scholarly journals Patrolling monocytes inhibit osteosarcoma metastasis to the lung

Aging ◽  
2020 ◽  
Author(s):  
Ting Chen ◽  
Lin Zhao
Keyword(s):  
Patrolling Monocytes

scholarly journals S1PR5 is pivotal for the homeostasis of patrolling monocytes

2013 ◽  
Vol 43 (6) ◽  
pp. 1667-1675 ◽  
Author(s):  
Emilie Debien ◽  
Katia Mayol ◽  
Vincent Biajoux ◽  
Cécile Daussy ◽  
Mercedes Gomez De Aguero ◽  
...  
Keyword(s):  
Patrolling Monocytes

scholarly journals The Impact of Ly6Clow Monocytes after Cerebral Hypoxia-Ischemia in Adult Mice

2014 ◽  
Vol 34 (7) ◽  
pp. e1-e9 ◽  
Author(s):  
Jean-Philippe Michaud ◽  
Pedro Moreno Pimentel-Coelho ◽  
Yannick Tremblay ◽  
Serge Rivest
Keyword(s):  
Ischemic Stroke ◽  
Cell Loss ◽  
Cerebral Hypoxia ◽  
Lesion Site ◽  
Phagocytic Cells ◽  
Inflammatory Monocytes ◽  
Adult Mice ◽  
Hypoxia Ischemia ◽  
The Impact ◽  
Patrolling Monocytes

After an ischemic stroke, mononuclear phagocytic cells such as microglia, macrophages, and monocytes migrate to the lesion site and coordinate an immune response. Monocytes, which are recruited from the bloodstream after ischemic brain injury, can be categorized into two subsets in mice: inflammatory and patrolling monocytes. Although inflammatory monocytes (Ly6Chi) seem to have a protective role in stroke progression, the impact of patrolling monocytes (Ly6Clow) is unknown. To address the role of Ly6Clow monocytes in stroke, we generated bone marrow chimeric mice in which their hematopoietic system was replaced by Nr4a1−/− cells, allowing the complete and permanent ablation of Ly6Clow monocytes without affecting the Ly6Chi subset. We then subjected adult mice to cerebral hypoxia-ischemia using the Levine/Vannucci model. Functional outcomes after stroke such as body weight change, neurologic score, motor functions and spatial learning were not affected. Moreover, depletion in Ly6Clow monocytes did not change significantly the total infarct size, cell loss, atrophy, the number, or the activation state of microglia/macrophages at the lesion site. These data suggest that Ly6Clow patrolling monocytes are redundant in the progression and recovery of ischemic stroke.

scholarly journals A Polecat’s View of Patrolling Monocytes

2017 ◽  
Vol 120 (11) ◽  
pp. 1699-1701 ◽  
Author(s):  
Jesse W. Williams ◽  
Gwendalyn J. Randolph ◽  
Bernd H. Zinselmeyer
Keyword(s):  
Patrolling Monocytes

scholarly journals Distinct signals and immune cells drive liver pathology and glomerulonephritis in ABIN1[D485N] mice

2019 ◽  
Vol 2 (6) ◽  
pp. e201900533 ◽  
Author(s):  
Sambit Kumar Nanda ◽  
Tsvetana Petrova ◽  
Francesco Marchesi ◽  
Marek Gierlinski ◽  
Momchil Razsolkov ◽  
...  
Keyword(s):  
Immune System ◽  
Adaptive Immune System ◽  
Liver Pathology ◽  
Disease Phenotype ◽  
Adaptive Immune ◽  
Inflammatory Monocytes ◽  
Diagnostic Potential ◽  
Ubiquitin Binding ◽  
Orally Active ◽  
Patrolling Monocytes

