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Published on: May 31, 2018
Melatonin attenuates lipopolysaccharide-induced immune dysfunction in dendritic cells
Tao Qin1, Danni Feng2, Bangyue Zhou3
1College of Veterinary Medicine, Yangzhou University, Yangzhou, Jiangsu, China; Joint International Research Laboratory of Agriculture and Agri-Product Safety, the Ministry of Education of China, Yangzhou University, Yangzhou, Jiangsu, China; Jiangsu Co-Innovation Center for the Prevention and Control of Important Animal Infectious Disease and Zoonoses, Yangzhou University, Yangzhou, Jiangsu, China.
Melatonin protects dendritic cells (DCs) from acute lung injury (ALI) by reducing inflammation and immune cell activation. This study reveals melatonin
Area of Science:
- Immunology
- Cell Biology
- Pharmacology
Background:
- Melatonin, a hormone with antioxidant and anti-inflammatory effects, has unknown roles in dendritic cell (DC) function during acute lung injury (ALI).
- Dendritic cells play a crucial role in immune responses and are implicated in the pathogenesis of ALI.
Purpose of the Study:
- To investigate the protective effects of melatonin on dendritic cells in a murine model of lipopolysaccharide (LPS)-induced ALI.
- To elucidate the mechanisms by which melatonin modulates DC function and immune responses during ALI.
Main Methods:
- Lipopolysaccharide (LPS)-induced ALI murine model.
- In vivo and in vitro assessment of DC phenotype, function, and cytokine secretion.
- Analysis of major histocompatibility complex II (MHCII), CD40, CD80, CD86, CD69, and C-C chemokine receptor 7 (CCR7) expression.
- Evaluation of DC-mediated T cell proliferation.
- Investigation of the nuclear factor erythroid-2-related factor 2 (Nrf-2)/heme oxygenase-1 (HO-1) signaling pathway.
Main Results:
- Melatonin treatment alleviated lung injury, reduced pro-inflammatory cytokines (TNF-α, IL-12p70, IL-17), and decreased MHCII expression on lung DCs in vivo.
- In vitro, melatonin inhibited LPS-induced DC activation markers (MHCII, CD40, CD80, CD86, CD69), promoted endocytosis, and reduced DC migration by downregulating CCR7.
- Melatonin-treated DCs showed impaired ability to stimulate allogeneic CD4+ T cell proliferation.
- Melatonin's effects on DCs were dependent on the Nrf-2/HO-1 pathway.
Conclusions:
- Melatonin exerts protective effects on dendritic cells against ALI-induced immunological stress.
- Melatonin modulates DC phenotype, function, and migration, thereby mitigating lung inflammation.
- Melatonin's mechanism involves the Nrf-2/HO-1 signaling pathway, suggesting its potential as a therapeutic agent for ALI targeting DC function.
