scholarly journals Neutrophil DREAM come true: The not-so-impossible quest for mechanisms of neutrophil function and heterogeneity

2021 ◽  
Vol 219 (1) ◽  
Author(s):  
John C. Gomez ◽  
Claire M. Doerschuk
Keyword(s):  
Endothelial Cells ◽  
Transcriptional Repressor ◽  
Neutrophil Function ◽  
Critical Response ◽  
Inflammatory Stimuli

Neutrophil functions and responses are heterogeneous, and the nature and categorization of this heterogeneity is achieving considerable interest. Work by Li et al. in this issue of JEM (2021. J. Exp. Med.https://doi.org/10.1084/jem.20211083) identifies how a transcriptional repressor, DREAM, regulates adhesion of neutrophils to endothelial cells and their transmigration into tissue. This study offers a mechanism for heterogeneity in this critical response of neutrophils to inflammatory stimuli.

High-density lipoproteins attenuate interleukin-6 production in endothelial cells exposed to pro-inflammatory stimuli

2005 ◽  
Vol 1736 (2) ◽  
pp. 136-143 ◽  
Author(s):  
Monica Gomaraschi ◽  
Nicoletta Basilico ◽  
Francesca Sisto ◽  
Donatella Taramelli ◽  
Sonia Eligini ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Interleukin 6 ◽  
High Density ◽  
High Density Lipoproteins ◽  
Inflammatory Stimuli

Tumor-promoting phorbol esters inhibit monocyte adherence to endothelial cells

1989 ◽  
Vol 66 (1) ◽  
pp. 437-442 ◽  
Author(s):  
D. W. Kamp ◽  
K. D. Bauer ◽  
D. B. Rubin ◽  
M. M. Dunn
Keyword(s):  
Endothelial Cells ◽  
Phorbol Esters ◽  
Kinetic Studies ◽  
Inhibitory Effect ◽  
Adhesive Interaction ◽  
Kinase C ◽  
Inflammatory Stimuli ◽  
Similar Inhibitory Effect ◽  
Monocyte Adherence ◽  
Activate Protein Kinase

Monocyte adherence to endothelial cells (EC) is an important event in the development of a monocytic inflammatory response, yet the effects of inflammatory mediators on monocyte adherence to EC are not well described. We compared the effects of phorbol esters known to activate protein kinase C, including phorbol myristate acetate (PMA) and phorbol 12,13-dibutyrate (PDA), on monocyte adherence to bovine aortic EC. Human monocytes (purity 90 +/- 1% SE) were isolated by centrifugal elutriation to obtain monocytes not previously exposed to a surface. Kinetic studies revealed that 51Cr-labeled monocyte adherence to EC reached a plateau after a 45-min incubation. Concentrations of PMA between 10 and 1,000 ng/ml significantly decreased monocyte adherence to EC (26 +/- 10 and 35 +/- 8% decrease compared with control, respectively). Concentrations of PDA of 100 and 1,000 ng/ml had a similar inhibitory effect. In contrast, the chemotactic stimulus, zymosan-activated serum, significantly increased monocyte adherence (40 +/- 14% increase compared with control). Thus inflammatory stimuli have different effects on the adhesive interaction of monocytes to EC. This may provide a mechanism to selectively modulate monocyte egress from the circulation into extravascular inflammatory sites.

scholarly journals The Response of Macrophages and Neutrophils to Hypoxia in the Context of Cancer and Other Inflammatory Diseases

2016 ◽  
Vol 2016 ◽  
pp. 1-10 ◽  
Author(s):  
Antje Egners ◽  
Merve Erdem ◽  
Thorsten Cramer
Keyword(s):  
Endothelial Cells ◽  
Inflammatory Diseases ◽  
Neutrophil Function ◽  
Proper Function ◽  
Low Oxygen ◽  
Bacterial Killing ◽  
Molecular Responses ◽  
Chronic Inflammatory Diseases ◽  
Hypoxic Conditions ◽  
Cellular Components

Lack of oxygen (hypoxia) is a hallmark of a multitude of acute and chronic diseases and can be either beneficial or detrimental for organ restitution and recovery. In the context of inflammation, hypoxia is particularly important and can significantly influence the course of inflammatory diseases. Macrophages and neutrophils, the chief cellular components of innate immunity, display distinct properties when exposed to hypoxic conditions. Virtually every aspect of macrophage and neutrophil function is affected by hypoxia, amongst others, morphology, migration, chemotaxis, adherence to endothelial cells, bacterial killing, differentiation/polarization, and protumorigenic activity. Prominent arenas of macrophage and neutrophil function, for example, acute/chronic inflammation and the microenvironment of solid tumors, are characterized by low oxygen levels, demonstrating the paramount importance of the hypoxic response for proper function of these cells. Members of the hypoxia-inducible transcription factor (HIF) family emerged as pivotal molecular regulators of macrophages and neutrophils. In this review, we will summarize the molecular responses of macrophages and neutrophils to hypoxia in the context of cancer and other chronic inflammatory diseases and discuss the potential avenues for therapeutic intervention that arise from this knowledge.

