Dysregulation of sputum columnar epithelial cells and products in distinct asthma phenotypes

Qin, Ling; Gibson, Péter G.; Simpson, Jodie L.; Baines, Katherine J.; McDonald, Vanessa M.; Wood, Lisa G.; Powell, Heather; Fricker, Michael

doi:10.1111/cea.13452

Cited by 11 publications

(10 citation statements)

References 42 publications

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“…Of note, POSTN acts on α M β 2 /CD11b [32] and may thus directly induce eosinophil migration, which may subsequently act to further increase mucus secretion as eosinophilic cationic protein is a well-known mediator of mucus production. It is also of interest to mention that high levels of POSTN were detected in epithelial columnar cell-high sputum of asthma patients with eosinophilia [33]. This may reflect an eosinophil and/or Type-2 immune signalling function of epithelial cells that secrete high levels of POSTN.…”

Section: Discussionmentioning

confidence: 90%

Periostin: contributor to abnormal airway epithelial function in asthma?

et al. 2020

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Periostin may serve as a biomarker for type-2-mediated eosinophilic airway inflammation in asthma. We hypothesised that type-2 cytokine IL-13 induces airway epithelial expression of periostin, which in turn contributes to epithelial changes observed in asthma.We studied the effect of IL-13 on periostin expression in BEAS-2B and air-liquid interface (ALI)-differentiated primary bronchial epithelial cells (PBECs). Additionally, effects of recombinant human periostin on epithelial-to-mesenchymal transition (EMT) markers and mucin genes were assessed. In bronchial biopsies and induced sputum from asthma patients and healthy controls, we analysed periostin single cell gene expression and protein levels.IL-13 increased POSTN expression in both cell types, which was accompanied by EMT-related features in BEAS-2B. In ALI-differentiated PBECs, IL-13 increased periostin basolateral and apical release. Apical administration of periostin increased the expression of MMP9, MUC5B and MUC5AC. In bronchial biopsies, POSTN expression was mainly confined to basal epithelial cells, ionocytes, endothelial cells and fibroblasts, showing higher expression in basal epithelial cells from asthma patients versus controls. Higher protein levels of periostin, expressed in epithelial and subepithelial layers, was confirmed in bronchial biopsies from asthma patients compared to healthy controls. Although sputum periostin levels were not higher in asthma, levels correlated with eosinophil numbers and coughing up mucus.Periostin expression is increased by IL-13 in bronchial epithelial cells and higher in bronchial biopsies from asthma patients. This may have important consequences, as administration of periostin increased epithelial expression of mucin genes, supporting the relationship of periostin with type-2 mediated asthma and mucus secretion.

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Section: Discussionmentioning

confidence: 90%

Periostin: contributor to abnormal airway epithelial function in asthma?

et al. 2020

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“…Other epigenomic events could be important after 2 weeks of infection with strain BL as suggested by the network analysis that informs expression of the nuclear receptor coactivator 1 (NCOA1 or SRC-1), which is a transcriptional co-regulatory protein that shows several nuclear receptor interacting domains and an intrinsic histone acetyltransferase activity that modulate gene expression [ 61 ]. Another significant cellular activity was cellular proliferation, considering the over-expression of the gene that codifies the protein Ctps2, which is the rate-limiting enzyme in the synthesis of cytosine nucleotides related to cellular replication [ 62 ]. Thus, BL strain produced a change in the expression profile after 2 weeks of infection that decreased the pro-inflammatory response, but at day 28 dpi the strong pro-inflammatory response returned as suggested by the lack of the sphingosine kinase gene expression, that probably contributed to the development of rapid and extensive pneumonia producing the animal’s death by respiratory insufficiency [ 63 ].…”

Section: Discussionmentioning

confidence: 99%

Profiling the immune response to Mycobacterium tuberculosis Beijing family infection: a perspective from the transcriptome