We report that TLR7, IL-6, and the adaptive immune system are essential for autoimmunity and glomerulonephritis but not for liver pathology in mice expressing the ubiquitin-binding–defective ABIN1[D485N] mutant. The blood and organs of ABIN1[D485N] mice have exceptionally high numbers of patrolling monocytes (pMo), which develop independently of IL-6 and the adaptive immune system. They are detectable in the blood months before autoimmunity and organ pathology are seen and may have diagnostic potential. The splenic pMo, inflammatory monocytes (iMo), and neutrophils of ABIN1[D485N] mice expressed high levels of mRNAs encoding proteins released during NETosis, which together with the high numbers of monocyte-derived dendritic cells (MoDCs) may drive the liver pathology in ABIN1[D485N] mice, and contribute to the pathology of other organs. The splenic iMo of ABIN1[D485N] mice displayed high expression of mRNAs encoding proteins controlling cell division and were actively dividing; this may underlie the increased pMo and MoDC numbers, which are derived from iMo. An orally active IRAK4 inhibitor suppressed all facets of the disease phenotype and prevented the increase in pMo numbers.

scholarly journals Patrolling monocytes are recruited and activated by diabetes to protect retinal microvessels

2020 ◽  
Author(s):  
Ada Admin ◽  
Francesco Tecilazich ◽  
Toan A. Phan ◽  
Fabio Simeoni ◽  
Giulia Maria Scotti ◽  
...  
Keyword(s):  
Gene Expression ◽  
Diabetic Retinopathy ◽  
General Circulation ◽  
Absolute Number ◽  
Retinal Vessels ◽  
Wild Type ◽  
Long Latency ◽  
History Of ◽  
Acellular Capillaries ◽  
Patrolling Monocytes

In diabetes there is a long latency between onset of hyperglycemia and appearance of structural microangiopathy. Because Ly6C<sup>low</sup> patrolling monocytes (PMo) behave as housekeepers of the vasculature, we tested whether PMo protect microvessels against diabetes. <p>We found that, in wild-type mice,<b> </b>diabetes reduced PMo in the general circulation but increased by 4-fold the absolute number of PMo adherent to retinal vessels (leukostasis). Conversely, in diabetic NR4A1<sup>-/-</sup> mice ─ a model of absence of PMo ─ there was no increase in leukostasis at all; and at 6 months of diabetes the number of retinal acellular capillaries almost doubled when compared to diabetic wild-type mice. Circulating PMo showed gene expression changes indicative of enhanced migratory, vasculo-protective, and housekeeping activities; as well as profound suppression of genes related to inflammation and apoptosis. Pro-migratory CXCR4 was no longer upregulated at longer duration, when retinal acellular capillaries begin to increase.</p> <p>Thus, after short diabetes duration, PMo are the cells preferentially recruited to the retinal vessels and protect vessels from diabetic damage. These observations support the need for reinterpretation of the functional meaning of leukostasis in diabetes, and document within the natural history of diabetic retinopathy processes of protection-repair that can provide novel paradigms for prevention. </p>

scholarly journals Relationship between dynamic changes in subpopulations of blood monocytes and the development of complications in patients with acute myocardial infarction

2020 ◽  
Vol 27 (4) ◽  
pp. 9-17
Author(s):  
T. V. Talayeva ◽  
O. M. Parkhomenko ◽  
I. V. Tretyak ◽  
O. V. Dovhan ◽  
O. V. Shumakov
Keyword(s):  
Myocardial Infarction ◽  
Absolute Number ◽  
Control Group ◽  
Blood Monocytes ◽  
The Absolute ◽  
Anti Inflammatory ◽  
Classical Monocytes ◽  
Intermediate Monocytes ◽  
Patrolling Monocytes

