PGC-1α Mediates a Metabolic Host Defense Response in Human Airway Epithelium during Rhinovirus Infections

Researchers observed that early Human rhinoviruses (HRV)-C15 infection induced a transitory barrier-protective metabolic state characterized by glycolysis that ultimately became exhausted as the infection progresses and led to cellular damage.
[Nature Communications]
Michi, A. N., Yipp, B. G., Dufour, A., Lopes, F., & Proud, D. (2021). PGC-1α mediates a metabolic host defense response in human airway epithelium during rhinovirus infections. Nature Communications, 12(1), 3669. https://doi.org/10.1038/s41467-021-23925-z Cite
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Single-Cell RNA Sequencing Identify SDCBP in ACE2-Positive Bronchial Epithelial Cells Negatively Correlates with COVID-19 Severity

Since angiotensin-converting enzyme 2 (ACE2)-positive cells were hosts for COVID-19, researchers focussed on this cell type to explore the underlying mechanisms of COVID-19.
[Journal of Cellular and Molecular Medicine]
Ma, D., Liu, S., Hu, L., He, Q., Shi, W., Yan, D., Cao, Y., Zhang, G., Wang, Z., Wu, J., & Jiang, C. (n.d.). Single-cell RNA sequencing identify SDCBP in ACE2-positive bronchial epithelial cells negatively correlates with COVID-19 severity. Journal of Cellular and Molecular Medicine, n/a(n/a). https://doi.org/https://doi.org/10.1111/jcmm.16714 Cite
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HDAC4 Induces the Development of Asthma by Increasing Slug-Upregulated CXCL12 Expression through KLF5 Deacetylation

Researchers used asthma model bronchial smooth muscle cells to measure the biological behaviors of Histone deacetylase 4 (HDAC4)-mediated Kruppel-like factor 5 (KLF5)/Slug/CXC chemokine ligand-12 (CXCL12) axis on the development of asthma in regulation of airway inflammation and remodeling.
[Journal of Translational Medicine]
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Inhibition of miR-1298-5p Attenuates Sepsis Lung Injury by Targeting SOCS6

miR-1298-5p and suppressor of cytokine signaling 6 (SOCS6) were silenced or overexpressed in human bronchial epithelial cells. PKH-67 Dye was used to trace exosome endocytosis.
[Molecular and Cellular Biochemistry]
Ma, J., Xu, L.-Y., Sun, Q.-H., Wan, X.-Y., & BingLi. (2021). Inhibition of miR-1298-5p attenuates sepsis lung injury by targeting SOCS6. Molecular and Cellular Biochemistry. https://doi.org/10.1007/s11010-021-04170-w Cite
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Synergistic Cycles of Protease Activity and Inflammation via PPARγ Degradation in Chronic Obstructive Pulmonary Disease

Scientists evaluated the effect of neutrophil elastase on lipopolysaccharide – induced interleukin 8 production and determined the molecular mechanism in human bronchial epithelial cells.
[Experimental and Molecular Medicine]
Kwak, N., Lee, K.-H., Woo, J., Kim, J., Lee, C.-H., & Yoo, C.-G. (2021). Synergistic cycles of protease activity and inflammation via PPARγ degradation in chronic obstructive pulmonary disease. Experimental & Molecular Medicine, 1–9. https://doi.org/10.1038/s12276-021-00626-7 Cite
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Pharmacological Activation of STING Blocks SARS-CoV-2 Infection

To identify potent antiviral innate immune agonists, researchers screened a panel of 75 microbial ligands that activate diverse signaling pathways and identified cyclic dinucleotides, canonical STING agonists, as antiviral.
[Science Immunology]
Li, M., Ferretti, M., Ying, B., Descamps, H., Lee, E., Dittmar, M., Lee, J. S., Whig, K., Kamalia, B., Dohnalová, L., Uhr, G., Zarkoob, H., Chen, Y.-C., Ramage, H., Ferrer, M., Lynch, K., Schultz, D. C., Thaiss, C. A., Diamond, M. S., & Cherry, S. (2021). Pharmacological activation of STING blocks SARS-CoV-2 infection. Science Immunology, 6(59). https://doi.org/10.1126/sciimmunol.abi9007 Cite
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Potential Role for EZH2 in Promotion of Asthma through Suppression of miR-34b Transcription by Inhibition of FOXO3

