The Gut and Lung Health Effects of Environmental Pollutants

A special issue of Toxics (ISSN 2305-6304). This special issue belongs to the section "Human Toxicology and Epidemiology".

Deadline for manuscript submissions: 25 April 2025 | Viewed by 817

Special Issue Editors


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Guest Editor
School of Public Health, Capital Medical University, Beijing 100069, China
Interests: environmental toxicology; gut homeostasis; metagenomics; particulate matter; epigenetics; pulmonary injury

E-Mail Website
Guest Editor
Yanjing Medical College, Capital Medical University, Beijing 101300, China
Interests: environmental toxicology; gut health effect; microplastics and health; air pollution; new pollutants

Special Issue Information

Dear Colleagues,

Environmental pollutants in air, water, and soil pose various known or potential threats to the environment and to human health. The health risks brought about by environmental pollutants have been a global public health issue that requires long-term attention. The health effects of environmental pollutants on the intestines and lungs, the main exposed organs, have aroused widespread interest from researchers. This Special Issue of Toxics focuses on the latest research progress concerning the effects of particulate matter and emerging environmental pollutants on intestinal and lung health. At the same time, we take this opportunity to encourage more people to devote themselves to promoting the development of this field.

Scope

  1. What are the new mechanisms of lung injury and intestinal effects caused by particulate matter?
  2. How does particulate matter exposure regulate gut and lung communication?
  3. How do the gut and lungs respond to emerging environmental pollutants exposure?

Dr. Meng Qingtao
Dr. Xianan Zhang
Guest Editors

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Keywords

  • emerging environmental pollutants
  • lung health
  • intestinal pulmonary interaction
  • new pollutants
  • gut health
  • intestinal immunity

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Published Papers (1 paper)

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Research

20 pages, 6301 KiB  
Article
miR-26a-5p/ADAM17-Mediated Proteolysis of TREM2 Regulates Neuroinflammation in Hypertensive Mice Following Lead Exposure
by Yuran Wang, Zeming Wang, Han Hao, Yuwei Zhao, Jian Wang and Weixuan Wang
Toxics 2025, 13(1), 37; https://doi.org/10.3390/toxics13010037 - 5 Jan 2025
Viewed by 553
Abstract
Hypertension is not merely a vascular disorder but a significant risk factor for neural impairment. Moreover, healthcare for the hypertensive population with environmental or occupational pollutants has become an issue of increasing concern in public health. As a traditional neurotoxic heavy metal, Pb [...] Read more.
Hypertension is not merely a vascular disorder but a significant risk factor for neural impairment. Moreover, healthcare for the hypertensive population with environmental or occupational pollutants has become an issue of increasing concern in public health. As a traditional neurotoxic heavy metal, Pb exposure results in neuroinflammation as well as neurodegenerative diseases. The current study aimed to investigate the mechanisms of neuroinflammation in hypertensive mice exposed to Pb. We demonstrated that hypertension exacerbated Pb-induced neuroinflammation in the prefrontal cortex (PFC), hippocampus, and hypothalamus, as evidenced by increased levels of proinflammatory cytokines (IL-6 and TNF-α) and decreased levels of anti-inflammatory cytokines (CD206 and IL-10). Additionally, hypertension enhanced the neuroinflammatory response in microglia, as indicated by similar changes in cytokine expression in an in vitro cell model. Importantly, we found that TREM2, a key regulator of microglial inflammation, was downregulated in hypertensive mice with Pb exposure. This decline in TREM2 expression was associated with increased proteolysis of TREM2 by a disintegrin and metalloproteases 10 (ADAM10) as well as a disintegrin and metalloproteases 17 (ADAM17), in which ADAM17 was verified as the main cleavage enzyme in terms of TREM2 proteolytic cleavage in hypertensive mice following Pb exposure. Furthermore, we identified miR-26a-5p as a potential regulator of ADAM17 expression, suggesting a potential mechanism for the downregulation of TREM2 in this context. Our findings provided new insights into the complex interplay between hypertension, Pb exposure, and neuroinflammation as well as highlight the potential role of TREM2, ADAM17, and miR-26a-5p as therapeutic targets for neuroinflammation in hypertensive populations with Pb exposure. Full article
(This article belongs to the Special Issue The Gut and Lung Health Effects of Environmental Pollutants)
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