Systemic Inflammation

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Catherine Fortier - One of the best experts on this subject based on the ideXlab platform.

  • the association between blast exposure and transdiagnostic health symptoms on Systemic Inflammation
    Neuropsychopharmacology, 2021
    Co-Authors: Jasmeet P Hayes, Meghan E Pierce, Kate E Valerio, Mark W Miller, Bertrand R Huber, Catherine Fortier
    Abstract:

    Chronic elevation of Systemic Inflammation is observed in a wide range of disorders including PTSD, depression, and traumatic brain injury. Although previous work has demonstrated a link between Inflammation and various diagnoses separately, few studies have examined transdiagnostic symptoms and Inflammation within the same model. The objective of this study was to examine relationships between psychiatric and health variables and Systemic Inflammation and to determine whether mild traumatic brain injury (mTBI) and/or exposure to blast munitions moderate these relationships. Confirmatory factor analysis in a large sample (N = 357) of post-9/11 Veterans demonstrated a good fit to a four-factor model reflecting traumatic stress, affective, somatic, and metabolic latent variables. Hierarchical regression models revealed that each of the latent variables were associated with higher levels of Systemic Inflammation. However, the strongest relationship with Inflammation emerged among those who had both war-zone blast exposures and metabolic dysregulation, even after adjusting for mental health latent variables. Exploratory analyses showed that blast exposure was associated with metabolic dysregulation in a dose-response manner, with self-reported closer blast proximity associated with the greatest metabolic dysregulation. Together, these results provide a greater understanding of the types of symptoms most strongly associated with Inflammation and underscore the importance of maintaining a healthy lifestyle to reduce the impact of obesity and other metabolic symptoms on future chronic disease in younger to middle-aged Veterans.

  • the association between blast exposure and transdiagnostic health symptoms on Systemic Inflammation
    medRxiv, 2021
    Co-Authors: Jasmeet P Hayes, Meghan E Pierce, Kate E Valerio, Mark W Miller, Bertrand R Huber, Catherine Fortier
    Abstract:

    ABSTRACT Chronic elevation of Systemic Inflammation is observed in a wide range of disorders including PTSD, depression, and traumatic brain injury, all of which are relatively common in United States Veterans. Although previous work has demonstrated a link between Inflammation and various diagnoses separately, few studies have examined transdiagnostic symptoms and Inflammation within the same model. The objective of this study was to examine relationships between psychiatric and health variables and Systemic Inflammation, and to determine whether mild traumatic brain injury (mTBI) and/or exposure to blast munitions moderate these relationships. Confirmatory factor analysis in a large sample (N = 357) of post-9/11 Veterans demonstrated good fit to a four-factor model reflecting traumatic stress, affective, somatic, and metabolic latent variables. Hierarchical regression models revealed that each of the latent variables were associated with higher levels of Systemic Inflammation. However, the strongest relationship with Inflammation emerged among those who had both war-zone blast exposures and metabolic dysregulation, even after adjusting for mental health latent variables. Exploratory analyses showed that blast exposure was associated with metabolic dysregulation in a dose-response manner, with self-reported closer blast proximity associated with the greatest metabolic dysregulation. Together, these results provide greater understanding of the types of symptoms most strongly associated with Inflammation, and underscore the importance of maintaining a healthy lifestyle to reduce the impact of obesity and other metabolic symptoms on future chronic disease in younger to middle-aged Veterans.

Julie Y H Chan - One of the best experts on this subject based on the ideXlab platform.

  • neuroInflammation and oxidative stress in rostral ventrolateral medulla contribute to neurogenic hypertension induced by Systemic Inflammation
    Journal of Neuroinflammation, 2012
    Co-Authors: Samuel H H Chan, Julie Y H Chan
    Abstract:

    Background In addition to Systemic Inflammation, neuroInflammation in the brain, which enhances sympathetic drive, plays a significant role in cardiovascular diseases, including hypertension. Oxidative stress in rostral ventrolateral medulla (RVLM) that augments sympathetic outflow to blood vessels is involved in neural mechanism of hypertension. We investigated whether neuroInflammation and oxidative stress in RVLM contribute to hypertension following chronic Systemic Inflammation.

