Highly purified human peripheral blood monocytes produce IL-6 but not TNFα in response to angiotensin II

Gelinas, Laura; Falkenham, Alec; Oxner, Adam; Sopel, Mryanda; Légaré, Jean‐François

doi:10.1177/1470320310391332

Cited by 16 publications

(8 citation statements)

References 38 publications

(55 reference statements)

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“…IMo also called M1 monocytes is a subtype of monocytes thought to be an important cellular source of IL-6 [21,22]. We found that CAWS injection resulted in mobilization of iMo into the periphery, as indicated by over a two-fold increase in the proportion of iMo in the blood and spleen of Ccr2 +/+ CAWS-injected compared to PBS injected mice (Figure 5E and F).…”

Section: Resultsmentioning

confidence: 79%

Important role of CCR2 in a murine model of coronary vasculitis

et al. 2012

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BackgroundChemokines and their receptors play a role in the innate immune response as well as in the disruption of the balance between pro-inflammatory Th17 cells and regulatory T cells (Treg), underlying the pathogenesis of coronary vasculitis in Kawasaki disease (KD).ResultsHere we show that genetic inactivation of chemokine receptor (CCR)-2 is protective against the induction of aortic and coronary vasculitis following injection of Candida albicans water-soluble cell wall extracts (CAWS). Mechanistically, both T and B cells were required for the induction of vasculitis, a role that was directly modulated by CCR2. CAWS administration promoted mobilization of CCR2-dependent inflammatory monocytes (iMo) from the bone marrow (BM) to the periphery as well as production of IL-6. IL-6 was likely to contribute to the depletion of Treg and expansion of Th17 cells in CAWS-injected Ccr2+/+ mice, processes that were ameliorated following the genetic inactivation of CCR2.ConclusionCollectively, our findings provide novel insights into the role of CCR2 in the pathogenesis of vasculitis as seen in KD and highlight novel therapeutic targets, specifically for individuals resistant to first-line treatments.

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Section: Resultsmentioning

confidence: 79%

Important role of CCR2 in a murine model of coronary vasculitis

et al. 2012

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“…Endogenous ANG II increased T-cell activation, leading to production of TNF-α [ 60 ] and blocking of ACE was found to increase Treg population in the spleen [ 61 ]. Additionally, ANG II increased IL-6 release in monocytes [ 62 ] and the increased IL-6 in CHC mice might affect to Treg population in CHC mice. It has been reported that IL-6 was required for overcoming Treg suppressive function with some other cytokines [ 63 ].…”

Section: Discussionmentioning

confidence: 99%

Chronic high dose of captopril induces depressive-like behaviors in mice: possible mechanism of regulatory T cell in depression

et al. 2017

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Major depression has various types of symptoms and disease courses with inconsistent response to monoamine-related antidepressants. Thus, monoamine theory may not be the only pathophysiologic pathway relevant to depression. Recently, it has been suggested that regulatory T cell (Treg) is associated with depression. Based on our previous study that showed decreased regulatory T cell (Treg) population following chronic high-dose captopril (CHC, 40 mg/kg/day * 21 days) administration, we examined whether CHC alone can induce depressive-like behaviors in mice even without stressful stimuli. In this study, we found that CHC induced depressive-like behaviors in tail suspension test (TST) and forced swimming test (FST) without systemic illness, while it did not induce anhedonic behavior, anxiety-like behaviors, or sociality-related behavior. The depressive-like behaviors were rescued by either CHC washout or antidepressant. CHC caused reduction in foxp3 and gata3 mRNA expression in the lymph nodes with elevation in plasma IL-1β and IL-6. Interestingly, CHC increased serum angiotensin II level. In the hippocampus, CHC increased TNF-α and IL-6 mRNA expression with microglia activation while reduced glucocorticoid receptor expression. However, CHC did not affect to hippocampal kynurenine pathway, serotonin level, hypothalamic corticotropin-releasing hormone mRNA level, or serum corticosterone level. Consequently, we propose that CHC may induce a specific form of depressive-like behaviors via Treg reduction and microglial activation.

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“…45 Briefly, PBMCs were separated from blood on a gradient (Histopaque-Ficoll; Sigma-Aldrich, Munich, Germany), washed twice at 1500 rpm for 10 minutes to remove platelets, and live cells were counted with a hemocytometer (MSUM Biochem and Biotech, Moorhead, MN) using the Trypan Blue exclusion method. Total blood monocytes, including both subsets of CD14þþCD16-and CD14þCD16þ monocytes were isolated using a negative selection kit (EasySep, Stemcell Technologies, Vancouver, Canada) according to manufacturer's instructions.…”

Section: Qpcrmentioning

confidence: 99%

Chemokine Receptor Expression in Peripheral Blood Monocytes from Patients with Neovascular Age-Related Macular Degeneration

Grunin

Burstyn‐Cohen

Hagbi-Levi

et al. 2012

Invest. Ophthalmol. Vis. Sci.

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PURPOSE. Chemokine signaling and monocytes/macrophages were implicated in the pathogenesis of AMD. We tested the association between chemokines involved in monocyte recruitment and AMD. METHODS.Immunophenotyping for white blood cell (WBC) populations including CD14þþCD16-and CD14þCD16þ monocytes, CD19þ, CD3þ, and CD16þ lymphocytes, and chemokine receptors CCR1, CCR2, CCR5, CX 3 CR1, and CXCR4 was performed on peripheral blood from treatment-naïve neovascular AMD (NV-AMD) patients and controls. The mRNA level of chemokine receptors in monocytes was measured with quantitative-PCR. Systemic levels of major chemokine ligands CCL2, CCL5, CCL3, and CXCL10 were evaluated by ELISA. Genotyping was performed for risk SNPs for AMD in the CFH, C3, and HTRA1 genes. RESULTS.The percentage of WBC subpopulations tested was similar between NV-AMD patients (n ¼ 18) and controls (n ¼ 20). CD14þCD16þ monocyte subpopulation showed a 3.5-fold increased expression of CCR1 (P ¼ 0.039; t-test) and a 2.2-fold increased expression of CCR2 (P ¼ 0.027) in patients compared with controls. Increased CCR1 and CCR2 expression was correlated with each other in patients (R 2 ¼ 0.64, P < 0.0001), but not controls (R 2 ¼ 0.02, P ¼ 0.57). Increased mRNA levels of CCR1 (1.6-fold, P ¼ 0.037) and CCR2 (1.6-fold, P ¼ 0.007) were found in monocytes from NV-AMD patients. Chemokine receptor expression was not correlated with the presence of risk SNPs, and was not associated with blood chemokine levels.CONCLUSIONS. CCR1 and CCR2 are coupregulated on the CD14þCD16þ monocyte population in NV-AMD patients. These data implicate CD14þCD16þ monocytes and chemokine signaling in AMD. Additional investigation is needed to elucidate the role of these monocytes and their potential as a biomarker or therapeutic target for AMD. (Invest Ophthalmol Vis Sci. 2012;53:5292-5300)

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Highly purified human peripheral blood monocytes produce IL-6 but not TNFα in response to angiotensin II

Cited by 16 publications

References 38 publications

Important role of CCR2 in a murine model of coronary vasculitis

Important role of CCR2 in a murine model of coronary vasculitis

Chronic high dose of captopril induces depressive-like behaviors in mice: possible mechanism of regulatory T cell in depression

Chemokine Receptor Expression in Peripheral Blood Monocytes from Patients with Neovascular Age-Related Macular Degeneration

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