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State-of-the-Art Molecular Mechanisms of Pulmonary Pathology in USA (Closed)

Editor

Division of Pulmonary, Allergy and Critical Care Medicine, Department of Medicine, University of Alabama at Birmingham, Birmingham, AL 35294, USA
Interests: inflammatory lung diseases; aging; fibroblast growth factor signaling; klotho; cystic fibrosis; chronic obstructive pulmonary disease; pulmonary vascular remodeling; fibroblast growth factor 23
Special Issues, Collections and Topics in MDPI journals

Topical Collection Information

Dear Colleagues,

This Topical Collection aims to provide an up-to-date and comprehensive view on the state-of-the-art research activities focusing on pulmonary disease in the USA.

Based on long-term traditions of fundamental science in the USA, we would like to provide a comprehensive insight into the state-of-the-art of research activities regarding molecular mechanisms of pathogenesis and treatment in pulmonary diseases. All kinds of articles are welcome, including contributions about original investigations as well as reviews in the field. The covered topics of interest include but are not limited to the following:

  1. Lung cancer
  2. Lung microbiota
  3. Chronic inflammatory lung diseases including COPD, cystic fibrosis, bronchiectasis
  4. Lung injury and repair
  5. Lung development
  6. Biomarkers
  7. Genomics and proteomics in lung disease
  8. Airway diseases including asthma
  9. Pulmonary fibrosis
  10. Lung infections
  11. Aging and lung disease
  12. Pulmonary vascular disease
  13. Pediatric lung disease
  14. Pathological organ crosstalk including the lung

Dr. Stefanie Krick
Collection Editor

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the collection website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

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Published Papers (2 papers)

2023

18 pages, 2941 KiB  
Article
Perfluoroalkyl Substances (PFAS) Affect Inflammation in Lung Cells and Tissues
Int. J. Mol. Sci. 2023, 24(10), 8539; https://doi.org/10.3390/ijms24108539 - 10 May 2023
Cited by 2 | Viewed by 2167
Abstract
Adverse lung outcomes from exposure to per-and polyfluoroalkyl substances (PFAS) are known; however, the mechanism of action is poorly understood. To explore this, human bronchial epithelial cells were grown and exposed to varied concentrations of short-chain (perfluorobutanoic acid, perflurobutane sulfonic acid and GenX) [...] Read more.
Adverse lung outcomes from exposure to per-and polyfluoroalkyl substances (PFAS) are known; however, the mechanism of action is poorly understood. To explore this, human bronchial epithelial cells were grown and exposed to varied concentrations of short-chain (perfluorobutanoic acid, perflurobutane sulfonic acid and GenX) or long-chain (PFOA and perfluorooctane sulfonic acid (PFOS)) PFAS, alone or in a mixture to identify cytotoxic concentrations. Non-cytotoxic concentrations of PFAS from this experiment were selected to assess NLRP3 inflammasome activation and priming. We found that PFOA and PFOS alone or in a mixture primed and activated the inflammasome compared with vehicle control. Atomic force microscopy showed that PFOA but not PFOS significantly altered the membrane properties of cells. RNA sequencing was performed on the lungs of mice that had consumed PFOA in drinking water for 14 weeks. Wild type (WT), PPARα knock-out (KO) and humanized PPARα (KI) were exposed to PFOA. We found that multiple inflammation- and immune-related genes were affected. Taken together, our study demonstrated that PFAS exposure could alter lung biology in a significant manner and may contribute to asthma/airway hyper-responsiveness. Full article
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18 pages, 3254 KiB  
Article
Activation of Endothelial Large Conductance Potassium Channels Protects against TNF-α-Induced Inflammation
Int. J. Mol. Sci. 2023, 24(4), 4087; https://doi.org/10.3390/ijms24044087 - 17 Feb 2023
Cited by 1 | Viewed by 1475
Abstract
Elevated TNF-α levels in serum and broncho-alveolar lavage fluid of acute lung injury patients correlate with mortality rates. We hypothesized that pharmacological plasma membrane potential (Em) hyperpolarization protects against TNF-α-induced CCL-2 and IL-6 secretion from human pulmonary endothelial cells through inhibition of inflammatory [...] Read more.
Elevated TNF-α levels in serum and broncho-alveolar lavage fluid of acute lung injury patients correlate with mortality rates. We hypothesized that pharmacological plasma membrane potential (Em) hyperpolarization protects against TNF-α-induced CCL-2 and IL-6 secretion from human pulmonary endothelial cells through inhibition of inflammatory Ca2+-dependent MAPK pathways. Since the role of Ca2+ influx in TNF-α-mediated inflammation remains poorly understood, we explored the role of L-type voltage-gated Ca2+ (CaV) channels in TNF-α-induced CCL-2 and IL-6 secretion from human pulmonary endothelial cells. The CaV channel blocker, Nifedipine, decreased both CCL-2 and IL-6 secretion, suggesting that a fraction of CaV channels is open at the significantly depolarized resting Em of human microvascular pulmonary endothelial cells (−6 ± 1.9 mV), as shown by whole-cell patch-clamp measurements. To further explore the role of CaV channels in cytokine secretion, we demonstrated that the beneficial effects of Nifedipine could also be achieved by Em hyperpolarization via the pharmacological activation of large conductance K+ (BK) channels with NS1619, which elicited a similar decrease in CCL-2 but not IL-6 secretion. Using functional gene enrichment analysis tools, we predicted and validated that known Ca2+-dependent kinases, JNK-1/2 and p38, are the most likely pathways to mediate the decrease in CCL-2 secretion. Full article
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Figure 1

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