scholarly journals Effect of pregnancy hormone mixtures on cytokine production and surface marker expression in naïve and LPS-activated THP-1 differentiated monocytes/macrophages

2019 ◽  
Vol 26 (2) ◽  
pp. 84-96
Author(s):  
María Isabel Mendoza-Cabrera ◽  
Rosa-Elena Navarro-Hernández ◽  
Anne Santerre ◽  
Pablo Cesar Ortiz-Lazareno ◽  
Ana Laura Pereira-Suárez ◽  
...  
Keyword(s):  
Inflammatory Response ◽  
Cytokine Production ◽  
Immune Cell ◽  
Surface Marker ◽  
Independent Manner ◽  
Surface Marker Expression ◽  
Monocytes And Macrophages ◽  
Marker Expression ◽  
Activated Monocytes ◽  
In Pregnancy

In pregnancy, maternal monocytes and macrophages acquire a specific phenotype that enables them to maintain immune tolerance and facilitate hormone–immune cell interactions, which are necessary for gestational progression. The aim of this study was to determine the effect of pregnancy hormone mixtures of the first and third trimesters on both resting and activated monocytes and macrophages. Pregnancy hormone levels (cortisol, estradiol, progesterone, and prolactin) were quantified at the first and third trimesters. The average of the levels obtained was used to prepare two mixtures of synthetic hormones: low and high. These mixtures were then used to stimulate THP-1 monocytes and macrophages, resting or activated with LPS. Cytokine production in the culture supernatants and surface marker expression (CD14, CD86, and CD163) were evaluated by ELISA and flow cytometry, respectively. We found that the hormones modulated the pro-inflammatory response of THP-1 cells, LPS-activated monocytes, and macrophages, inducing high levels of IL-10 and low levels of IL-8, IL-1-β, and IL-6. All hormone stimulation increased the CD163 receptor in both resting and LPS-activated monocytes and macrophages in a dose-independent manner, unlike CD14 and CD86. Pregnancy hormones promote the expression of the markers associated with the M2-like phenotype, modulating their pro-inflammatory response. This phenotype regulation by hormones could be a determinant in pregnancy.

scholarly journals The Fasciola hepatica Tegumental Antigen Suppresses Dendritic Cell Maturation and Function

2009 ◽  
Vol 77 (6) ◽  
pp. 2488-2498 ◽  
Author(s):  
Clare M. Hamilton ◽  
David J. Dowling ◽  
Christine E. Loscher ◽  
Russell M. Morphew ◽  
Peter M. Brophy ◽  
...  
Keyword(s):  
Cell Surface ◽  
Cytokine Production ◽  
Fasciola Hepatica ◽  
Surface Marker ◽  
Cell Surface Marker ◽  
Surface Marker Expression ◽  
Marker Expression ◽  
Anti Inflammatory ◽  
And Function ◽  
Cell Surface Marker Expression

ABSTRACT Parasitic worms and molecules derived from them have powerful anti-inflammatory properties and are shown to have therapeutic effects on inflammatory diseases. The helminth Fasciola hepatica has been reported to suppress antigen-specific Th1 responses in concurrent bacterial infections, thus demonstrating its anti-inflammatory ability in vivo. Here, F. hepatica tegumental antigen (Teg) was shown to significantly suppress serum levels of gamma interferon (IFN-γ) and interleukin-12p70 (IL-12p70) in a model of septic shock. Since dendritic cells (DCs) are a good source of IL-12p70 and critical in driving adaptive immunity, we investigated the effects of F. hepatica Teg on the activation and function of murine DCs. While Teg alone did not induce cytokine production or cell surface marker expression on DCs, it significantly suppressed cytokine production (IL-12p70, IL-6, IL-10, tumor necrosis factor alpha, and nitrite) and cell surface marker expression (CD80, CD86, and CD40) in DCs matured with a range of Toll-like receptor (TLR) and non-TLR ligands. Teg works independently of the TLR4 pathway, since it still functioned in DCs generated from TLR4 mutant and knockout mice. It impaired DC function by inhibiting their phagocytic capacity and their ability to prime T cells. It does not appear to target the common components (extracellular signal-regulated kinase, Jun N-terminal protein kinase, or p38) of the TLR pathways; however, it suppressed the active p65 subunit of the transcription factor NF-κB in mature DCs, which could explain the impairment of proinflammatory cytokine production. Overall, our results demonstrate the potent anti-inflammatory properties of F. hepatica Teg and its therapeutic potential as an anti-inflammatory agent.