The aim – to determine the extent of different subpopulations of blood monocytes in acute myocardial infarction (AMI) with ST-segment elevation patients on day 1 and 7 and to evaluate the relationship between their content and the dynamics of changes and the risk of complications after AMI.Materials and methods. The composition of individual subpopulations of monocytes in the peripheral venous blood (and general clinical and biochemical blood tests) was evaluated in 50 pts with STEMI (who were admitted within 6 hours after the onset of the disease) at admission (before primary PCI) and on day 7. All patients received standard recommended therapy. Dynamic heart echocardiography was also performed on the 1st and 7th day. All patients were divided into 2 groups depending on the dynamical increase (1 group – 21 pts) or decrease (2 group – 29 pts) of classical monocytes (CD14hiCD16–) subpopulation during 7 days of follow-up. The control group included 15 healthy subjects with no signs of coronary heart disease and 23 pts with chronic coronary heart disease without AMI.Results and discussion. In subgroup 1, the percentage of the «classical» fraction of monocytes during the observation increased to 89.0±1.2 %, which was 4.2 % more than on the 1st day and 12.5 % more than in the control group (р<0.05), while the absolute amount of classic monocytes on day 7 increased by 48 % compared to initial value (р<0.01). The percentage of «intermediate» (CD14hiCD16+) blood monocytes in patients of this subgroup on the 1st day of hospitalization was 70 % higher than in the control group, and 42 % higher than in the 2nd subgroup of patients (р<0,001), however, on the 7th day it decreased by 30 % compared to baseline, although it remained by 8 % more than in the control group (the absolute number of «intermediate» monocytes did not change). The activation index (IA) of the «intermediate» monocytes on the first day did not differ between subgroups and was 40 % higher than in the control group (р<0.001). However, in the dynamics of observation, in patients of subgroup 1, this figure did not change, while in subgroup 2 IA decreased by 60 % (р<0.001). Despite the fact that the absolute number of anti-inflammatory («patrolling») (CD14+lowCD16++) monocytes did not change until the 7th day of observation (and their percentage decreased slightly), their IA was significantly lower than in the control group (95 %) and in patients of subgroup 2 (92 %, р<0,001). In patients of subgroup 2, the decrease of the percentage of «classic» monocytes was –7.7 % (from 90.4±0.8 to 83.4±1.2 %). Despite the fact that the number and percentage of intermediate monocytes increased in dynamics, their IA decreased almost 2 times, which may indicate a decrease in the pro-inflammatory ability these monocytes. The percentage and number of «patrolling» monocytes increased in dynamics by 37.4 % (р<0.0001) and by 268.3 % (р<0.01), respectively. IA of patrolling monocytes was almost 12 and 7 times higher than in patients of subgroup 1 on the 1st and 7th day of observation, respectively, which may indicate a significant activation of anti-inflammatory activity of patrolling monocytes. Intracardiac thrombosis was 3.3 times more common in patients of subgroup 1, in this subgroup was also more often noted (compared to the subgroup 2): dilatation of the left ventricle (almost 8 times), reduction of left ventricular ejection fraction (4 times), and pathological post-infarction remodeling of the left ventricle (almost 7 times).Conclusions. The results of the study indicate the important role of different subpopulations of blood monocytes in the processes of myocardial damage and recovery (in particular, the pro-inflammatory role of increasing the number of classical monocytes and increasing the activity of intermediate monocytes, as well as the anti-inflammatory role of increasing the number, percentage and activity of patrolling monocytes) in patients with AMI and can be the basis for developing new approaches to the diagnosis and prevention of complications of this disease.

scholarly journals HO-1hi patrolling monocytes protect against vaso-occlusion in sickle cell disease

Blood ◽  
2018 ◽  
Vol 131 (14) ◽  
pp. 1600-1610 ◽  
Author(s):  
Yunfeng Liu ◽  
Fangmiao Jing ◽  
Woelsung Yi ◽  
Avital Mendelson ◽  
Patricia Shi ◽  
...  
Keyword(s):  
Sickle Cell Disease ◽  
Sickle Cell ◽  
Cell Disease ◽  
Key Points ◽  
Patrolling Monocytes ◽  
Lower Frequencies

