Long-term IL-33–producing epithelial progenitor cells in chronic obstructive lung disease

Abstract

Some expressions and notations related to Equations 1 and 2 were presented incorrectly. The correct text and equations are below.The coefficients (β) in Cox's regression model are estimated by maximizing the partial likelihood function subject to a constraint on the L1-norm of the coefficients. The lasso estimator (β ) maximizes the objective function given below:Here l(β) is the log partial likelihood in the Cox model; for the exact form of this function, see ref. 41. The tuning parameter, λ in Equation 1, was chosen by 10-fold cross-validation. For the implementation, we used the R package "glmnet" (39).PROVAR was defined for each of the 222 TCGA samples as the sum of the estimated coefficients multiplied by protein expression levels, as shown below. Here i represents patients (i = 1,...,222), j represents proteins with nonzero coefficients (j = 1, ..., m), β j is the lasso coefficient of the jth protein marker, and X ij is the expression level of the jth protein for the ith patient. (Equation 2)The JCI regrets the error.

HMGB1 regulates IL-33 expression in acute respiratory distress syndrome

“…As with HMGB1, IL-33 is a nuclear protein and has been suggested to be an alarmin because it is released with epithelial or endothelial cell damage [24]. Moreover, IL-33 plays a proinflammatory role in many pulmonary inflammatory, such as chronic obstructive pulmonary disease (COPD), allergic asthma, lung fibrosis and pneumonia [25][26][27][28]. We therefore hypothesized that IL-33 has a proinflammatory role in ARDS, similarly as with HMGB1.…”

IL-33 and Thymic Stromal Lymphopoietin in mast cell functions

“…Although IL-33 expression is constitutive in these tissues during homeostasis it can be further enhanced during inflammatory conditions. Increased expression of IL-33 in the nuclei of human airway epithelial cells has been observed in patients with asthma (Prefontaine et al, 2010) and chronic obstructive pulmonary disease (Byers et al, 2013). Moreover, IL-33 expression is inducible in immune cells such as macrophages (Chang et al, 2011), dendritic cells (Tjota et al, 2013) and mast cells (Hsu et al, 2010) during inflammation, although at much lower levels than in epithelial cells.…”

Harnessing the potential of lung stem cells for regenerative medicine

“…More goblet cells are also found in human proximal airways and the basal cell-lined pseudostratified epithelium extends distally all the way down to the small bronchiolar airways in the human lung. However, a number of studies have recently reported the expression of basal cell markers in the distal lungs of mice after virus infection (Byers et al, 2013;Kumar et al, 2011), which indicates that the cellular composition of the lung epithelium is influenced by environmental exposure. Therefore, one could speculate that the variance in cellular diversity between mouse and human lungs could be attributed, at least in part, to the specific pathogen-free conditions of laboratory housing.…”

“…Recent insight into epithelial regeneration after viral infection has also identified a unique population of p63 + K5 + basal-like cells in regenerating bronchiolar airways and alveoli (Byers et al, 2013;Kumar et al, 2011). Basal cells are normally never seen in the bronchiolar airways or alveoli of mice and lineage-tracing studies using Krt5-CreER/ACTB-mT-EGFP mice have revealed that p63 + K5 + basal-like cells that accumulate in the alveolar parenchyma after influenza or bleomycin injury are not descendent from basal cells in the upper airways (Zheng et al, 2014).…”

“…Evidence showing that K14-expression on basal cells increases from 20% in the steady state to 100% after naphthalene injury suggests that K14 expression is context dependent (Cole et al, 2010). The association between basal cells and the transient expression of basal cell markers in bronchiolar and alveolar epithelium after viral infection (Byers et al, 2013;Kumar et al, 2011) also remains to be investigated.…”