Irene

Rodríguez-Castillo

López-Leal³

et al. 2021

Virulence

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Tuberculosis continues to be an important public health problem. Particularly considering Beijingfamily strains of Mycobacterium tuberculosis, which have been associated with drug-resistance and hypervirulence. The Beijing-like SIT190 (BL) is the most prevalent Beijing strain in Colombia. The pathogenic mechanism and immune response against this pathogen is unknown. Thus, we compared the course of pulmonary TB in BALB/c mice infected with Classical-Beijing strain 391 and BL strain 323. The disease course was different among infected animals with Classical-Beijing and BL strain. Mice infected with BL had a 100% mortality at 45 days post-infection (dpi), with high bacillary loads and massive pneumonia, whereas infected animals with Classical-Beijing survived until 60 dpi and showed extensive pneumonia and necrosis. Lung RNA extraction was carried out at early (day 3 dpi), intermediate (day 14 dpi), and late (days 28 and 60 dpi) time points of infection. Transcriptional analysis of infected mice with Classical-Beijing showed several overexpressed genes, associated with a pro-inflammatory profile, including those for coding for CCL3 and CCL4 chemokines, both biomarkers of disease severity. Conversely, mice infected with BL displayed a profile which included the over-expression of several genes associated with immunesuppression, including Nkiras, Dleu2, and Sphk2, highlighting an anti-inflammatory milieu which would allow high bacterial replication followed by an intense inflammatory response. In summary, both Beijing strains induced a non-protective immune response which induced extensive tissue damage, BL strain induced rapidly extensive pneumonia and death, whereas Classical-Beijing strain produced slower extensive pneumonia later associated with extensive necrosis.

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“…Thus, these 8 genes are considered as potential prognostic markers for ESCC. In previous study, CFAP53 has been detected in the bronchial epithelium (22), and is highly expressed in the sputum of asthmatics. FCGR2A gene polymorphism is related to the prognosis and treatment response of a variety of cancer types.…”

Section: Discussionmentioning

confidence: 75%

Development of a prognostic nomogram based on an eight-gene signature for esophageal squamous cell carcinoma by weighted gene co-expression network analysis (WGCNA)

Xie¹,

Yang²,

Wei³

et al. 2022

Ann Transl Med

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Background: Esophageal squamous cell carcinoma (ESCC) is a highly aggressive malignant tumor. This study aims to develop a robust prognostic model for ESCC. Methods: Expression profiles of ESCC were downloaded from the Gene Expression Omnibus (GEO) andThe Cancer Genome Atlas (TCGA) databases. Co-expressed modules were constructed by weighted gene co-expression network analysis (WGCNA). Differentially expressed genes (DEGs) between ESCC and normal samples were identified with the screening criteria of adjusted P value <0.05 and log |fold change (FC)| >1. After univariate and multivariate Cox regression analysis, an 8-gene module was constructed. A receiver operating characteristic (ROC) curve for overall survival (OS) was used to assess the prediction efficacy of the risk score. A nomogram was developed based on the risk score, age, gender, and stage for 1-, 2and 3-year survival. The potential biological functions and pathways of the 8 genes were predicted using the Metascape database. Results:The 2 ESCC-related co-expression modules were built via WGCNA. Among all DEGs, 55 survival-related genes were identified for ESCC. Based on these genes, an 8-gene module was constructed, composed of CFAP53, FCGR2A, FCGR3A, GNGT1, IGF2, LINC01524, MAGEA3, and MAGEA6. The area under the curve (AUC) was 0.961, suggesting that the risk score could effectively predict the OS of patients with ESCC. Furthermore, the nomogram exhibited high accuracy in predicting the survival rate of ESCC patients at 1, 2, and 3 years. These genes were mainly involved in ESCC-related pathways such as extracellular matrix organization, collagen formation, and blood vessel development.Conclusions: Our nomogram based on the 8-gene risk score could be a reliable prognostic tool for ESCC.

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Dysregulation of sputum columnar epithelial cells and products in distinct asthma phenotypes

Cited by 11 publications

References 42 publications

Periostin: contributor to abnormal airway epithelial function in asthma?

Periostin: contributor to abnormal airway epithelial function in asthma?

Profiling the immune response to Mycobacterium tuberculosis Beijing family infection: a perspective from the transcriptome

Development of a prognostic nomogram based on an eight-gene signature for esophageal squamous cell carcinoma by weighted gene co-expression network analysis (WGCNA)

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