Key Points SCD patients with a recent VOC episode have lower frequencies and numbers of HO-1hi patrolling monocytes. Heme-driven SCD vaso-occlusion is exacerbated in mice lacking patrolling monocytes and reversed following patrolling monocyte transfer.

scholarly journals Murine cytomegalovirus disseminates independently of CX3CR1, CCL2 or its m131/m129 chemokine homologue

2019 ◽  
Vol 100 (12) ◽  
pp. 1695-1700 ◽  
Author(s):  
Helen E. Farrell ◽  
Kimberley Bruce ◽  
Alec J. Redwood ◽  
Philip G. Stevenson
Keyword(s):  
Salivary Gland ◽  
Murine Cytomegalovirus ◽  
Entry Site ◽  
Fractalkine Receptor ◽  
Systemic Spread ◽  
Infected Cells ◽  
Initial Seeding ◽  
Receptor Cx3cr1 ◽  
Patrolling Monocytes

Cytomegaloviruses (CMVs) use myeloid cells to move within their hosts. Murine CMV (MCMV) colonizes the salivary glands for long-term shedding, and reaches them via CD11c+ infected cells. A need to recruit patrolling monocytes for systemic spread has been proposed, based on poor salivary gland infection in fractalkine receptor (CX3CR1)-deficient mice. We found no significant CX3CR1 dependence of salivary gland infection. CCL2 and the viral m131/m129 chemokine homologue were also redundant for acute MCMV spread, arguing against a need for inflammation or infection to recruit additional monocytes to the entry site. M131/m129 promoted salivary gland infection, but only after the initial seeding of infected cells to this site. Our data support the idea that MCMV disseminates by infecting and mobilizing tissue-resident dendritic cells.

scholarly journals Patrolling monocytes scavenge endothelial-adherent sickle RBCs: a novel mechanism of inhibition of vaso-occlusion in SCD

Blood ◽  
2019 ◽  
Vol 134 (7) ◽  
pp. 579-590 ◽  
Author(s):  
Yunfeng Liu ◽  
Hui Zhong ◽  
Weili Bao ◽  
Avital Mendelson ◽  
Xiuli An ◽  
...  
Keyword(s):  
Muramyl Dipeptide ◽  
Organ Damage ◽  
Heme Oxygenase 1 ◽  
Cytotoxic Effects ◽  
Mechanism Of Inhibition ◽  
Promising Therapeutic Target ◽  
Cellular Debris ◽  
Selective Depletion ◽  
Acute Crisis ◽  
Patrolling Monocytes

Abstract Painful vaso-occlusive crisis (VOC) is the most common complication of sickle cell disease (SCD). Increasing evidence suggests that vaso-occlusion is initiated by increased adherence of sickle red blood cells (RBCs) to the vascular endothelium. Thus, the mechanisms that remove endothelial-attached sickle RBCs from the microvasculature are expected to be critical for optimal blood flow and prevention of VOC in SCD. We hypothesized that patrolling monocytes (PMos), which protect against vascular damage by scavenging cellular debris, could remove endothelial-adherent sickle RBCs and ameliorate VOC in SCD. We detected RBC (GPA+)-engulfed material in circulating PMos of patients with SCD, and their frequency was further increased during acute crisis. RBC uptake by PMos was specific to endothelial-attached sickle, but not control, RBCs and occurred mostly through ICAM-1, CD11a, and CD18. Heme oxygenase 1 induction, by counteracting the cytotoxic effects of engulfed RBC breakdown products, increased PMo viability. In addition, transfusions, by lowering sickle RBC uptake, improved PMo survival. Selective depletion of PMos in Townes sickle mice exacerbated vascular stasis and tissue damage, whereas treatment with muramyl dipeptide (NOD2 ligand), which increases PMo mass, reduced stasis and SCD associated organ damage. Altogether, these data demonstrate a novel mechanism for removal of endothelial attached sickle RBCs mediated by PMos that can protect against VOC pathogenesis, further supporting PMos as a promising therapeutic target in SCD VOC.

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