scholarly journals Brain Morphometry and Chronic Inflammation in Bangladeshi Children Growing up in Extreme Poverty

2021 ◽  
Author(s):  
Ted K Turesky ◽  
Laura Pirazzoli ◽  
Talat Shama ◽  
Shahria Hafiz Kakon ◽  
Rashidul Haque ◽  
...  
Keyword(s):  
Brain Development ◽  
Chronic Inflammation ◽  
Maternal Education ◽  
Inflammatory Responses ◽  
Inflammatory Marker ◽  
Growing Up ◽  
Tissue Segmentation ◽  
Extreme Poverty ◽  
Brain Morphometry ◽  
Sulcal Depth

Over 300 million children grow up in environments of extreme poverty, and the biological and psychosocial hazards endemic to these environments often expose these children to infection, disease, and consequent inflammatory responses. Chronic inflammation in early childhood has been associated with diminished cognitive outcomes and despite this established relationship, the mechanisms explaining how inflammation affects brain development are not well known. Importantly, chronic inflammation is very common in areas of extreme poverty, raising the possibility that it may serve as a mechanism explaining the known relationship between low socioeconomic status (SES) and atypical brain development. To examine these potential pathways, seventy-nine children growing up in an extremely poor, urban area of Bangladesh underwent structural MRI scanning at six years of age. Structural brain images were submitted to Mindboggle software, a Docker-compliant and high-reproducibility tool for tissue segmentation and regional estimations of volume, surface area, cortical thickness, sulcal depth, and mean curvature. Concentration of C-reactive protein was assayed at eight time points between infancy and five years of age and the frequency with which children had elevated concentrations of inflammatory marker served as the measure of chronic inflammation. SES was measured with years of maternal education and income-to-needs. Chronic inflammation predicted total brain volume, total white matter volume, average sulcal depth, and bilateral putamen volumes. Chronic inflammation also mediated the link between maternal education and bilateral putamen volumes. These findings suggest that chronic inflammation is associated with brain morphometry globally and in the putamen, and further suggests that inflammation may be a potential mechanism linking SES to brain development.

scholarly journals Brain Morphometry and Diminished Physical Growth in Bangladeshi Children Growing up in Extreme Poverty: a Longitudinal Study

2021 ◽  
Author(s):  
Ted K. Turesky ◽  
Talat Shama ◽  
Shahria Hafiz Kakon ◽  
Rashidul Haque ◽  
Nazrul Islam ◽  
...  
Keyword(s):  
Brain Development ◽  
Physical Growth ◽  
Growing Up ◽  
Tissue Segmentation ◽  
Brain Images ◽  
Extreme Poverty ◽  
Brain Morphometry ◽  
Common Marker ◽  
Neurocognitive Outcomes ◽  
The Relationship

AbstractDiminished physical growth is a common marker of malnutrition and it affects approximately 200 million children worldwide. Despite its importance and prevalence, it is not clear whether diminished growth affects brain development and neurocognitive outcomes. Further, diminished growth is more common in areas of extreme poverty, raising the possibility that it may serve as a mechanism for previously shown links between poverty and brain development. To address these questions, 79 children growing up in an extremely poor, urban area of Bangladesh underwent MRI at 6 years. Structural brain images were submitted to Mindboggle software, a Docker-compliant and highly reproducible tool for tissue segmentation and regional estimations of volume, surface area, cortical thickness, travel depth, and mean curvature. Diminished growth predicted brain morphometry and mediated the link between poverty and brain morphometry most consistently for white matter and subcortical volumes. Meanwhile, brain volume in left pallidum and right ventral diencephalon mediated the relationship between diminished growth and full-scale IQ. These findings offer malnutrition as one possible mechanism by which poverty affects brain development and neurocognitive outcomes in areas of extreme poverty.

scholarly journals Brain Morphometry and Diminished Physical Growth in Bangladeshi Children Growing up in Extreme Poverty: a Longitudinal Study

2021 ◽  
pp. 101029
Author(s):  
Ted K. Turesky ◽  
Talat Shama ◽  
Shahria Hafiz Kakon ◽  
Rashidul Haque ◽  
Nazrul Islam ◽  
...  
Keyword(s):  
Longitudinal Study ◽  
Physical Growth ◽  
Growing Up ◽  
Extreme Poverty ◽  
Brain Morphometry

scholarly journals Unfulfilled Inflammatory Resolution: A Key Factor in the Pathogenesis of Psoriasis

2020 ◽  
Author(s):  
Zohreh Jadali
Keyword(s):  
Inflammatory Response ◽  
Chronic Inflammation ◽  
Molecular Mechanisms ◽  
Inflammatory Responses ◽  
Inflammatory Diseases ◽  
Relevant Literature ◽  
Regulatory Mechanisms ◽  
Immune Mediated ◽  
Key Factor ◽  
Inflammation Resolution

