Response biomarkers of inhalation exposure to cigarette smoke in the mouse          lung

Suzuki, Shigenori; Asai, Kuniya; Gi, Min; Kojima, Kazuyuki; Kakehashi, Anna; Oishi, Yushi; Matsue, Taisuke; Yukimatsu, Nao; Hirata, Kazuto; Kawaguchi, Tomoya; Wanibuchi, Hideki

doi:10.1293/tox.2021-0077

Cited by 4 publications

(2 citation statements)

References 23 publications

(30 reference statements)

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“…Increased levels of LCN2 have also been reported in bleomycin-induced lung in ammation and tobacco exposure that causes neutrophilic in ammation [42,43]. In addition, CXCL6 is a chemokine with neutrophil chemotaxis, and it has been reported that CXCL6 expression is observed in acute lung in ammation caused by bleomycin administration and lung injury caused by nanomaterials [44,45].…”

Section: Discussionmentioning

confidence: 96%

Investigation of Pulmonary Inflammatory Responses Following Intratracheal instillation of and Inhalation exposure to Polypropylene Microplastics

Tomonaga,

Higashi,

Izumi

et al. 2024

Preprint

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Background Microplastics have been detected in the atmosphere as well as in the ocean, and there is concern about their biological effects in the lungs. We conducted a short-term inhalation exposure and intratracheal instillation using rats to evaluate lung disorders related to microplastics. We conducted an inhalation exposure of polypropylene fine powder at a low concentration of 2 mg/m3 and a high concentration of 10 mg/m3 on 8-week-old male Fischer 344 rats for 6 hours a day, 5 days a week for 4 weeks. We also conducted an intratracheal instillation of polypropylene at a low dose of 0.2 mg/rat and a high dose of 1.0 mg/rat on 12-week-old male Fischer 344 rats. Rats were dissected from 3 days to 6 months after both exposures, and bronchoalveolar lavage fluid (BALF) and lung tissue were collected to analyze lung inflammation and lung injury. Results Both exposures to polypropylene induced a persistent influx of inflammatory cells and expression of CINC-1, CINC-2, and MPO in BALF from 1 month after exposure. Genetic analysis showed a significant increase in inflammation-related factors for up to 6 months. The low concentration in the inhalation exposure of polypropylene also induced mild lung inflammation. Conclusion These findings suggest that inhaled polypropylene, which is a microplastic, induces persistent lung inflammation and has the potential for lung disorder. Exposure to 2 mg/m3 induced inflammatory changes and was thought to be the Lowest Observed Adverse Effect Level (LOAEL) for acute effects of polypropylene.

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Section: Discussionmentioning

confidence: 96%

Investigation of Pulmonary Inflammatory Responses Following Intratracheal instillation of and Inhalation exposure to Polypropylene Microplastics

Tomonaga,

Higashi,

Izumi

et al. 2024

Preprint

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“…This gene is responsible for encoding the NGAL protein, essential in regulating innate immunity and iron homeostasis [80]. Research indicates that cigarette smoke significantly alters LCN2 expression, suggesting its potential as a marker for the harmful effects of smoke exposure [81]. Notably, LCN2 expression markedly increased in rat and mouse lungs after 13 and 6 months of cigarette smoke exposure, respectively [82,83].…”

Section: Qualitative Features In Lung Immune Cellsmentioning

confidence: 99%

Machine Learning Reveals Impacts of Smoking on Gene Profiles of Different Cell Types in Lung

Ma,

Shen,

Guo

et al. 2024

Life

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Smoking significantly elevates the risk of lung diseases such as chronic obstructive pulmonary disease (COPD) and lung cancer. This risk is attributed to the harmful chemicals in tobacco smoke that damage lung tissue and impair lung function. Current research on the impact of smoking on gene expression in specific lung cells is limited. This study addresses this gap by analyzing gene expression profiles at the single-cell level from 43,539 lung endothelial cells, 234,349 lung epithelial cells, 189,843 lung immune cells, and 16,031 lung stromal cells using advanced machine learning techniques. The data, categorized by different lung cell types, were classified into three smoking states: active smoker, former smoker, and never smoker. Each cell sample encompassed 28,024 feature genes. Employing an incremental feature selection method within a computational framework, several specific genes have been identified as potential markers of smoking status in different lung cell types. These include B2M, EEF1A1, and TPT1 in lung endothelial cells; FTL and MT-ATP8 in lung epithelial cells; HLA-B and HLA-C in lung immune cells; and HSP90B1 and LCN2 in lung stroma cells. Additionally, this study developed quantitative rules for representing the gene expression patterns related to smoking. This research highlights the potential of machine learning in oncology, enhancing our molecular understanding of smoking’s harm and laying the groundwork for future mechanism-based studies.

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Paclobutrazol ameliorates cigarette smoke-induced chronic obstructive pulmonary disease (COPD) in experimental rats

Xuan

Zhang

Wang

et al. 2023

Arabian Journal of Chemistry

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Response biomarkers of inhalation exposure to cigarette smoke in the mouse lung

Cited by 4 publications

References 23 publications

Investigation of Pulmonary Inflammatory Responses Following Intratracheal instillation of and Inhalation exposure to Polypropylene Microplastics

Investigation of Pulmonary Inflammatory Responses Following Intratracheal instillation of and Inhalation exposure to Polypropylene Microplastics

Machine Learning Reveals Impacts of Smoking on Gene Profiles of Different Cell Types in Lung

Paclobutrazol ameliorates cigarette smoke-induced chronic obstructive pulmonary disease (COPD) in experimental rats

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