Salt increases monocyte CCR2 expression and inflammatory responses in humans

Wenstedt, Eliane F. E.; Verberk, Sanne G.S.; Kroon, Jeffrey; Neele, Annette E.; Baardman, Jeroen; Claessen, Nike; Paşaoğlu, Özge Tuğçe; Rademaker, Emma; Schrooten, Esmee M.; Wouda, Rosa D; Winther, Menno P.J. de; Aten, Jan; Vogt, Liffert; Bossche, Jan Van den

doi:10.1172/jci.insight.130508

Cited by 35 publications

(49 citation statements)

References 52 publications

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“…The flow chart for study selection is shown in Figure 1 . Eight studies [ 13 , 27 , 37 , 38 , 39 , 40 , 41 , 42 ] met the inclusion criteria for examining the effect of sodium intake on circulating inflammatory biomarkers and were included in the systematic review. Detailed descriptive data, as well as results for all the included studies are provided in Table 1 and Table 2 .…”

Section: Resultsmentioning

confidence: 99%

Does Sodium Intake Induce Systemic Inflammatory Response? A Systematic Review and Meta-Analysis of Randomized Studies in Humans

et al. 2021

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Experimental studies suggest that sodium induced inflammation might be another missing link leading to atherosclerosis. To test the hypothesis that high daily sodium intake induces systemic inflammatory response in humans, we performed a systematic review according to PRISMA guidelines of randomized controlled trials (RCTs) that examined the effect of high versus low sodium dose (HSD vs. LSD), as defined per study, on plasma circulating inflammatory biomarkers. Eight RCTs that examined CRP, TNF-a and IL-6 were found. Meta-analysis testing the change of each biomarker in HSD versus LSD was possible for CRP (n = 5 studies), TNF-a (n = 4 studies) and IL-6 (n = 4 studies). The pooled difference (95% confidence intervals) per biomarker was for: CRP values of 0.1(−0.3, 0.4) mg/L; TNF-a −0.7(−5.0, 3.6) pg/mL; IL-6 −1.1(−3.3 to 1.1) pg/mL. Importantly, there was inconsistency between RCTs regarding major population characteristics and the applied methodology, including a very wide range of LSD (460 to 6740 mg/day) and HSD (2800 to 7452 mg/day). Although our results suggest that the different levels of daily sodium intake are not associated with significant changes in the level of systemic inflammation in humans, this outcome may result from methodological issues. Based on these identified methodological issues we propose that future RCTs should focus on young healthy participants to avoid confounding effects of comorbidities, should have three instead of two arms (very low, “normal” and high) of daily sodium intake with more than 100 participants per arm, whereas an intervention duration of 14 days is adequate.

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Section: Resultsmentioning

confidence: 99%

Does Sodium Intake Induce Systemic Inflammatory Response? A Systematic Review and Meta-Analysis of Randomized Studies in Humans

et al. 2021

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“…Of note, the exact role of NFAT5 and macrophages in local ionic balance has been reviewed elsewhere [22,26,38]. In humans, an experimental HSD (≥ approximately 12 g NaCl/day for 7-14 days) also resulted in the accumulation of Na + [39] and macrophages [40] in the skin, strongly suggesting that this system might be operative in humans as well.…”

Section: Trends Trends In In Immunology Immunologymentioning

confidence: 99%

Sodium and its manifold impact on our immune system

Jobin

Müller

Kurts

2021

Trends in Immunology

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The Western diet is rich in salt, and a high salt diet (HSD) is suspected to be a risk factor for cardiovascular diseases. It is now widely accepted that an experimental HSD can stimulate components of the immune system, potentially exacerbating certain autoimmune diseases, or alternatively, improving defenses against certain infections, such as cutaneous leishmaniasis. However, recent findings show that an experimental HSD may also aggravate other infections (e.g., pyelonephritis or systemic listeriosis). Here, we discuss the modulatory effects of a HSD on the microbiota, metabolic signaling, hormonal responses, local sodium concentrations, and their effects on various immune cell types in different tissues. We describe how these factors are integrated, resulting either in immune stimulation or suppression in various tissues and disease settings.Salt (NaCl) used to be so rare and valuable that in the 17th century for instance, the Duchy of Bavaria and the city of Salzburg entered into war over it. Even the word 'salary' reflects the preciousness that salt once had [1]. Due to geotechnological advances, salt nowadays is neither rare nor expensive. We love it and, thus, we eat a lot of it. Typical diets in Western countries and China contain more than 10 g per day [2].

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“…13 Furthermore, a salt-sensitive blood pressure increase in 11 healthy human volunteers was shown to coincide with an increased pro-inflammatory monocyte phenotype (increased CCR2 expression) and macrophage phenotype (increased HLA-DR expression and reduced CD206 expression; and increased proinflammatory cytokine secretion in vitro). 69 Successful translation to humans, however, requires very specific interventions (since general macrophage interventions are unfeasible), which necessitates more detailed knowledge on when and which macrophages are protective vs. harmful in hypertension development.…”

Section: Group By Route Of Administrationmentioning

confidence: 99%

The effect of macrophage-targeted interventions on blood pressure – a systematic review and meta-analysis of preclinical studies

Wenstedt

Croonenburg

Born

et al. 2021

Translational Research

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An increasing body of evidence shows a role for macrophages and monocytes (as their precursors) in hypertension, but with conflicting results with regard to whether they are protective or harmful. Therefore, we systematically reviewed the effect of macrophage interventions on blood pressure in animal models, to explore which factors determine the blood pressure increasing vs. decreasing effect. A search in PubMED and EMBASE yielded 9620 records, 26 of which were included. Eighteen studies (involving 22 different experiments (k = 22)) performed macrophage depletion, whereas 12 studies specifically deleted certain macrophage proteins. The blood pressure effects of macrophage depletion were highly various and directed toward both directions, as expected, which could not be reduced to differences in animal species or methods of hypertension induction. Prespecified subgroup analysis did reveal a potential role for the route in which the macrophage-depleting agent is being administrated (intraperitoneal vs intravenous subgroup difference of P = 0.07 (k = 22), or P < 0.001 in studies achieving considerable (ie, >50%) depletion (k = 18)). Along with findings from specific macrophage protein deletion studiesshowing that deletion of one single macrophage protein (like TonEBP, endothelin-B, EP 4 , NOX-2 and the angiotensin II type 1 receptor) can alter blood pressure responses to hypertensive stimuli-the indication that each route has its specific depletion pattern regarding targeted tissues and macrophage phenotypes suggests a determinative role for these features. These hypothesis-generating results encourage more detailed depletion characterization of each technique by direct experimental comparisons, providing a chance to obtain more knowledge on which macrophages are beneficial versus detrimental in hypertension development.

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Salt increases monocyte CCR2 expression and inflammatory responses in humans

Cited by 35 publications

References 52 publications

Does Sodium Intake Induce Systemic Inflammatory Response? A Systematic Review and Meta-Analysis of Randomized Studies in Humans

Does Sodium Intake Induce Systemic Inflammatory Response? A Systematic Review and Meta-Analysis of Randomized Studies in Humans

Sodium and its manifold impact on our immune system

The effect of macrophage-targeted interventions on blood pressure – a systematic review and meta-analysis of preclinical studies

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