Sodium chloride promotes pro-inflammatory macrophage polarization thereby aggravating CNS autoimmunity

Hucke, Stephanie; Eschborn, Melanie; Liebmann, Marie; Herold, Martin; Freise, Nicole; Engbers, Annika; Ehling, Petra; Meuth, Sven G.; Roth, Johannes; Kuhlmann, Tanja; Wiendl, Heinz; Klotz, Luisa

doi:10.1016/j.jaut.2015.11.001

Cited by 142 publications

(183 citation statements)

References 46 publications

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“…A possible explanation of these divergent results is the different treatments and baseline characteristics of the MS patients included in the studies, as well as the divergent approaches to assess sodium intake in these retrospective analyses. Several studies have shown that high sodium diets could exacerbate EAE 74, 75, 77, 79. When analyzing CD4 + T cells, this effect was accompanied by increased numbers of T H 17 cells and a higher infiltration of T H 17 cells into the CNS 74, 75.…”

Section: Salt and Msmentioning

confidence: 99%

“…The salt consumption varies considerably among countries, ranging from 1.5 g of sodium per day in East African countries to 3.9 g of sodium per day in high‐income countries 73. Recently, many studies have demonstrated that a high intake of sodium chloride can be an important factor potentially influencing autoimmunity in both humans and rodents 74, 75, 76, 77, 78, 79, 80, 81, 82. In patients with RRMS in Argentina, increased sodium intake was associated with enhanced disease exacerbation and new lesion development 76.…”

Section: Salt and Msmentioning

confidence: 99%

“…In addition to its effects on T cells, a high salt diet was also associated with altered macrophage responses in EAE 77. Enhanced infiltration and activation of macrophages in the CNS was accompanied by increased levels of the myeloid‐attracting chemokines CCL2 and CXCL10.…”

Section: Salt and Msmentioning

confidence: 99%

“…Both in vitro and in vivo high salt concentrations promoted a proinflammatory M1 phenotype of macrophages, with upregulation of iNOS and IL‐1β. Mechanistically, macrophages pretreated with NaCl showed activation of members of the MAPK pathway, such as ERK1/2, JNK, p38, and p38‐dependent NFAT5, leading to increased production of nitric oxide and tumor necrosis factor‐α 77, 86. Moreover, adoptive transfer of salt‐treated bone marrow–derived macrophages (BMMs) aggravated ongoing EAE compared with control BMMs 77.…”

Section: Salt and Msmentioning

confidence: 99%

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Western lifestyle and immunopathology of multiple sclerosis

Matveeva

Bogie

Hendriks

et al. 2018

Annals of the New York Academy of Sciences

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There is increasing evidence for a sudden and unprecedented rise in the incidence of multiple sclerosis (MS) in Westernized countries over the past decades, emphasizing the role of environmental factors. Among many candidates, rapid changes in dietary habits seem to play a role in the pathogenesis of MS. Here, we summarize and discuss the available evidence for the role of dietary nutrients, such as table salt, fatty acids, and flavonoids, in the development and pathogenesis of MS. We also discuss new and emerging risk factors accompanying Western lifestyle, such as shift work, sleep, and circadian disruption.

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Section: Salt and Msmentioning

confidence: 99%

Section: Salt and Msmentioning

confidence: 99%

Section: Salt and Msmentioning

confidence: 99%

Section: Salt and Msmentioning

confidence: 99%

See 2 more Smart Citations

Western lifestyle and immunopathology of multiple sclerosis

Matveeva

Bogie

Hendriks

et al. 2018

Annals of the New York Academy of Sciences

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“…High salt treatment also decreases anti-inflammatory cytokines and increases inflammatory cytokines by mouse and human macrophages in vitro [24,25].…”

Section: Salt-derived Inflammationmentioning

confidence: 99%

Salt and Pregnancy Complications: A Proposal for Future Research

Abdoli¹

2016

J Women's Health Care

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Spleen‐Targeted Glabridin‐Loaded Nanoparticles Regulate Polarization of Monocyte/Macrophage (M_o/M_φ) for the Treatment of Cerebral Ischemia‐Reperfusion Injury

