ArticleAmerican journal of physiology. Lung cellular and molecular physiology2016
Cadmium attenuates the macrophage response to LPS through inhibition of the NF-κB pathway.
Article in American journal of physiology. Lung cellular and molecular physiology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 39 citations in OpenAlex.
- Article
- Environmental pollutant risk factors for worse COVID-19 related clinical outcomes in predominately hispanic and latino populations.Environmental research · 2024Article
- Association between heavy metals exposure and persistent infections: the mediating role of immune function.Frontiers in public health · 2024Article
- Adverse health effects of emerging contaminants on inflammatory bowel disease.Frontiers in public health · 2023Review
- Role of Macrophages in Air Pollution Exposure Related Asthma.International journal of molecular sciences · 2022Review
- White adipose tissue as a target for cadmium toxicity.Frontiers in pharmacology · 2022Article
- Cadmium and wild boar: Environmental exposure and immunological impact on macrophages.Toxicology reports · 2022Article
- The adverse impact of cadmium on immune function and lung host defense.Seminars in cell & developmental biology · 2021Article
- Cadmium Exchange with Zinc in the Non-Classical Zinc Finger Protein Tristetraprolin.Inorganic chemistry · 2021Article
- The effects of some essential and toxic metals/metalloids in COVID-19: A review.Food and chemical toxicology : an international journal published for the British Industrial Biological Research Association · 2021Review
- Receptor-Interacting Protein Kinase 3 Inhibition Prevents Cadmium-Mediated Macrophage Polarization and Subsequent AtherosclerosisFrontiers in cardiovascular medicine · 2021Article
- Effects of Cadmium Exposure on the Immune System and Immunoregulation.Frontiers in immunology · 2021Review
- Cadmium-mediated lung injury is exacerbated by the persistence of classically activated macrophages.The Journal of biological chemistry · 2020Article
- Cadmium in tobacco smokers: a neglected link to lung disease?European respiratory review : an official journal of the European Respiratory Society · 2018Review
- Cadmium-induced ER stress and inflammation are mediated through C/EBP-DDIT3 signaling in human bronchial epithelial cells.Experimental & molecular medicine · 2017Article
- Zinc Modulates Endotoxin-Induced Human Macrophage Inflammation through ZIP8 Induction and C/EBPβ Inhibition.PloS one · 2017Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
Chronic obstructive pulmonary disease (COPD) in the U.S. is primarily caused by cigarette smoking. COPD patients are highly susceptible to respiratory infections in part due to alveolar macrophage dysfunction despite a substantial increase in macrophages in the lung. Cadmium (Cd) is a toxic metal that is concentrated within tobacco and accumulates in the lung of smokers. We hypothesized that Cd uptake into macrophages alters immune function thereby impairing the macrophage response to invading pathogens. Our hypothesis was tested by comparing primary human monocytes and macrophages, primary mouse bronchoalveolar lavage myeloid cells, and related cell lines. Strikingly, Cd exposure followed by LPS stimulation resulted in a dose-dependent, significant decrease in nuclear p65 activity in macrophages that was not observed in monocytes. This corresponded with Cd-mediated inhibition of IKKβ and an impaired ability to transcribe and release cytokines in response to LPS challenge in vivo. These findings provide novel evidence that Cd has the capacity to disrupt macrophage immune function compared with monocytes. Importantly, Cd results in immune dysfunction in macrophages through inhibition of the NF-κB signaling pathway. Based on these findings, we provide new evidence that Cd contributes to immune dysfunction in the lung of COPD subjects and may increase susceptibility to infection.
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Registered trials
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