Air pollution accelerates the development of obesity and Alzheimer's disease: the role of leptin and inflammation - a mini-review.

Autor: Campolim CM; Department of Internal Medicine, School of Medical Science, State University of Campinas (UNICAMP), Campinas, SP, Brazil.; Division of Endocrinology, Diabetes, and Metabolism, Department of Medicine, Beth Israel Deaconess Medical Center, and Harvard Medical School, Boston, MA, United States., Schimenes BC; School of Applied Sciences, State University of Campinas (UNICAMP), Limeira, SP, Brazil., Veras MM; Laboratory of Environmental and Experimental Pathology LIM05, Department of Pathology, School of Medicine, University of São Paulo (USP), São Paulo, SP, Brazil., Kim YB; Division of Endocrinology, Diabetes, and Metabolism, Department of Medicine, Beth Israel Deaconess Medical Center, and Harvard Medical School, Boston, MA, United States., Prada PO; Department of Internal Medicine, School of Medical Science, State University of Campinas (UNICAMP), Campinas, SP, Brazil.; Obesity and Comorbidities Research Center, Campinas, SP, Brazil.; Department of Structural and Functional Biology, Institute of Biology (IB), University of Campinas, Campinas, SP, Brazil.
Jazyk: angličtina
Zdroj: Frontiers in immunology [Front Immunol] 2024 Jun 12; Vol. 15, pp. 1401800. Date of Electronic Publication: 2024 Jun 12 (Print Publication: 2024).
DOI: 10.3389/fimmu.2024.1401800
Abstrakt: Air pollution is an urgent concern linked to numerous health problems in low- and middle-income countries, where 92% of air pollution-related deaths occur. Particulate matter 2.5 (PM 2.5 ) is the most harmful component of air pollutants, increasing inflammation and changing gut microbiota, favoring obesity, type 2 diabetes, and Alzheimer's Disease (AD). PM 2.5 contains lipopolysaccharides (LPS), which can activate the Toll-like receptor 4 (TLR4) signaling pathway. This pathway can lead to the release of pro-inflammatory markers, including interleukins, and suppressor of cytokine signaling-3 (SOCS3), which inhibits leptin action, a hormone that keeps the energy homeostasis. Leptin plays a role in preventing amyloid plaque deposition and hyperphosphorylation of tau-protein (p-tau), mechanisms involved in the neurodegeneration in AD. Approximately 50 million people worldwide are affected by dementia, with a significant proportion living in low-and middle-income countries. This number is expected to triple by 2050. This mini-review focuses on the potential impact of PM 2.5 exposure on the TLR4 signaling pathway, its contribution to leptin resistance, and dysbiosis that exacerbates the link between obesity and AD.
Competing Interests: The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest. The author(s) declared that they were an editorial board member of Frontiers, at the time of submission. This had no impact on the peer review process and the final decision.
(Copyright © 2024 Campolim, Schimenes, Veras, Kim and Prada.)
Databáze: MEDLINE
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