Lung epithelial cells serve as the first line of defense against various inhaled pollutant particles. To investigate the adverse health effects of organic components of fine particulate matter (PM) collected in Seoul, South Korea, we selected 12 PM samples from May 2016 to January 2017 and evaluated the effects of organic compounds of PM on inflammation, cellular aging, and macroautophagy in human lung epithelial cells isolated directly from healthy donors. Organic extracts of PM specifically induced neutrophilic chemokine and interleukin-8 expression via extracellular signal-regulated kinase activation. Moreover, PM significantly increased the expression of aging markers (p16, p21, and p27) and activated macroautophagy. Average mass concentrations of organic and elemental carbon had no significant correlations with PM effects. However, polycyclic aromatic hydrocarbons and n-alkanes were the most relevant components of PM that correlated with neutrophilic inflammation. Vegetative detritus and residential bituminous coal combustion sources strongly correlated with neutrophilic inflammation, aging, and macroautophagy activation. These data suggest that the chemical composition of PM is important for determining the adverse health effects of PM. Our study provides encouraging evidence to regulate the harmful components of PM in Seoul.
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http://dx.doi.org/10.1007/s11356-021-14850-1 | DOI Listing |
Sci Rep
December 2024
Division of Pulmonary, Allergy, Critical Care, and Sleep Medicine, University of Pittsburgh, Pittsburgh, PA, USA.
E-cigarette/vaping-associated lung injury (EVALI) is strongly associated with vitamin E acetate and often occurs with concomitant tetrahydrocannabinol (THC) use. To uncover pathways associated with EVALI, we examined cytokines, transcriptomic signatures, and lipidomic profiles in bronchoalveolar lavage fluid (BALF) from THC-EVALI patients. At a single center, we prospectively enrolled mechanically ventilated patients with EVALI from THC-containing products (N = 4) and patients with non-vaping acute lung injury and airway controls (N = 5).
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December 2024
Department of Thoracic Surgery, Affiliated Hospital of Nantong University, Nantong, Jiangsu, China.
Lung cancer remains the primary cause of cancer-related mortality, with factors such as postoperative tumor recurrence, metastasis, and therapeutic drug resistance exacerbating patient outcomes. Immunotherapy has emerged as a transformative approach, challenging conventional treatment paradigms for lung cancer. Consequently, advancing research in lung cancer immunotherapy is imperative.
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December 2024
Department of Immunology and Rheumatology, Division of Advanced Preventive Medical Sciences, Nagasaki University Graduate School of Biomedical Sciences, Nagasaki, Japan.
Objectives: Little is known about how various treatments impact the progression of interstitial lung disease (ILD) in rheumatoid arthritis (RA) patients. Here, we compared ILD progression in RA patients treated with Janus kinase inhibitors (JAKi) or biological disease-modifying anti-rheumatic drugs (bDMARDs). experiments were also performed to evaluate the potential effects of the drugs on epithelial-mesenchymal transition (EMT), a key event in pulmonary fibrosis.
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November 2024
Department of Respiratory and Critical Care Medicine, Wuyi County First People's Hospital, Jinhua, Zhejiang, China.
Objective: Epithelial-mesenchymal transition (EMT) and metastasis are the primary causes of mortality in non-small-cell lung cancer (NSCLC). 5'-3' exoribonuclease 2 (XRN2) plays an important role in the process of tumor EMT. Thus, this investigation mainly aimed to clarify the precise molecular pathways through which XRN2 contributes to EMT and metastasis in NSCLC.
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November 2024
Medical College, Ningbo University Health Science Center, Ningbo, China.
Objective: Patients with non-small cell lung cancer (NSCLC) have poor prognoses. Sulfatase 1 (SULF1) is an extracellular neutral sulfatase and is involved in multiple physiological processes. Hence, this study investigated the function and possible mechanisms of SULF1 in NSCLC.
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