Researchers investigated the molecular mechanism of enhancer of zeste homolog 2 (EZH2) in the development of asthma.
[Laboratory Investigation]
Liu, B., Sun, H., Wang, J., Liu, H., & Zhao, C. (2021). Potential role for EZH2 in promotion of asthma through suppression of miR-34b transcription by inhibition of FOXO3. Laboratory Investigation, 1–13. https://doi.org/10.1038/s41374-021-00585-7 Cite
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Incense Smoke-Induced Oxidative Stress Disrupts Tight Junctions and Bronchial Epithelial Barrier Integrity and Induces Airway Hyperresponsiveness in Mouse Lungs

Using mouse and cell culture models, the authors evaluated the effects of incense smoke exposure on airway hyperresponsiveness, expression of multiple epithelial tight junction- and adherens junction-associated mRNAs and proteins in the lungs, and the barrier function of bronchial epithelial cells assessed by transepithelial electronic resistance.
[Scientific Reports]
Yamamoto, N., Kan-o, K., Tatsuta, M., Ishii, Y., Ogawa, T., Shinozaki, S., Fukuyama, S., Nakanishi, Y., & Matsumoto, K. (2021). Incense smoke-induced oxidative stress disrupts tight junctions and bronchial epithelial barrier integrity and induces airway hyperresponsiveness in mouse lungs. Scientific Reports, 11(1), 7222. https://doi.org/10.1038/s41598-021-86745-7 Cite
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SARS-CoV-2 Variants Reveal Features Critical for Replication in Primary Human Cells

By integrating viral sequencing data from patient material, virus stocks, and passaging experiments, together with kinetic virus replication data from nonhuman Vero-CCL81 cells and primary differentiated human bronchial epithelial cells (BEpCs), scientists observed several SARS-CoV-2 features that associated with distinct phenotypes.
[PLOS Biology]
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Panaxydol Attenuates Ferroptosis against LPS-Induced Acute Lung Injury in Mice by Keap1-Nrf2/HO-1 Pathway

In vivo, the role of panaxydol (PX) on lipopolysaccharide (LPS)-induced acute lung injury in mice was tested by determination of LPS-induced pulmonary inflammation, pulmonary edema and ferroptosis. In vitro, BEAS-2B cells were used to investigate the molecular mechanisms by which PX functions via determination of inflammation, ferroptosis and their relationship.
[Journal of Translational Medicine]
Panaxydol attenuates ferroptosis against LPS-induced acute lung injury in mice by Keap1-Nrf2/HO-1 pathway | Journal of Translational Medicine | Full Text. (n.d.). Retrieved March 4, 2021, from https://translational-medicine.biomedcentral.com/articles/10.1186/s12967-021-02745-1 Cite
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PGC-1α Regulates Airway Epithelial Barrier Dysfunction Induced by House Dust Mite

BEAS-2B cells were exposed to house dust mite and the expressions of PGC-1α and E-cadherin were examined by immunoblotting.
[Respiratory Research]
Saito, T., Ichikawa, T., Numakura, T., Yamada, M., Koarai, A., Fujino, N., Murakami, K., Yamanaka, S., Sasaki, Y., Kyogoku, Y., Itakura, K., Sano, H., Takita, K., Tanaka, R., Tamada, T., Ichinose, M., & Sugiura, H. (2021). PGC-1α regulates airway epithelial barrier dysfunction induced by house dust mite. Respiratory Research, 22(1), 63. https://doi.org/10.1186/s12931-021-01663-6 Cite
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