Tasco-Forage: II. Monocyte immune cell response and performance of beef steers grazing tall fescue treated with a seaweed extract.

2001 ◽  
Vol 79 (4) ◽  
pp. 1022 ◽  
Author(s):  
K E Saker ◽  
V G Allen ◽  
J P Fontenot ◽  
C P Bagley ◽  
R L Ivy ◽  
...  
Keyword(s):  
Tall Fescue ◽  
Cell Response ◽  
Immune Cell ◽  
Seaweed Extract ◽  
Beef Steers ◽  
And Performance ◽  
Immune Cell Response

Monocyte immune cell response and copper status in beef steers that grazed endophyte-infected tall fescue.

1998 ◽  
Vol 76 (10) ◽  
pp. 2694 ◽  
Author(s):  
K E Saker ◽  
V G Allen ◽  
J Kalnitsky ◽  
C D Thatcher ◽  
W S Swecker ◽  
...  
Keyword(s):  
Tall Fescue ◽  
Cell Response ◽  
Immune Cell ◽  
Beef Steers ◽  
Copper Status ◽  
Immune Cell Response ◽  
And Copper Status

scholarly journals RhoA Signaling in Immune Cell Response and Cardiac Disease

Cells ◽  
2021 ◽  
Vol 10 (7) ◽  
pp. 1681
Author(s):  
Lucia Sophie Kilian ◽  
Derk Frank ◽  
Ashraf Yusuf Rangrez
Keyword(s):  
Cardiac Disease ◽  
Cell Response ◽  
Cell Activation ◽  
Immune Cell ◽  
Inflammatory Diseases ◽  
Heart Diseases ◽  
Small Gtpase ◽  
Cardiac Inflammation ◽  
Immune Cell Activation ◽  
Immune Cell Response

Chronic inflammation, the activation of immune cells and their cross-talk with cardiomyocytes in the pathogenesis and progression of heart diseases has long been overlooked. However, with the latest research developments, it is increasingly accepted that a vicious cycle exists where cardiomyocytes release cardiocrine signaling molecules that spiral down to immune cell activation and chronic state of low-level inflammation. For example, cardiocrine molecules released from injured or stressed cardiomyocytes can stimulate macrophages, dendritic cells, neutrophils and even T-cells, which then subsequently increase cardiac inflammation by co-stimulation and positive feedback loops. One of the key proteins involved in stress-mediated cardiomyocyte signal transduction is a small GTPase RhoA. Importantly, the regulation of RhoA activation is critical for effective immune cell response and is being considered as one of the potential therapeutic targets in many immune-cell-mediated inflammatory diseases. In this review we provide an update on the role of RhoA at the juncture of immune cell activation, inflammation and cardiac disease.

scholarly journals IMMU-68. SINGLE-CELL PROTEOMIC ANALYSIS OF IMMUNE CELL RESPONSE TO CHECKPOINT BLOCKADE USING 30-PARAMETER FLOW CYTOMETRY

2018 ◽  
Vol 20 (suppl_6) ◽  
pp. vi137-vi137
Author(s):  
Amber Giles ◽  
Leonard Nettey ◽  
Thomas Liechti ◽  
Margaret Beddall ◽  
Elizabeth Vera ◽  
...  
Keyword(s):  
Flow Cytometry ◽  
Single Cell ◽  
Cell Response ◽  
Proteomic Analysis ◽  
Immune Cell ◽  
Checkpoint Blockade ◽  
Immune Cell Response

scholarly journals Postoperative cellular stress in the kidney is associated with an early systemic γδ T-cell immune cell response

Critical Care ◽  
2018 ◽  
Vol 22 (1) ◽  
Author(s):  
Ivan Göcze ◽  
Katharina Ehehalt ◽  
Florian Zeman ◽  
Paloma Riquelme ◽  
Karin Pfister ◽  
...  
Keyword(s):  
T Cell ◽  
Cell Response ◽  
Immune Cell ◽  
Cellular Stress ◽  
Γδ T Cell ◽  
Immune Cell Response

scholarly journals Immune cells as targets for cardioprotection: new players and novel therapeutic opportunities

