Particulate matter exposure disturbs inflammatory cytokine homeostasis associated with changes in trace metal levels
Xuemei Liu1, Jinhua Wang2, Mengfan Zhou3
1State Key Laboratory of Pollution Control and Resources Reuse, School of the Environment, Nanjing University, Nanjing, China; Huaiyin Institute of Technology, School of the Chemical Engineering, Huaian, China.
Abstract:
Few studies have focused on the impact of particulate matter (PM) exposure with respect to the relationship between PM-induced inflammation and the levels of trace metals in tissues and organs. In this study, C57BL/6 male mice were exposed to ambient air alongside control mice breathing air filtered through a high-efficiency particulate air (HEPA) filter. In both groups, mRNA levels of pro- and anti-inflammatory cytokines were measured after 4, 8 and 12 weeks together with the trace metal contents of the lungs, heart, liver, hippocampus and blood. PM exposure resulted in a general upward trend in the levels of pro-inflammatory cytokines in lung, heart, liver and hippocampus. By contrast, IL-10 mRNA expression varied depending on the organ, with a continuous upward trend in heart and liver and an up-regulation at 8 weeks followed by a down-regulation at 12 weeks in lung and hippocampus. The disturbed homeostasis of inflammatory cytokines was accompanied by changes in trace metal levels in the mice. These alterations may have constituted a compensatory effect conferring protection from inflammatory damage. However, prolonged PM exposure finally resulted in the deficiency of several essential trace metals in the lungs and hippocampus, which may have contributed to the observed histological changes typical of an inflammatory response.
Insights
Particulate matter (PM) exposure increases inflammation and alters trace metal levels in mouse organs. Prolonged exposure led to essential trace metal deficiencies in lungs and hippocampus, potentially worsening inflammation.
Area of Science:
- Environmental Health
- Toxicology
- Immunology
Background:
- Particulate matter (PM) exposure is a growing public health concern.
- Limited research exists on the interplay between PM-induced inflammation and trace metal accumulation in organs.
- Understanding these relationships is crucial for assessing health risks associated with air pollution.
Purpose of the Study:
- To investigate the impact of ambient particulate matter exposure on inflammatory cytokine levels.
- To determine the relationship between PM exposure and trace metal concentrations in various tissues and organs.
- To explore potential compensatory mechanisms and long-term consequences of PM exposure.
Main Methods:
- C57BL/6 male mice were exposed to ambient air or filtered air (HEPA control).
- mRNA levels of pro- and anti-inflammatory cytokines were measured at 4, 8, and 12 weeks.
- Trace metal content was analyzed in lung, heart, liver, hippocampus, and blood.
Main Results:
- PM exposure generally increased pro-inflammatory cytokine mRNA in lung, heart, liver, and hippocampus.
- Interleukin-10 (IL-10) mRNA expression showed organ-specific patterns.
- Disturbed cytokine homeostasis correlated with altered trace metal levels, suggesting a compensatory response.
- Prolonged PM exposure resulted in essential trace metal deficiencies in lungs and hippocampus.
Conclusions:
- PM exposure disrupts inflammatory cytokine balance and alters trace metal homeostasis.
- Initial trace metal changes may offer protection, but prolonged exposure leads to deficiencies.
- These deficiencies may contribute to PM-induced inflammatory histological changes in organs like the lungs and hippocampus.