scholarly journals Therapies with CCL25 require controlled release via microparticles to avoid strong inflammatory reactions

2021 ◽  
Vol 19 (1) ◽  
Author(s):  
J. Spinnen ◽  
K. Fröhlich ◽  
N. Sinner ◽  
M. Stolk ◽  
J. Ringe ◽  
...  
Keyword(s):  
Immune Cell ◽  
Surface Marker ◽  
M2 Macrophage ◽  
Prolonged Release ◽  
Direct Stimulation ◽  
Inflammatory Reactions ◽  
Surface Marker Expression ◽  
Immune Cell Subsets ◽  
Plga Microparticles ◽  
Marker Expression

Abstract Background Chemokine therapy with C–C motif chemokine ligand 25 (CCL25) is currently under investigation as a promising approach to treat articular cartilage degeneration. We developed a delayed release mechanism based on Poly (lactic-co-glycolic acid) (PLGA) microparticle encapsulation for intraarticular injections to ensure prolonged release of therapeutic dosages. However, CCL25 plays an important role in immune cell regulation and inflammatory processes like T-cell homing and chronic tissue inflammation. Therefore, the potential of CCL25 to activate immune cells must be assessed more thoroughly before further translation into clinical practice. The aim of this study was to evaluate the reaction of different immune cell subsets upon stimulation with different dosages of CCL25 in comparison to CCL25 released from PLGA particles. Results Immune cell subsets were treated for up to 5 days with CCL25 and subsequently analyzed regarding their cytokine secretion, surface marker expression, polarization, and migratory behavior. The CCL25 receptor C–C chemokine receptor type 9 (CCR9) was expressed to a different extent on all immune cell subsets. Direct stimulation of peripheral blood mononuclear cells (PBMCs) with high dosages of CCL25 resulted in strong increases in the secretion of monocyte chemoattractant protein-1 (MCP-1), interleukin-8 (IL-8), interleukin-1β (IL-1β), tumor-necrosis-factor-α (TNF-α) and interferon-γ (IFN-γ), upregulation of human leukocyte antigen-DR (HLA-DR) on monocytes and CD4+ T-cells, as well as immune cell migration along a CCL25 gradient. Immune cell stimulation with the supernatants from CCL25 loaded PLGA microparticles caused moderate increases in MCP-1, IL-8, and IL-1β levels, but no changes in surface marker expression or migration. Both CCL25-loaded and unloaded PLGA microparticles induced an increase in IL-8 and MCP-1 release in PBMCs and macrophages, and a slight shift of the surface marker profile towards the direction of M2-macrophage polarization. Conclusions While supernatants of CCL25 loaded PLGA microparticles did not provoke strong inflammatory reactions, direct stimulation with CCL25 shows the critical potential to induce global inflammatory activation of human leukocytes at certain concentrations. These findings underline the importance of a safe and reliable release system in a therapeutic setup. Failure of the delivery system could result in strong local and systemic inflammatory reactions that could potentially negate the benefits of chemokine therapy.

scholarly journals FACS-Based Isolation, Propagation and Characterization of Mouse Embryonic Cardiomyocytes Based on VCAM-1 Surface Marker Expression

PLoS ONE ◽  
2013 ◽  
Vol 8 (12) ◽  
pp. e82403 ◽  
Author(s):  
Annica Pontén ◽  
Stuart Walsh ◽  
Daniela Malan ◽  
Xiaojie Xian ◽  
Susanne Schéele ◽  
...  
Keyword(s):  
Surface Marker ◽  
Surface Marker Expression ◽  
Embryonic Cardiomyocytes ◽  
Marker Expression
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