Recent literature has highlighted the importance of chronic inflammation in psoriasis pathogenesis. Non-resolving inflammation can trigger progressive tissue damage and inflammatory mediator release which in turn perpetuate the inflammatory cycle. Under normal conditions, inflammatory responses are tightly controlled through several mechanisms that restore normal tissue function and structure. Defects in regulatory mechanisms of the inflammatory response can result in persistent unresolved inflammation and further increases of inflammation. Therefore, this review focuses on defects in regulatory mechanisms of inflammatory responses that lead to uncontrolled chronic inflammation in psoriasis. Databases such as Pubmed Embase, ISI, and Iranian databases including Iranmedex, and SID were researched to identify relevant literature. The results of this review indicate that dysregulation of the inflammatory response may be a likely cause of various immune-mediated inflammatory disorders such as psoriasis. Based on current findings, advances in understanding the cellular and molecular mechanisms involved in inflammation resolution are not only improving our knowledge of the pathogenesis of chronic inflammatory diseases but also supporting the development of new therapeutic strategies.

scholarly journals Massage Therapy Modulates Inflammatory Mediators Following Sprint Exercise in Healthy Male Athletes

2020 ◽  
Vol 5 (1) ◽  
pp. 9
Author(s):  
Gillian E. White ◽  
Sarah L. West ◽  
Jessica E. Caterini ◽  
Alex P. Di Battista ◽  
Shawn G. Rhind ◽  
...  
Keyword(s):  
Inflammatory Responses ◽  
Inflammatory Marker ◽  
Massage Therapy ◽  
Muscle Performance ◽  
Drop Jump ◽  
Healthy Male ◽  
Necrosis Factor Alpha ◽  
Male Athletes ◽  
Jump Performance ◽  
Baseline Levels

Massage therapy is a common postexercise muscle recovery modality; however, its mechanisms of efficacy are uncertain. We evaluated the effects of massage on systemic inflammatory responses to exercise and postexercise muscle performance and soreness. In this crossover study, nine healthy male athletes completed a high-intensity intermittent sprint protocol, followed by massage therapy or control condition. Inflammatory markers were assessed pre-exercise; postexercise; and at 1, 2, and 24 h postexercise. Muscle performance was measured by squat and drop jump, and muscle soreness on a Likert scale. Significant time effects were observed for monocyte chemoattractant protein-1 (MCP-1), interleukin-8 (IL-8), interleukin-6 (IL-6), interleukin-10 (IL-10), tumor necrosis factor alpha (TNFα), drop jump performance, squat jump performance, and soreness. No significant effects for condition were observed. However, compared with control, inflammatory marker concentrations (IL-8, TNFα, and MCP-1) returned to baseline levels earlier following the massage therapy condition (p < 0.05 for all). IL-6 returned to baseline levels earlier following the control versus massage therapy condition (p < 0.05). No differences were observed for performance or soreness variables. MCP-1 area under the curve (AUC) was negatively associated with squat and drop jump performance, while IL-10 AUC was positively associated with drop jump performance (p < 0.05 for all). In conclusion, massage therapy promotes resolution of systemic inflammatory signaling following exercise but does not appear to improve performance or soreness measurements.

scholarly journals ZMPSTE24 Is Associated with Elevated Inflammation and Progerin mRNA

Cells ◽  
2020 ◽  
Vol 9 (9) ◽  
pp. 1981
Author(s):  
Moritz Messner ◽  
Santhosh Kumar Ghadge ◽  
Thomas Maurer ◽  
Michael Graber ◽  
Simon Staggl ◽  
...  
Keyword(s):  
Chronic Inflammation ◽  
Significant Positive Correlation ◽  
Inflammatory Marker ◽  
Cross Sectional Study ◽  
Premature Aging ◽  
Lamin A ◽  
Cross Sectional ◽  
Positive Correlation ◽  
Hs Crp ◽  
Hutchinson Gilford Progeria Syndrome

Lamins are important filaments forming the inner nuclear membrane. Lamin A is processed by zinc metalloproteinase (ZMPSTE24). Failure to cleave a truncated form of prelamin A—also called progerin—causes Hutchinson–Gilford progeria syndrome a well-known premature aging disease. Minor levels of progerin are readily expressed in the blood of healthy individuals due to alternative splicing. Previously, we found an association of increased progerin mRNA with overweight and chronic inflammation (hs-CRP). Here, we aimed to elucidate correlations of ZMPSTE24, lamin A/C and progerin with the inflammatory marker hs-CRP. In this retrospective, cross-sectional study we analyzed blood samples from 110 heart failure patients for quantitative mRNA expression of ZMPSTE24, lamin A/C, progerin and hs-CRP protein. Spearman correlations and linear regression analyses including adjustments for age, gender and ejection fraction showed a significant positive correlation of lnprogerin with lnZMPSTE24 (n = 110; r = 0.33; p = 0.0004) and lnlamin A/C (n = 110; r = 0.82, p < 0.0001), whereas no association was observed between lnlamin A/C and lnZMPSTE24 expression. Further analyses showed a significant positive correlation of lnhs-CRP with lnZMPSTE24 (n = 110; r = 0.21; p = 0.01) and lnlamin A/C (n = 110; r = 0.24; p = 0.03). We conclude that chronic inflammation is associated with increased expression of ZMPSTE24 and lamin A/C mRNA. Both markers also positively correlate with increased expression of the premature aging marker progerin which may be linked to cardiovascular aging.

