ArticleToxicological sciences : an official journal of the Society of Toxicology2012
An NF-κB-independent and Erk1/2-dependent mechanism controls CXCL8/IL-8 responses of airway epithelial cells to cadmium.
Article in Toxicological sciences : an official journal of the Society of Toxicology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 55 citations in OpenAlex.
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- The N-terminal domain of precursor IL-1α enhances IL-6 expression via an intracrine mechanism in oral squamous cell carcinoma.Molecular biology reports · 2025Article
- IL-8 (CXCL8) Correlations with Psychoneuroimmunological Processes and Neuropsychiatric Conditions.Journal of personalized medicine · 2024Review
- MEK1/2 inhibition decreases pro-inflammatory responses in macrophages from people with cystic fibrosis and mitigates severity of illness in experimental murine methicillin-resistantFrontiers in cellular and infection microbiology · 2024Article
- ROS and ERK Pathway Mechanistic Approach on Hepatic Insulin Resistance After Chronic Oral Exposure to Cadmium NOAEL Dose.Biological trace element research · 2023Article
- microRNA-149-5p mediates the PMCell biology and toxicology · 2023Article
- Pancreas-Liver-Adipose Axis: Target of Environmental Cadmium Exposure Linked to Metabolic Diseases.Toxics · 2023Review
- Korean Red Ginseng water extract inhibits cadmium-induced lung injury via suppressing MAPK/ERK1/2/AP-1 pathway.Journal of ginseng research · 2022Article
- Targeting the EGFR-ERK axis using the compatible solute ectoine to stabilize CFTR mutant F508del.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2022Article
- Pulmonary toxicity of inhaled nano-sized cerium oxide aerosols in Sprague-Dawley rats.Nanotoxicology · 2019Article
- Involvement of Alveolar Macrophages and Neutrophils in Acute Lung Injury After Scorpion Envenomation: New Pharmacological Targets.Inflammation · 2018Article
- Cadmium-induced ER stress and inflammation are mediated through C/EBP-DDIT3 signaling in human bronchial epithelial cells.Experimental & molecular medicine · 2017Article
- Cigarette smoke exposure reveals a novel role for the MEK/ERK1/2 MAPK pathway in regulation of CFTR.Biochimica et biophysica acta · 2015Article
- Subtoxic Doses of Cadmium Modulate Inflammatory Properties of Murine RAW 264.7 Macrophages.BioMed research international · 2015Article
- Transcriptional mechanisms and protein kinase signaling mediate organic dust induction of IL-8 expression in lung epithelial and THP-1 cells.American journal of physiology. Lung cellular and molecular physiology · 2015Article
- Cadmium exposure and cancer mortality in a prospective cohort: the strong heart study.Environmental health perspectives · 2014Article
- Early secreted antigenic target of 6 kDa (ESAT-6) protein of Mycobacterium tuberculosis induces interleukin-8 (IL-8) expression in lung epithelial cells via protein kinase signaling and reactive oxygen species.The Journal of biological chemistry · 2013Article
- Modulation of airway epithelial cell functions by Pidotimod: NF-kB cytoplasmatic expression and its nuclear translocation are associated with an increased TLR-2 expression.Italian journal of pediatrics · 2013Article
- Long lasting effects of smoking: breast cancer survivors' inflammatory responses to acute stress differ by smoking history.Psychoneuroendocrinology · 2013Article
- Curcumin regulates airway epithelial cell cytokine responses to the pollutant cadmium.Biochemical and biophysical research communications · 2012Article
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Authors and funding
9 authors at 2 institutions in 1 country.
Funding
Abstract
Airway epithelial cells in the lung are the first line of defense against pathogens and environmental pollutants. Inhalation of the environmental pollutant cadmium has been linked to the development of lung cancer and chronic obstructive pulmonary disease, which are diseases characterized by chronic inflammation. To address the role of airway epithelial cells in cadmium-induced lung inflammation, we investigated how cadmium regulates secretion of interleukin 8 (IL-8) by airway epithelial cells. We show that exposure of human airway epithelial cells to subtoxic doses of cadmium in vitro promotes a characteristic inflammatory cytokine response consisting of IL-8, but not IL-1β or tumor necrosis factor-alpha. We also found that intranasal delivery of cadmium increases lung levels of the murine IL-8 homologs macrophage inflammatory protein-2 and keracinocyte-derived chemokine and results in an influx of Gr1+ cells into the lung. We determined that inhibition of the nuclear factor-κB (NF-κB) pathway had no effect on cadmium-induced IL-8 secretion by human airway epithelial cells, suggesting that IL-8 production was mediated through an NF-κB-independent pathway. Mitogen-activated protein kinases (MAPKs) are often involved in proinflammatory signaling. Cadmium could activate the main MAPKs (i.e., p38, JNK, and Erk1/2) in human airway epithelial cells. However, only pharmacological inhibition of Erk1/2 pathway or knockdown of the expression of Erk1 and Erk2 using small interfering RNAs suppressed secretion of IL-8 induced by cadmium. Our findings identify cadmium as a potent activator of the proinflammatory cytokine IL-8 in lung epithelial cells and reveal for the first time the role of an NF-κB-independent but Erk1/2-dependent pathway in cadmium-induced lung inflammation.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.