Virulence Factors of Pseudomonas aeruginosa Induce Both the Unfolded Protein and Integrated Stress Responses in Airway Epithelial Cells The authors showed that cell-free conditioned medium of the PAO1 strain of P. aeruginosa, containing secreted virulence factors, induces endoplasmic reticulum stress in primary bronchial epithelial cells as evidenced by splicing of XBP1 mRNA and induction of CHOP, GRP78 and GADD34 expression. [PLoS Pathog] Full Article Morphine Compromises Bronchial Epithelial TLR2/IL17R Signaling Crosstalk, Necessary for Lung IL17 Homeostasis Researchers showed that early induction of IL17 from the bronchial epithelium, following pathogenic encounter is a protective response, which contributes to pathogenic clearance and currently attributed to TLR2 activation in immune cells. [Sci Rep] Full Article Aryl Hydrocarbon Receptor Agonists Upregulate VEGF Secretion from Bronchial Epithelial Cells By treating HBE-135, Beas-2B, and primary human bronchial epithelial cells (BECs) with aryl hydrocarbon receptor (AhR) agonists, the mechanisms through which AhR modulated vascular endothelial growth factor (VEGF) expression in human BECs were investigated. [J Mol Med] Abstract Aspergillus fumigatus Activates PAR-2 and Skews Toward a Th2 Bias in Airway Epithelial Cells Researchers tested the hypothesis that A. fumigatus (AF) can modulate the response of airway epithelial cells to favor a Th2 response. Exposure of bronchial epithelial cells to AF extract suppressed poly I:C and HRV16 signaling via PAR-2 activation. [Am J Respir Cell Mol Biol] Abstract Fibroblast-Epithelial Cell Interactions Drive Epithelial-Mesenchymal Transition Differently in Cells from Normal and COPD Patients Scientists investigated the hypothesis that epithelial-to-mesenchymal transition (EMT) is active in human bronchial epithelial cells of chronic obstructive pulmonary disease (COPD) patients, and that mediators secreted by lung fibroblasts from COPD patients induce EMT. [Respir Res] Abstract | Full Article LUNG CANCER A Non-Tight Junction Function of Claudin-7—Interaction with Integrin Signaling in Suppressing Lung Cancer Cell Proliferation and Detachment Claudin-7 co-localizes and forms a stable complex with integrin β1. Both suppressing claudin-7 expression by lentivirus shRNA in human lung cancer cells and deletion of claudin-7 in mouse lungs lead to the reduction in integrin β1 and phospho-FAK levels. [Mol Cancer] Full Article Novel EPHB4 Receptor Tyrosine Kinase Mutations and Kinomic Pathway Analysis in Lung Cancer Scientists reported the identification of novel EPHB4 mutations that lead to putative structural alterations as well as increased cellular proliferation and motility. They showed that EPHB4 mutations can induce broad changes in the kinome signature of lung cancer cells. [Sci Rep] Full Article Genetic and Functional Analysis of Polymorphisms in the Human Dopamine Receptor and Transporter Genes in Small Cell Lung Cancer Cell treatment with the dopamine (DA) D1 receptor antagonist SCH23390 inhibited SKF38393 effects. In contrast, the DA D2 receptor agonist quinpirole counteracted, in a dose and time dependent way, small cell lung cancer cell proliferation, it did not affect cAMP levels and decreased phosphorylated AKT that was induced by DA D2 receptor antagonist sulpiride. [J Cell Physiol] Abstract Epigenetic Regulation of miR-129-2 and Its Effects on the Proliferation and Invasion in Lung Cancer Cells To investigate whether DNA methylation alters the expression of microRNA (miR)-129 in lung cancer, scientists performed DNA methylation assays and found that 5′ untranslated region of miR-129-2 gene was absolutely methylated in both A549 and SPCA-1 lung cancer cells, but totally un-methylated in 95-D cells. [J Cell Mol Med] Full Article Sanguinarine-Induced Apoptosis in Lung Adenocarcinoma Cells Is Dependent on Reactive Oxygen Species Production and Endoplasmic Reticulum Stress The authors explored the anticancer properties of sanguinarine (SAN) in lung cancer using the human lung adenocarcinoma cell line SPC-A1. They revealed that SAN inhibited SPC-A1 cell growth and induced apoptosis in a dose-dependent manner. [Oncol Rep] Abstract |