Correction: Plasma polymeric immunoglobulin receptor exacerbates lung injury in Klebsiella pneumoniae-induced pneumosepsis

Shuaiwei Wang¹Hao Fu²Xiaoqing Li³Hongrui Xu¹Yu Bai¹Wenjun Jiang¹Xiaozhe Cheng¹Na Chen¹Yijie Zhang⁴Wei Li^1*

• ¹Henan University, Kaifeng, China
• ²The Fifth Affiliated Hospital of Zunyi Medical University, Zhuhai, Guangdong, China
• ³The First People’s Hospital, Shangqiu, Henan, China
• ⁴Luohe Medical College, Luohe, China

In the published article, there was a typographical error in the legend for Figure 2B as published. The symbol (&) needs to be removed. The corrected legend appears below.(B) Comparisons of pIgR concentrations in CAP subjects (SOFA = 0, n = 33) with PIS subjects with different degrees of organ dysfunctions (SOFA scores). The n values are 29, 69, 48, 43, 40, 39, 25, 35, 33, 20, 22 and 46 for SOFA groups 2 to ≥ 13, respectively. Kruskal-Wallis test was used to calculate p values. *p < 0.05; ***p < 0.001.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. In the published article, there was an error. During the typographical process, an ampersand (&) was added to the body text of the article. A correction has been made to 3 Results, 3.2 Elevation of plasma pIgR is associatedwith sepsis mortality, Paragraph 3. This sentence previously stated:"The median concentrations of pIgR were 779.76, 780.27 and 1041.87 ng/mL in healthy, CAP and PIS subjects, respectively (Figure 2A). pIgR concentrations were not different between healthy and CAP subjects (p = 0.47), but 34% higher in PIS group (p = 0.01, Figure 2A). Among PIS subjects, only those with multiple organ failures (SOFA score &> 12) had a significantly higher level of pIgR than CAP subjects (SOFA = 0, Figure 2B). In addition, pIgR concentration was higher in PIS patients that were destined to die (1463 ng/ml) than those survived 28 days of hospitalization (924 ng/ml, p <0.0001, Figure 2C). Consistent with the TMT-MS results, higher pIgR concentrations (> median) were associated with increased risk of death (hazard ratio = 1.912, p < 0.0001, Figure 2D)."The corrected sentence appears below:"The median concentrations of pIgR were 779.76, 780.27 and 1041.87 ng/mL in healthy, CAP and PIS subjects, respectively (Figure 2A). pIgR concentrations were not different between healthy and CAP subjects (p = 0.47), but 34% higher in PIS group (p = 0.01, Figure 2A). Among PIS subjects, only those with multiple organ failures (SOFA score > 12) had a significantly higher level of pIgR than CAP subjects (SOFA = 0, Figure 2B). In addition, pIgR concentration was higher in PIS patients that were destined to die (1463 ng/ml) than those survived 28 days of hospitalization (924 ng/ml, p <0.0001, Figure 2C). Consistent with the TMT-MS results, higher pIgR concentrations (> median) were associated with increased risk of death (hazard ratio = 1.912, p < 0.0001, Figure 2D)."In the published article, there was an error. The word 'not' is missing from the body text of the article. A correction has been made to 4 Discussion, 4.3 AT2-targeting by plasma pIgR, Paragraph 6. This sentence previously stated:"KP infection causes widespread injuries of alveolar epithelial cells, such as AT1 and AT2, as indicated by the marked reduction in GP36, SPA and SPC in KPS mouse lungs. The significant impacts of r_pIgR and pIgR_Ab on SPA and SPC, but not GP36, suggest that AT2 are preferentially targeted by plasma pIgR. This notion is consistent with the virtually exclusive localization of pIgR immunoreactivity in AT2, among all alveolar cells, in KPS mouse lungs. Since AT2 do express endogenous pIgR under physiological conditions or after bacterial infection (9, 11), the emergence of pIgR immunoreactivity likely results from a binding of extracellular pIgR. Indeed, pIgR was not detectable in primary AT2 cells before and after LPS treatment, but was evident after an exposure to r_pIgR. The further increase in pIgR in LPS-treated cells suggests