Soy Biodiesel and Petrodiesel Emissions Differ in Size, Chemical Composition and Stimulation of Inflammatory Responses in Cells and Animals Researchers demonstrated that particulate matter generated by combustion of the two fuels induced different responses in in vitro and in vivo models. [Environ Sci Technol] Abstract Curcumin Prevents Replication of Respiratory Syncytial Virus and the Epithelial Responses to it in Human Nasal Epithelial Cells Researchers investigated the effects of the nuclear factor kappa B in human nasal epithelial cells infected with respiratory syncytial virus (RSV). Curcumin prevented the replication and budding of RSV and the epithelial responses to it without cytotoxicity. [PLoS One] Full Article Mitochondrial Fragmentation in Cigarette Smoke Induced-Bronchial Epithelial Cell Senescence Mitochondria in bronchial epithelial cells were prone to be more fragmented in chronic obstructive pulmonary disease lung tissues. Cigarette smoke extract induced mitochondrial fragmentation and mitochondrial reactive oxygen species production, which were responsible for acceleration of cellular senescence in human bronchial epithelial cells. [Am J Physiol Lung Cell Mol Physiol] Abstract Metabolic Shift in Lung Alveolar Cell Mitochondria following Acrolein Exposure Researchers examined the role of acrolein in altering mitochondrial function and metabolism in lung specific cells. Low-dose acrolein exposure decreased mitochondrial respiration in a dose-dependent manner due to alteration in the metabolism of glucose in three cell types. [Am J Physiol Lung Cell Mol Physiol] Abstract Respiratory Syncytial Virus Infection Disrupts Monolayer Integrity and Function in Cystic Fibrosis Airway Cells Researchers examined respiratory syncytial virus (RSV) infection in immortalized bronchial epithelial cells expressing wild-type or F508del cystic fibrosis transmembrane conductance regulator, for monolayer integrity and RSV replication. [Viruses] Abstract | Full Article LUNG CANCER The HDAC Inhibitor, MPT0E028, Enhances Erlotinib-Induced Cell Death in EGFR-TKI-Resistant NSCLC Cells Researchers combined the histone deacetylase (HDAC) inhibitor, MPT0E028, with erlotinib in an effort to increase their antitumor effects in erlotinib-resistant lung adenocarcinoma cells. This combined treatment yielded significant growth inhibition, induced the expression of apoptotic proteins, increased the levels of acetylated histone H3, and showed synergistic effects in vitro and in vivo. [Cell Death Dis] Full Article Orai3 Constitutes a Native Store-Operated Calcium Entry that Regulates Non-Small Cell Lung Adenocarcinoma Cell Proliferation Scientists investigated the expression and the role of Orai3 in cell proliferation in non-small cell lung cancer. They showed that Orai3 is over-expressed in cancer tissues as compared to the non-tumoral ones. [PLoS One] Abstract Induction of Apoptosis and Cell Cycle Arrest in A549 Human Lung Adenocarcinoma Cells by Surface Encapping Selenium Nanoparticles: An Effect Enhanced by Polysaccharides-Protein Complexes from Polyporus rhinocerus Exposure to Polyporus rhinocerus water-soluble polysaccharides-protein complexes-selenium nanoparticles significantly inhibited the growth of A549 cells through induction of apoptosis and G2/M phase arrest supported by an increase of sub-G1 and G2/M phase cell populations, DNA fragmentation and chromatin condensation. [J Agric Food Chem] Abstract Linobiflavonoid Inhibits Human Lung Adenocarcinoma A549 Cells: Effect on Tubulin Protein The antitumor bioactivities of linobiflavonoid were studied through evaluating its in vitro cytotoxicity against several cell lines, with the aid of 3-(4,5-dimethylthiazolyl)-3,5-diphenytetrazolium bromide assay. Researchers found that linobiflavonoid showed more notable inhibiting activity against A549 cells. [Mol Biol Rep] Abstract Selective Modulation of MHC Class II Chaperons by a Novel IFN-γ-Inducible Class II Transactivator Variant in Lung Adenocarcinoma A549 Cells Unlike class II transactivator (CIITA)-TAG, CIITAΔE7 is expressed more abundantly in lung adenocarcinoma A549 cells than in the non-transformed counterpart BEAS-2B cells following interferon (IFN)-γ stimulation. [Biochem Biophys Res Commun] Abstract |