2019 ◽  
Vol 115 (7) ◽  
pp. 1117-1130 ◽  
Author(s):  
Ioanna Andreadou ◽  
Hector A Cabrera-Fuentes ◽  
Yvan Devaux ◽  
Nikolaos G Frangogiannis ◽  
Stefan Frantz ◽  
...  
Keyword(s):  
Heart Failure ◽  
Inflammatory Reaction ◽  
Immune Cells ◽  
Cell Response ◽  
Immune Cell ◽  
Left Ventricular ◽  
Lymphoid Cells ◽  
Inflammatory Phase ◽  
Anti Inflammatory ◽  
Immune Cell Response

Abstract New therapies are required to reduce myocardial infarct (MI) size and prevent the onset of heart failure in patients presenting with acute myocardial infarction (AMI), one of the leading causes of death and disability globally. In this regard, the immune cell response to AMI, which comprises an initial pro-inflammatory reaction followed by an anti-inflammatory phase, contributes to final MI size and post-AMI remodelling [changes in left ventricular (LV) size and function]. The transition between these two phases is critical in this regard, with a persistent and severe pro-inflammatory reaction leading to adverse LV remodelling and increased propensity for developing heart failure. In this review article, we provide an overview of the immune cells involved in orchestrating the complex and dynamic inflammatory response to AMI—these include neutrophils, monocytes/macrophages, and emerging players such as dendritic cells, lymphocytes, pericardial lymphoid cells, endothelial cells, and cardiac fibroblasts. We discuss potential reasons for past failures of anti-inflammatory cardioprotective therapies, and highlight new treatment targets for modulating the immune cell response to AMI, as a potential therapeutic strategy to improve clinical outcomes in AMI patients. This article is part of a Cardiovascular Research Spotlight Issue entitled ‘Cardioprotection Beyond the Cardiomyocyte’, and emerged as part of the discussions of the European Union (EU)-CARDIOPROTECTION Cooperation in Science and Technology (COST) Action, CA16225.

Abstract 435: Brown Adipose Tissue Activation in the Postprandial State Reflects on Plasma Lipoproteins and Immune Cell Response in Humans

2014 ◽  
Vol 34 (suppl_1) ◽  
Author(s):  
Alexandra Mellerowicz ◽  
Madelene Ericsson ◽  
Mattias Hedlund ◽  
Stefan K Nilsson
Keyword(s):  
Adipose Tissue ◽  
Brown Adipose Tissue ◽  
Cell Response ◽  
Immune Cell ◽  
Plasma Lipoproteins ◽  
Emg Activity ◽  
Cold Stimulation ◽  
Postprandial State ◽  
Brown Adipose ◽  
Immune Cell Response

Background: Brown adipose tissue (BAT) has a unique to ability to use excess energy for heat production. It is therefore an attractive target organ for counteracting obesity and related metabolic diseases where overfeeding is an underlying cause. BAT has in murine models been shown to clear postprandial lipids quickly. The postprandial response is associated to systemic inflammatory alterations and an increased lipid pressure possibly driving atherosclerosis development. We hypothesized that BAT activation would affect postprandial lipid clearance and that this would reflect in an altered immune cell response. Methods: Young male volunteers were subject to an oral fat tolerance test at two separate occasions during both cold stimulation and in thermoneutral control conditions. Body temperature and EMG activity was monitored and energy expenditure (EE) was measured. Blood samples were taken at baseline and every 30 min for 2 h. Plasma lipids and the immune cell response. Results: Cold stimulation during OFTT resulted in a 19,4 % higher EE compared to warm conditions (P=0,007). Surprisingly, no changes in plasma TG were observed. A 2-fold elevation in free fatty acids (FFA) was seen in cold which also correlated positively with EE (P=0,008). Total plasma cholesterol increased compared to warm conditions by 0,56 mmol/L (P=0,050). LDL-c and HDL-c were increased in cold (0,20 mmol/L difference P=0,048 and 0,16 mmol/L P=0,002) whereas remnant-c was unaltered between the two thermal conditions. White blood cell count (WBC) after OFTT was significantly increased in cold (P = 0,018) by 0,29 х 109/L. Discussion: BAT activation in the postprandial state results in increased HDL-c, possibly indicating increased vascular lipolysis and associated pre-β HDL particle formation. Increased VLDL production due to elevated FFA levels in the cold state and might explain why plasma TG is unaltered and also why LDL-c remains at a higher concentration in the cold. Conclusions: BAT might be an attractive target for obesity treatment but potentially displays pro-atherogenic properties that must be addressed in longitudinal studies.

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