Biomarkers of neuroinflammation: Focus on monocyte chemotaxis

2021 ◽  
Vol 429 ◽  
pp. 118009
Author(s):  
Carlo Ferrarese ◽  
Lucio Tremolizzo
Keyword(s):  
Monocyte Chemotaxis

scholarly journals Extracellular vesicles from dHL-60 cells as delivery vehicles for diverse therapeutics

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Jun-Kyu Kim ◽  
Young-Jin Youn ◽  
Yu-Bin Lee ◽  
Sun-Hwa Kim ◽  
Dong-Keun Song ◽  
...  
Keyword(s):  
Drug Delivery ◽  
Extracellular Vesicles ◽  
Macrophage Polarization ◽  
Promyelocytic Leukemia ◽  
Leukemia Cells ◽  
Effector Functions ◽  
Potential Source ◽  
Monocyte Chemotaxis ◽  
Delivery Vehicles ◽  
Intercellular Communications

AbstractExtracellular vesicles (EVs) are membrane-derived heterogeneous vesicles that mediate intercellular communications. They have recently been considered as ideal vehicles for drug-delivery systems, and immune cells are suggested as a potential source for drug-loaded EVs. In this study, we investigated the possibility of neutrophils as a source for drug-loaded EVs. Neutrophil-like differentiated human promyelocytic leukemia cells (dHL-60) produced massive amounts of EVs within 1 h. The dHL-60 cells are also easily loaded with various cargoes such as antibiotics (penicillin), anticancer drug (paclitaxel), chemoattractant (MCP-1), miRNA, and Cas9. The EVs derived from the dHL-60 cells showed efficient incorporation of these cargoes and significant effector functions, such as bactericidal activity, monocyte chemotaxis, and macrophage polarization. Our results suggest that neutrophils or neutrophil-like promyelocytic cells could be an attractive source for drug-delivery EVs.

Neuropeptide S stimulates human monocyte chemotaxis via NPS receptor activation

Peptides ◽  
2013 ◽  
Vol 39 ◽  
pp. 16-20 ◽  
Author(s):  
M. Filaferro ◽  
C. Novi ◽  
V. Ruggieri ◽  
S. Genedani ◽  
S. Alboni ◽  
...  
Keyword(s):  
Human Monocyte ◽  
Receptor Activation ◽  
Neuropeptide S ◽  
Monocyte Chemotaxis

Decreased Mononuclear and Polymorphonuclear Chemotaxis in Human Newborns,Infants, and Young Children

PEDIATRICS ◽  
1977 ◽  
Vol 60 (4) ◽  
pp. 467-472
Author(s):  
Robert B. Klein ◽  
Thomas J. Fischer ◽  
Sherrie E. Gard ◽  
Michael Biberstein ◽  
Kenneth C. Rich ◽  
...  
Keyword(s):  
Young Infant ◽  
Skin Tests ◽  
Boyden Chamber ◽  
High Power Field ◽  
Inflammatory Reactions ◽  
Adult Control ◽  
Susceptibility To Infection ◽  
Significant Difference ◽  
Monocyte Chemotaxis ◽  
Hypersensitivity Skin

A new method, chemotaxis under agarose gel, was used to assess the directed motility of polymorphonuclear (PMN) and mononuclear (MN) phagocytes of 21 newborns, 71 infants and children, and 50 adults. This assay requires only small quantities of cells and is rapid, easy, reproducible, and provides a permanent record. The chemotactic substance was zymosan-activated human serum. Monocyte chemotaxis in the newborn was approximately 50% of adult control values, using the Boyden chamber (8.1 ± 2 cells per high-power field[HPF] [SE] in newborns compared to 17 ± 3 cells per HPF in adults), and 25% of adult control values, using the agarose method (50 ± 10 cells in newborns compared to 216 ± 15 cells in adults). Both are significant differences (P < .005). MN chemotaxis remains extremely low through age 5, and remains moderately reduced until age 10. PMN chemotaxis in the newborn was 82 ± 21 cells compared to adult controls of 300± 42 cells, also a significant difference (P < .05). PMN chemotaxis remains markedly depressed through age 2. Thereafter, PMN chemotaxis increases but remains significantly less than in adults until age 16. These chemotactic defects may play an important role in depressed delayed hypersensitivity skin tests, diminished inflammatory reactions, and increased susceptibility to infection present in the newborn and young infant.

Human monocyte chemotaxis to complement-derived chemotaxins is enhanced by Gc-globulin

1994 ◽  
Vol 55 (3) ◽  
pp. 349-354 ◽  
Author(s):  
C. A. Piquette ◽  
R. Robinson-Hill ◽  
R. O. Webster
Keyword(s):  
Human Monocyte ◽  
Monocyte Chemotaxis

In Vitro Effect of Isotretinoin on Monocyte Chemotaxis

1986 ◽  
Vol 86 (5) ◽  
pp. 550-552 ◽  
Author(s):  
Ronald H Falcon ◽  
Wei-Li Lee ◽  
Alan R Shalita ◽  
Kamala Suntharalingam ◽  
Senih M Fikrig
Keyword(s):  
Monocyte Chemotaxis ◽  
Vitro Effect

scholarly journals Tat–Human Immunodeficiency Virus-1 Induces Human Monocyte Chemotaxis by Activation of Vascular Endothelial Growth Factor Receptor-1

