scholarly journals Dietary Sodium Nitrite Causes Similar Modifications to Splenic Inflammatory Gene Expression as a High-Fat Diet

2021 ◽  
Vol 67 (6) ◽  
pp. 404-416
Author(s):  
Motoko OARADA ◽  
Yuushi OKUMURA ◽  
Katsuya HIRASAKA ◽  
Kosuke SUGIURA ◽  
Nobuhiko TACHIBANA ◽  
...  
Keyword(s):  
Gene Expression ◽  
Sodium Nitrite ◽  
High Fat Diet ◽  
Dietary Sodium ◽  
High Fat ◽  
Inflammatory Gene Expression ◽  
Inflammatory Gene

scholarly journals Maternal high-fat diet induces sex-specific changes to glucocorticoid and inflammatory signaling in response to corticosterone and lipopolysaccharide challenge in adult rat offspring

2019 ◽  
Author(s):  
Sanoji Wijenayake ◽  
Mouly F. Rahman ◽  
Christine M.W. Lum ◽  
Wilfred C. De Vega ◽  
Aya Sasaki ◽  
...  
Keyword(s):  
Gene Expression ◽  
High Fat Diet ◽  
Maternal Obesity ◽  
Inflammatory Responses ◽  
Physiological Stress ◽  
High Fat ◽  
Inflammatory Gene Expression ◽  
Inflammatory Genes ◽  
Inflammatory Gene ◽  
Rat Offspring

ABSTRACTBackgroundAcute elevations in endogenous corticosterone (CORT) with psychosocial stress or exogenous administration potentiate inflammatory gene expression. Maternal obesity as a result of high-fat diet (HFD) consumption has been linked to higher basal levels of neuroinflammation, including increased expression of pro-inflammatory genes in the amygdala. These findings suggest that exposure to maternal HFD may elicit pro-inflammatory responses in the presence of an immune stressor such as lipopolysaccharide (LPS), a component of gram-negative bacteria, as well as acute elevated CORT.MethodsRat offspring were exposed to maternal HFD or control diet (CHD) throughout pre and postnatal development until weaning, when all offspring were provided CHD until adulthood. In adulthood, offspring were ‘challenged’ with administration of exogenous CORT, to simulate an acute physiological stress, LPS, to induce an immune stress, or both. qPCR was used to measure transcript abundance of CORT receptors and downstream inflammatory genes in the amygdala, hippocampus and prefrontal cortex, brain regions that mediate neuroendocrine and behavioral responses to stress.ResultsHFD female offspring exhibited elevations in anti-inflammatory transcripts, whereas HFD male offspring responded with greater pro-inflammatory gene expression to simultaneous CORT and LPS administration.ConclusionsThese findings suggest that exposure to maternal HFD leads to sex-specific alterations that may alter inflammatory responses in the brain, possibly as an adaptive response to basal inflammation.

scholarly journals Maternal high-fat diet-induced programing of gut taste receptor and inflammatory gene expression in rat offspring is ameliorated by CLA supplementation

2015 ◽  
Vol 3 (10) ◽  
pp. e12588 ◽  
Author(s):  
Clare M. Reynolds ◽  
Stephanie A. Segovia ◽  
Xiaoyuan D. Zhang ◽  
Clint Gray ◽  
Mark H. Vickers
Keyword(s):  
Gene Expression ◽  
High Fat Diet ◽  
Taste Receptor ◽  
High Fat ◽  
Inflammatory Gene Expression ◽  
Inflammatory Gene ◽  
Rat Offspring

scholarly journals Neutrophil microvesicles drive atherosclerosis by deliveringmiR-155to atheroprone endothelium

2018 ◽  
Author(s):  
Ingrid Gomez ◽  
Ben Ward ◽  
Celine Souilhol ◽  
Chiara Recarti ◽  
Mark Ariaans ◽  
...  
Keyword(s):  
Gene Expression ◽  
Endothelial Cells ◽  
Risk Factor ◽  
High Fat Diet ◽  
Vascular Inflammation ◽  
Atherosclerotic Plaques ◽  
High Fat ◽  
Complex Flow ◽  
Inflammatory Gene Expression ◽  
Disturbed Flow

AbstractNeutrophils have been implicated in the pathogenesis of atherosclerosis, a lipid-driven disease of arteries, but they are seldom found in atherosclerotic plaques. To resolve this longstanding paradox, we investigated whether neutrophil-derived microvesicles may influence arterial pathophysiology. Clinical and pre-clinical studies revealed that levels of circulating neutrophil microvesicles were enhanced by exposure to a high fat diet, a known risk factor for atherosclerosis. Neutrophil microvesicles accumulated at disease-prone regions of arteries that are exposed to complex flow patterns, and they promoted vascular inflammation and atherosclerosis in a murine model. Using cultured endothelial cells exposed to disturbed flow, it was demonstrated that neutrophil microvesicles promoted inflammatory gene expression by delivering a microRNA (miR-155) that enhanced NF-κB activation. Similary, neutrophil microvesicles increased miR-155 and enhanced NF-κB at disease-prone sites of disturbed flow in arteries of mice. We conclude that delivery of microvesicles carrying miR-155 to disease-prone regions of arteries provides a novel mechanism by which neutrophils contribute to vascular inflammation and atherogenesis.

scholarly journals Neutrophil microvesicles drive atherosclerosis by delivering miR-155 to atheroprone endothelium

2020 ◽  
Vol 11 (1) ◽  
Author(s):  
Ingrid Gomez ◽  
Ben Ward ◽  
Celine Souilhol ◽  
Chiara Recarti ◽  
Mark Ariaans ◽  
...  
Keyword(s):  
Gene Expression ◽  
High Fat Diet ◽  
Vascular Inflammation ◽  
Plaque Formation ◽  
Atherosclerotic Plaques ◽  
High Fat ◽  
Inflammatory Gene Expression ◽  
Disturbed Flow ◽  
Atherosclerotic Plaque Formation

AbstractNeutrophils are implicated in the pathogenesis of atherosclerosis but are seldom detected in atherosclerotic plaques. We investigated whether neutrophil-derived microvesicles may influence arterial pathophysiology. Here we report that levels of circulating neutrophil microvesicles are enhanced by exposure to a high fat diet, a known risk factor for atherosclerosis. Neutrophil microvesicles accumulate at disease-prone regions of arteries exposed to disturbed flow patterns, and promote vascular inflammation and atherosclerosis in a murine model. Using cultured endothelial cells exposed to disturbed flow, we demonstrate that neutrophil microvesicles promote inflammatory gene expression by delivering miR-155, enhancing NF-κB activation. Similarly, neutrophil microvesicles increase miR-155 and enhance NF-κB at disease-prone sites of disturbed flow in vivo. Enhancement of atherosclerotic plaque formation and increase in macrophage content by neutrophil microvesicles is dependent on miR-155. We conclude that neutrophils contribute to vascular inflammation and atherogenesis through delivery of microvesicles carrying miR-155 to disease-prone regions.

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