  • neuroInflammation and oxidative stress in rostral ventrolateral medulla contribute to neurogenic hypertension induced by Systemic Inflammation
    Journal of Neuroinflammation, 2012
    Co-Authors: Samuel H H Chan, Julie Y H Chan
    Abstract:

    In addition to Systemic Inflammation, neuroInflammation in the brain, which enhances sympathetic drive, plays a significant role in cardiovascular diseases, including hypertension. Oxidative stress in rostral ventrolateral medulla (RVLM) that augments sympathetic outflow to blood vessels is involved in neural mechanism of hypertension. We investigated whether neuroInflammation and oxidative stress in RVLM contribute to hypertension following chronic Systemic Inflammation. In normotensive Sprague-Dawley rats, Systemic Inflammation was induced by infusion of Escherichia coli lipopolysaccharide (LPS) into the peritoneal cavity via an osmotic minipump. Systemic arterial pressure and heart rate were measured under conscious conditions by the non-invasive tail-cuff method. The level of the inflammatory markers in plasma or RVLM was analyzed by ELISA. Protein expression was evaluated by Western blot or immunohistochemistry. Tissue level of superoxide anion (O2 ·-) in RVLM was determined using the oxidation-sensitive fluorescent probe dihydroethidium. Pharmacological agents were delivered either via infusion into the cisterna magna with an osmotic minipump or microinjection bilaterally into RVLM. Intraperitoneal infusion of LPS (1.2 mg/kg/day) for 14 days promoted sustained hypertension and induced a significant increase in plasma level of C-reactive protein, tumor necrosis factor-α (TNF-α), or interleukin-1β (IL-1β). This LPS-induced Systemic Inflammation was accompanied by activation of microglia, augmentation of IL-1β, IL-6, or TNF-α protein expression, and O2 ·- production in RVLM, all of which were blunted by intracisternal infusion of a cycloxygenase-2 (COX-2) inhibitor, NS398; an inhibitor of microglial activation, minocycline; or a cytokine synthesis inhibitor, pentoxifylline. NeuroInflammation in RVLM was also associated with a COX-2-dependent downregulation of endothelial nitric oxide synthase and an upregulation of intercellular adhesion molecule-1. Finally, the LPS-promoted long-term pressor response and the reduction in expression of voltage-gated potassium channel, Kv4.3 in RVLM were antagonized by minocycline, NS398, pentoxifylline, or a superoxide dismutase mimetic, tempol, either infused into cisterna magna or microinjected bilaterally into RVLM. The same treatments, on the other hand, were ineffective against LPS-induced Systemic Inflammation. These results suggest that Systemic Inflammation activates microglia in RVLM to induce COX-2-dependent neuroInflammation that leads to an increase in O2 ·- production. The resultant oxidative stress in RVLM in turn mediates neurogenic hypertension.

Samuel H H Chan - One of the best experts on this subject based on the ideXlab platform.

  • neuroInflammation and oxidative stress in rostral ventrolateral medulla contribute to neurogenic hypertension induced by Systemic Inflammation
    Journal of Neuroinflammation, 2012
    Co-Authors: Samuel H H Chan, Julie Y H Chan
    Abstract:

    Background In addition to Systemic Inflammation, neuroInflammation in the brain, which enhances sympathetic drive, plays a significant role in cardiovascular diseases, including hypertension. Oxidative stress in rostral ventrolateral medulla (RVLM) that augments sympathetic outflow to blood vessels is involved in neural mechanism of hypertension. We investigated whether neuroInflammation and oxidative stress in RVLM contribute to hypertension following chronic Systemic Inflammation.