Blood ◽  
1997 ◽  
Vol 90 (4) ◽  
pp. 1365-1372 ◽  
Author(s):  
Stefania Mitola ◽  
Silvano Sozzani ◽  
Walter Luini ◽  
Luca Primo ◽  
Alessandro Borsatti ◽  
...  
Keyword(s):  
Vascular Endothelial Growth Factor ◽  
Human Immunodeficiency Virus ◽  
Growth Factor ◽  
Tyrosine Kinase ◽  
Vascular Endothelial ◽  
Immunodeficiency Virus ◽  
Monocyte Chemotaxis ◽  
Endothelial Growth Factor ◽  
Hiv 1 ◽  
Human Immunodeficiency Virus 1

Human immunodeficiency virus-1 (HIV-1) Tat protein can be released by infected cells and activates mesenchymal cells. Among these, monocytes respond to Tat by migrating into tissues and releasing inflammatory mediators. In the present study, we have examined the molecular mechanism of monocyte activation by Tat, showing that this viral protein signals inside the cells through the tyrosine kinase receptor for vascular endothelial growth factor encoded by fms-like tyrosine kinase gene (VEGFR-1/Flt-1). Subnanomolar concentrations of Tat induced monocyte chemotaxis, which was inhibited by cell preincubation with vascular-endothelial growth factor-A (VEGF-A). This desensitisation was specific for VEGF-A, because it not was observed with FMLP. In addition, the soluble form of VEGFR-1 specifically inhibited polarization and migration induced by Tat and VEGF-A, thus confirming the common use of this receptor. Binding studies performed at equilibrium by using radiolabeled Tat showed that monocytes expressed a unique class of binding site, with a kd of approximately 0.2 nmol/L. The binding of radiolabeled Tat to monocyte surface and the cross-linking to a protein of 150 kD was inhibited specifically by an excess of cold Tat or VEGF-A. Western blot analysis with an antibody anti–VEGFR-1/Flt-1 performed on monocyte phosphoproteins immunoprecipitated by an monoclonal antibody antiphosphotyrosine showed that Tat induced a rapid phosphorylation in tyrosine residue of the 150-kD VEGFR-1/Flt-1. Taken together, these results suggest that biologic activities of HIV-1 Tat in human monocytes may, at least in part, be elicited by activation of VEGFR-1/Flt-1.

Abstract 450: Monocytic Glutaredoxin 1 Protects Mice Against Obesity, Hyperglycemia and Atherosclerosis

2017 ◽  
Vol 37 (suppl_1) ◽  
Author(s):  
Kevin Downs ◽  
Sina Tavakoli ◽  
John D Short ◽  
Huynh N Nguyen ◽  
Reto Asmis
Keyword(s):  
High Fat Diet ◽  
Statistical Significance ◽  
Gene Array ◽  
Metabolic Stress ◽  
Wild Type ◽  
Adipose Tissues ◽  
Atherosclerotic Lesions ◽  
Monocyte Chemotaxis

Overexpression of glutaredoxin 1 (Grx1) protects monocytes from metabolic stress-induced priming, i.e. dysregulation and hypersensitization to chemokines (Ullevig et al. ATVB 2012). To address the role of monocytic Grx1 in mice and in the development of atherogenesis and obesity, we transplanted bone marrow (BM) from either wild-type (WT) or Grx1 -/- donor mice into atherosclerosis-prone LDLR -/- mice and fed these mice a high-fat diet (HFD) for up to 20 weeks. Grx1 Leuko -/- mice showed accelerated weight gain after 9 weeks followed by early onset of hyperglycemia. After 6 weeks on HFD, atherosclerotic lesions were slightly larger in Grx1 Leuko -/- mice than in WT mice, but the differences did not reach statistical significance. However, after 20 weeks, Grx1 Leuko -/- mice showed 36% larger lesions than WT-BM recipients, and monocyte chemotaxis in vivo was increased 1.6-fold. Furthermore, compared to WT-BM recipients, adipose tissues and livers of Grx1 Leuko -/- mice also showed increased macrophage content and elevated tissue inflammation as determined by IHC and qRT-PCR-based gene array. Adipose tissue in particular, showed significant increases in the expression of proinflammatory genes in addition to an increased abundance of proinflammatory “crown-like” structures. In contrast, genes associated with inflammation resolving macrophages were significantly suppressed. Macrophages isolated from Grx1 -/- mice and stimulated with INFγ+TNFα also showed increased expression of pro-inflammatory M1-associated genes, whereas M2-associated genes were suppressed in Grx-1 -/- macrophages activated with IL-4. Furthermore, macrophages from Grx1 -/- mice exposed to metabolic stress also display increased protein S -glutathionylation, enhanced hypersensitization to chemokine, and impaired autophagy compared to macrophages from wild-type mice. Taken together, our data show that loss of monocytic Grx1 worsens monocyte priming in response to HFD-induced metabolic stress and accelerates the infiltration of dysfunctional monocyte-derived macrophages into tissues, such as aorta, liver and adipose tissues. We conclude that monocytic Grx1 is critical for maintaining metabolic homeostasis in mice and protects mice against obesity and atherogenesis.

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