A line of transgenic pigs in which the expression of human decay-accelerating factor by endothelial cells is increased in the presence of inflammatory stimuli

1996 ◽  
Vol 3 (1) ◽  
pp. 87-91 ◽  
Author(s):  
Christine A. Carrington ◽  
Andrew C. Richards ◽  
Alexander W. Tucker ◽  
Anna L. Peters ◽  
David J.G. White
Keyword(s):  
Endothelial Cells ◽  
Transgenic Pigs ◽  
Decay Accelerating Factor ◽  
Inflammatory Stimuli

Angiopoietin-2 promotes inflammatory lymphangiogenesis and its effect can be blocked by the specific inhibitor L1-10

2012 ◽  
Vol 302 (1) ◽  
pp. H215-H223 ◽  
Author(s):  
Zhi-Xin Yan ◽  
Zhao-Hua Jiang ◽  
Ning-Fei Liu
Keyword(s):  
Endothelial Cells ◽  
Vascular Endothelial Cells ◽  
Transplant Rejection ◽  
Lymphatic Vessels ◽  
Specific Inhibitor ◽  
Biological Behavior ◽  
Tnf Α ◽  
Inflammatory Stimuli ◽  
Angiopoietin 2

Angiopoietin (Ang)-2, a ligand of the receptor tyrosine kinase Tie2, is known to be involved in the regulation of embryonic lymphangiogenesis. However, the role of Ang-2 in postnatal pathological lymphangiogenesis, such as inflammation, is largely unknown. We used a combination of imaging, molecular, and cellular approaches to investigate whether Ang-2 is involved in inflammatory lymphangiogenesis. We observed strong and continuous expression of Ang-2 on newly generated lymphatic vessels for 2 wk in sutured corneas of BALB/c mice. This expression was concurrent with an increased number of lymphatic vessels. TNF-α expression also increased, with peak TNF-α expression occurring before peak Ang-2 expression was reached. In vitro experiments showed that TNF-α stimulates Ang-2 and Tie2 and ICAM-1 expression on human lymphatic endothelial cells (LECs) and blood vascular endothelial cells (BECs). Ang-2 alone did not affect the biological behavior of LECs, whereas Ang-2 combined with TNF-α significantly promoted the proliferation of LECs but not BECs. In mouse models, blockade of Ang-2 with L1-10, an Ang-2-specific inhibitor, significantly inhibited lymphangiogenesis but promoted angiogenesis. These results clearly indicate that Ang-2 acts as a crucial regulator of inflammatory lymphangiogenesis by sensitizing the lymphatic vasculature to inflammatory stimuli, thereby directly promoting lymphangiogenesis. The involvement of Ang-2 in inflammatory lymphangiogenesis provides a strong rationale for the exploitation of anti-Ang-2 treatment in the prevention and treatment of tumor metastasis and transplant rejection.

scholarly journals Dephosphorylation of the catenins p120 and p100 in endothelial cells in response to inflammatory stimuli

1999 ◽  
Vol 338 (2) ◽  
pp. 471-478 ◽  
Author(s):  
Marianne J. RATCLIFFE ◽  
Caroline SMALES ◽  
James M. STADDON
Keyword(s):  
Endothelial Cells ◽  
Protein Kinase C ◽  
Protein Kinase ◽  
Tight Junction ◽  
Adherens Junction ◽  
Receptor Activation ◽  
Protein Kinase C Inhibitors ◽  
Kinase C ◽  
Inflammatory Stimuli ◽  
Tight Junction Permeability

Inflammatory mediators such as histamine and thrombin increase the tight-junction permeability of endothelial cells. Tight-junction permeability may be independently controlled, but is dependent on the adherens junction, where adhesion is achieved through homotypic interaction of cadherins, which in turn are associated with cytoplasmic proteins, the catenins. p120, also termed p120cas/p120ctn, and its splice variant, p100, are catenins. p120, originally discovered as a substrate of the tyrosine kinase Src, is also a target for a protein kinase C-stimulated pathway in epithelial cells, causing its serine/threonine dephosphorylation. The present study shows that pharmacological activation of protein kinase C stimulated a similar pathway in endothelial cells. Activation of receptors for agents such as histamine (H1), thrombin and lysophosphatidic acid in the endothelial cells also caused serine/threonine dephosphorylation of p120 and p100, suggesting physiological relevance. However, protein kinase C inhibitors, although blocking the effect of pharmacological activation of protein kinase C, did not block the effects due to receptor activation. Calcium mobilization and the myosin-light-chain-kinase pathway do not participate in p120/p100 signalling. In conclusion, endothelial cells possess protein kinase C-dependent and -independent pathways regulating p120/p100 serine/threonine phosphorylation. These data describe a new connection between inflammatory agents, receptor-stimulated signalling and pathways potentially influencing intercellular adhesion in endothelial cells.

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