  • neuroInflammation and oxidative stress in rostral ventrolateral medulla contribute to neurogenic hypertension induced by Systemic Inflammation
    Journal of Neuroinflammation, 2012
    Co-Authors: Samuel H H Chan, Julie Y H Chan
    Abstract:

    In addition to Systemic Inflammation, neuroInflammation in the brain, which enhances sympathetic drive, plays a significant role in cardiovascular diseases, including hypertension. Oxidative stress in rostral ventrolateral medulla (RVLM) that augments sympathetic outflow to blood vessels is involved in neural mechanism of hypertension. We investigated whether neuroInflammation and oxidative stress in RVLM contribute to hypertension following chronic Systemic Inflammation. In normotensive Sprague-Dawley rats, Systemic Inflammation was induced by infusion of Escherichia coli lipopolysaccharide (LPS) into the peritoneal cavity via an osmotic minipump. Systemic arterial pressure and heart rate were measured under conscious conditions by the non-invasive tail-cuff method. The level of the inflammatory markers in plasma or RVLM was analyzed by ELISA. Protein expression was evaluated by Western blot or immunohistochemistry. Tissue level of superoxide anion (O2 ·-) in RVLM was determined using the oxidation-sensitive fluorescent probe dihydroethidium. Pharmacological agents were delivered either via infusion into the cisterna magna with an osmotic minipump or microinjection bilaterally into RVLM. Intraperitoneal infusion of LPS (1.2 mg/kg/day) for 14 days promoted sustained hypertension and induced a significant increase in plasma level of C-reactive protein, tumor necrosis factor-α (TNF-α), or interleukin-1β (IL-1β). This LPS-induced Systemic Inflammation was accompanied by activation of microglia, augmentation of IL-1β, IL-6, or TNF-α protein expression, and O2 ·- production in RVLM, all of which were blunted by intracisternal infusion of a cycloxygenase-2 (COX-2) inhibitor, NS398; an inhibitor of microglial activation, minocycline; or a cytokine synthesis inhibitor, pentoxifylline. NeuroInflammation in RVLM was also associated with a COX-2-dependent downregulation of endothelial nitric oxide synthase and an upregulation of intercellular adhesion molecule-1. Finally, the LPS-promoted long-term pressor response and the reduction in expression of voltage-gated potassium channel, Kv4.3 in RVLM were antagonized by minocycline, NS398, pentoxifylline, or a superoxide dismutase mimetic, tempol, either infused into cisterna magna or microinjected bilaterally into RVLM. The same treatments, on the other hand, were ineffective against LPS-induced Systemic Inflammation. These results suggest that Systemic Inflammation activates microglia in RVLM to induce COX-2-dependent neuroInflammation that leads to an increase in O2 ·- production. The resultant oxidative stress in RVLM in turn mediates neurogenic hypertension.

Winfried Marz - One of the best experts on this subject based on the ideXlab platform.

  • genetically determined nlrp3 inflammasome activation associates with Systemic Inflammation and cardiovascular mortality
    European Heart Journal, 2021
    Co-Authors: Stefan J Schunk, Marcus E Kleber, Winfried Marz, Shichao Pang, Stephen Zewinger, Sarah Triem, Philipp Ege
    Abstract:

    AIMS: Inflammation plays an important role in cardiovascular disease (CVD) development. The NOD-like receptor protein-3 (NLRP3) inflammasome contributes to the development of atherosclerosis in animal models. Components of the NLRP3 inflammasome pathway such as interleukin-1β can therapeutically be targeted. Associations of genetically determined inflammasome-mediated Systemic Inflammation with CVD and mortality in humans are unknown. METHODS AND RESULTS: We explored the association of genetic NLRP3 variants with prevalent CVD and cardiovascular mortality in 538 167 subjects on the individual participant level in an explorative gene-centric approach without performing multiple testing. Functional relevance of single-nucleotide polymorphisms on NLRP3 inflammasome activation has been evaluated in monocyte-enriched peripheral blood mononuclear cells (PBMCs). Genetic analyses identified the highly prevalent (minor allele frequency 39.9%) intronic NLRP3 variant rs10754555 to affect NLRP3 gene expression. rs10754555 carriers showed significantly higher C-reactive protein and serum amyloid A plasma levels. Carriers of the G allele showed higher NLRP3 inflammasome activation in isolated human PBMCs. In carriers of the rs10754555 variant, the prevalence of coronary artery disease was significantly higher as compared to non-carriers with a significant interaction between rs10754555 and age. Importantly, rs10754555 carriers had significantly higher risk for cardiovascular mortality during follow-up. Inflammasome inducers (e.g. urate, triglycerides, apolipoprotein C3) modulated the association between rs10754555 and mortality. CONCLUSION: The NLRP3 intronic variant rs10754555 is associated with increased Systemic Inflammation, inflammasome activation, prevalent coronary artery disease, and mortality. This study provides evidence for a substantial role of genetically driven Systemic Inflammation in CVD and highlights the NLRP3 inflammasome as a therapeutic target. Published on behalf of the European Society of Cardiology. All rights reserved. © The Author(s) 2021. For permissions, please email: journals.permissions@oup.com. (Less)

