John D. Snyder1,2†Tae Won Yoon1,2†Sangmin Lee2Priyanka Halder2Elizabeth Ann Fitzpatrick1,2Ae-Kyung Yi1,2*1Integrated Biomedical Science Graduate Program, The University of Tennessee Health Science Center, Memphis, TN, United States2Department of Microbiology, Immunology and Biochemistry, The University of Tennessee Health Science Center, Memphis, TN, United States

In the published article, there was an error in Figure 2 as published. The panel numbers (A, B, C) are missing. The corrected Figure 2 and its caption appear below.

Figure 2. PKD1 in myeloid lineage cells is dispensable for the initial cytokine and chemokine expression in the lungs of mice in response to S. rectivirgula inhalation. PKD1fl/fl mice (WT) and PKD1fl/fl-LyZCre mice (PKD1mKO) were exposed intranasally to saline or S. rectivirgula (100 μg) for 2 h (A) or 6 h (B, C). (A, B) Total RNA was purified from lung lobes isolated from each individual mouse and reverse transcribed, and then mRNA levels of the indicated genes were analyzed in duplicate by real-time qPCR using SYBR Green Assay. The data on genes that were differentially expressed were normalized to the expression of the housekeeping gene [Actin for panel (A) and GAPDH for panel (B)]. Fold change comparing S. rectivirgula-exposed WT mice and S. rectivirgula-exposed PKD1mKO mice to control saline-exposed mice were calculated by comparative quantification algorithm-delta delta Ct method (fold difference = 2−ΔΔCt). Data represent the mean (Fold) ± SD. (C) Bronchoalveolar lavage (BAL) was performed. Levels of the indicated cytokines and chemokines in BAL fluid were detected by multiplex sandwich assay. Data present the mean concentration (pg/mL) ± SD. Number of mice used for each group is as follows: Saline, n = 2 to 6; WT-SR, n = 3 to 4; PKD1mKO-SR, n = 4 to 5. Statistically significant difference determined by one-way ANOVA with Tukey’s post-hoc test is indicated (*p < 0.05; **p < 0.01; ***p < 0.001; ****p < 0.0001). ns, not significant.

The authors apologize for this error and state that this does not change the scientific conclusions of the article in any way. The original article has been updated.

All claims expressed in this article are solely those of the authors and do not necessarily represent those of their affiliated organizations, or those of the publisher, the editors and the reviewers. Any product that may be evaluated in this article, or claim that may be made by its manufacturer, is not guaranteed or endorsed by the publisher.

Keywords: protein kinase D1, cytokines/chemokines, inflammation, alveolitis, Saccharopolyspora rectivirgula, hypersensitivity pneumonitis, toll-like receptor signaling

Citation: Snyder JD, Yoon TW, Lee S, Halder P, Fitzpatrick EA and Yi A-K (2024) Corrigendum: Protein kinase D1 in myeloid lineage cells contributes to the accumulation of CXCR3+CCR6+ nonconventional Th1 cells in the lungs and potentiates hypersensitivity pneumonitis caused by S. rectivirgula. Front. Immunol. 15:1513635. doi: 10.3389/fimmu.2024.1513635

Received: 18 October 2024; Accepted: 21 October 2024;
Published: 05 November 2024.

Copyright © 2024 Snyder, Yoon, Lee, Halder, Fitzpatrick and Yi. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

*Correspondence: Ae-Kyung Yi, ayi@uthsc.edu

†These authors have contributed equally to this work