CR1-null FA exposed). Data for other experiments are from three to eight mice per group (WT-FA, WT-ozone, CX3CR1-null-FA, and CX3CR1-null-ozone).

Modeling the Role of Lanthionine Synthetase C-Like 2 (LANCL2) in the Modulation of Immune Responses to Helicobacter pylori Infection

“…For instance, we hypothesize that a population of CX3CR1+ macrophages may be required for the promotion of a regulatory environment that balances excessive inflammation and effector responses. In support of this hypothesis, this population has been associated with beneficial effects in inflammatory bowel disease (IBD), allergic responses in the lung, gastrointestinal cancers and steatohepatitis [15,16,17,18]. As a cell type that has only recently gained prominence, relatively little is known about the differentiation into and maturation of this phenotype.…”