Bertrand R Huber - One of the best experts on this subject based on the ideXlab platform.

  • the association between blast exposure and transdiagnostic health symptoms on Systemic Inflammation
    Neuropsychopharmacology, 2021
    Co-Authors: Jasmeet P Hayes, Meghan E Pierce, Kate E Valerio, Mark W Miller, Bertrand R Huber, Catherine Fortier
    Abstract:

    Chronic elevation of Systemic Inflammation is observed in a wide range of disorders including PTSD, depression, and traumatic brain injury. Although previous work has demonstrated a link between Inflammation and various diagnoses separately, few studies have examined transdiagnostic symptoms and Inflammation within the same model. The objective of this study was to examine relationships between psychiatric and health variables and Systemic Inflammation and to determine whether mild traumatic brain injury (mTBI) and/or exposure to blast munitions moderate these relationships. Confirmatory factor analysis in a large sample (N = 357) of post-9/11 Veterans demonstrated a good fit to a four-factor model reflecting traumatic stress, affective, somatic, and metabolic latent variables. Hierarchical regression models revealed that each of the latent variables were associated with higher levels of Systemic Inflammation. However, the strongest relationship with Inflammation emerged among those who had both war-zone blast exposures and metabolic dysregulation, even after adjusting for mental health latent variables. Exploratory analyses showed that blast exposure was associated with metabolic dysregulation in a dose-response manner, with self-reported closer blast proximity associated with the greatest metabolic dysregulation. Together, these results provide a greater understanding of the types of symptoms most strongly associated with Inflammation and underscore the importance of maintaining a healthy lifestyle to reduce the impact of obesity and other metabolic symptoms on future chronic disease in younger to middle-aged Veterans.

  • the association between blast exposure and transdiagnostic health symptoms on Systemic Inflammation
    medRxiv, 2021
    Co-Authors: Jasmeet P Hayes, Meghan E Pierce, Kate E Valerio, Mark W Miller, Bertrand R Huber, Catherine Fortier
    Abstract:

    ABSTRACT Chronic elevation of Systemic Inflammation is observed in a wide range of disorders including PTSD, depression, and traumatic brain injury, all of which are relatively common in United States Veterans. Although previous work has demonstrated a link between Inflammation and various diagnoses separately, few studies have examined transdiagnostic symptoms and Inflammation within the same model. The objective of this study was to examine relationships between psychiatric and health variables and Systemic Inflammation, and to determine whether mild traumatic brain injury (mTBI) and/or exposure to blast munitions moderate these relationships. Confirmatory factor analysis in a large sample (N = 357) of post-9/11 Veterans demonstrated good fit to a four-factor model reflecting traumatic stress, affective, somatic, and metabolic latent variables. Hierarchical regression models revealed that each of the latent variables were associated with higher levels of Systemic Inflammation. However, the strongest relationship with Inflammation emerged among those who had both war-zone blast exposures and metabolic dysregulation, even after adjusting for mental health latent variables. Exploratory analyses showed that blast exposure was associated with metabolic dysregulation in a dose-response manner, with self-reported closer blast proximity associated with the greatest metabolic dysregulation. Together, these results provide greater understanding of the types of symptoms most strongly associated with Inflammation, and underscore the importance of maintaining a healthy lifestyle to reduce the impact of obesity and other metabolic symptoms on future chronic disease in younger to middle-aged Veterans.