Wang

et al. 2022

Advanced Materials

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ischemia can cause an ischemic core and salvageable surrounding tissue (termed as penumbra). The penumbra has been regarded as a pharmacological target for ischemic stroke treatment. [2] Restoring cerebral blood flow is currently the most effective approach for reducing the number of damaged neuron in the ischemic penumbra. [3] Although intravenous thrombolysis can effectively restore blood supply in the penumbra, its use is limited by a short time window during which it can be safely and effectively performed. [4] Additionally, restoring blood flow can arouse a cerebral ischemicreperfusion (I-R) injury, which results in the amplification of the inflammatory response and the aggravation of secondary damage. The infiltration of peripheral monocytes/macrophages (M o /M ϕ ) is a crucial inflammatory injury mechanism, which induces neuronal apoptosis and nervous system dysfunction. In addition, a recent study has also highlighted the pivotal role of M o /M ϕ in the repair process, indicating that regulation of the balance of M o /M ϕ can be an effective method for the treatment of cerebral I-R injury. [5] The spleen is an immediate reservoir of M o /M ϕ , which has more M o /M ϕ than the entire circulatory system. [6] The spleen is also the primary source of inflammatory cells, which can infiltrate the ischemic penumbra during the early phase of an ischemic stroke. [7] In the ischemic penumbra, M o /M ϕ can be classically activated to the M1 phenotype of macrophages (M1-macrophage), secrete pro-inflammatory cytokines, and release oxygen free radicals. [8] Due to their heterogeneity and high versatility, M o /M ϕ can also be polarized into M2-macrophages, which are involved in anti-inflammatory and repair processes through their capability to secrete anti-inflammatory cytokines. [9] Therefore, reducing the number of splenic M1-macrophages and increasing the number of splenic M2-macrophages can effectively protect neurons from the damaged microenvironment in the penumbra.Glabridin (Gla) possesses multiple pharmacological activities, including antioxidant, anti-inflammatory, and neuroprotective. [10] As a peroxisome proliferator-activated receptor-γ (PPARγ) specific antagonist, Gla is also involved in cell proliferation and differentiation. [11] Previous studies demonstrated that PPAR-γ activation could result in the M2 polarization of During cerebral ischemia-reperfusion (I-R) injury, the infiltration of monocyte/ macrophages (M o /M ϕ ) into the ischemic penumbra causes inflammatory damage but also regulates tissue repair in the penumbra. The regulation and balance of M o /M ϕ polarization is considered as a potential therapeutic target for treating cerebral I-R injury. Herein, these findings demonstrate that glabridin (Gla)-loaded nanoparticles (i.e., NP Gla -5k) can effectively inhibit M1-polarization and enhance M2-polarization of M o /M ϕ . Positron emission tomography (PET) imaging shows that NP Gla -5k can selectively accumulate in the spleen following intravenous injection. Spleen-targeted Cy5-NP Gla -5k can...

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Sodium chloride promotes pro-inflammatory macrophage polarization thereby aggravating CNS autoimmunity

Cited by 142 publications

References 46 publications

Western lifestyle and immunopathology of multiple sclerosis

Western lifestyle and immunopathology of multiple sclerosis

Salt and Pregnancy Complications: A Proposal for Future Research

Spleen‐Targeted Glabridin‐Loaded Nanoparticles Regulate Polarization of Monocyte/Macrophage (M_o/M_φ) for the Treatment of Cerebral Ischemia‐Reperfusion Injury

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Sodium chloride promotes pro-inflammatory macrophage polarization thereby aggravating CNS autoimmunity

Cited by 142 publications

References 46 publications

Western lifestyle and immunopathology of multiple sclerosis

Western lifestyle and immunopathology of multiple sclerosis

Salt and Pregnancy Complications: A Proposal for Future Research

Spleen‐Targeted Glabridin‐Loaded Nanoparticles Regulate Polarization of Monocyte/Macrophage (Mo/Mφ) for the Treatment of Cerebral Ischemia‐Reperfusion Injury

Contact Info

Product

Resources

About

Spleen‐Targeted Glabridin‐Loaded Nanoparticles Regulate Polarization of Monocyte/Macrophage (M_o/M_φ) for the Treatment of Cerebral Ischemia‐Reperfusion Injury