Platelets, inflammation and anti-inflammatory effects of antiplatelet drugs in ACS and CAD

2015 ◽  
Vol 114 (09) ◽  
pp. 498-518 ◽  
Author(s):  
Karin Müller ◽  
Madhumita Chatterjee ◽  
Dominik Rath ◽  
Tobias Geisler
Keyword(s):  
Cardiovascular Disease ◽  
Chronic Inflammation ◽  
Platelet Activation ◽  
Inflammatory Marker ◽  
Antiplatelet Agents ◽  
Prognostic Impact ◽  
Chronic Inflammatory Condition ◽  
Anti Inflammatory ◽  
Coronary Events

SummaryPlatelets play a pivotal role in chronic inflammation leading to progression of atherosclerosis and acute coronary events. Recent discoveries on novel mechanisms and platelet-dependent inflammatory targets underpin the role of platelets to maintain a chronic inflammatory condition in cardiovascular disease. There is strong and clinically relevant crosslink between chronic inflammation and platelet activation. Antiplatelet therapy is a cornerstone in the prevention and treatment of acute cardiovascular events. The benefit of antiplatelet agents has mainly been attributed to their direct anti-aggregatory impact. Some anti-inflammatory off-target effects have also been described. However, it is unclear whether these effects are secondary due to inhibition of platelet activation or are caused by direct distinct mechanisms interfering with inflammatory pathways. This article will highlight novel platelet associated targets that contribute to inflammation in cardiovascular disease and elucidate mechanisms by which currently available antiplatelet agents evolve anti-inflammatory capacities, in particular by carving out the differential mechanisms directly or indirectly affecting platelet mediated inflammation. It will further illustrate the prognostic impact of antiplatelet therapies by reducing inflammatory marker release in recent cardiovascular trials.

scholarly journals A Consideration of Biomarkers to be Used for Evaluation of Inflammation in Human Nutritional Studies

2013 ◽  
Vol 109 (S1) ◽  
pp. S1-S34 ◽  
Author(s):  
P.C. Calder ◽  
N. Ahluwalia ◽  
R. Albers ◽  
N. Bosco ◽  
R. Bourdet-Sicard ◽  
...  
Keyword(s):  
Inflammatory Markers ◽  
Inflammatory Process ◽  
Inflammatory Responses ◽  
Task Force ◽  
Inflammatory Marker ◽  
Low Grade ◽  
Future Health ◽  
Modifying Factors ◽  
Markers Of Inflammation ◽  
Nutritional Studies

To monitor inflammation in a meaningful way, the markers used must be valid: they must reflect the inflammatory process under study and they must be predictive of future health status. In 2009, the Nutrition and Immunity Task Force of the International Life Sciences Institute, European Branch, organized an expert group to attempt to identify robust and predictive markers, or patterns or clusters of markers, which can be used to assess inflammation in human nutrition studies in the general population. Inflammation is a normal process and there are a number of cells and mediators involved. These markers are involved in, or are produced as a result of, the inflammatory process irrespective of its trigger and its location and are common to all inflammatory situations. Currently, there is no consensus as to which markers of inflammation best represent low-grade inflammation or differentiate between acute and chronic inflammation or between the various phases of inflammatory responses. There are a number of modifying factors that affect the concentration of an inflammatory marker at a given time, including age, diet and body fatness, among others. Measuring the concentration of inflammatory markers in the bloodstream under basal conditions is probably less informative compared with data related to the concentration change in response to a challenge. A number of inflammatory challenges have been described. However, many of these challenges are poorly standardised. Patterns and clusters may be important as robust biomarkers of inflammation. Therefore, it is likely that a combination of multiple inflammatory markers and integrated readouts based upon kinetic analysis following defined challenges will be the most informative biomarker of inflammation.

scholarly journals Cytosolic Self-DNA—A Potential Source of Chronic Inflammation in Aging

Cells ◽  
2021 ◽  
Vol 10 (12) ◽  
pp. 3544
Author(s):  
Mansour Akbari ◽  
Daryl P. Shanley ◽  
Vilhelm A. Bohr ◽  
Lene Juel Rasmussen
Keyword(s):  
Innate Immunity ◽  
Chronic Inflammation ◽  
Inflammatory Responses ◽  
Experimental Models ◽  
Therapeutic Interventions ◽  
Low Grade ◽  
Innate Immune Responses ◽  
And Function ◽  
The Life Course ◽  
Cellular Components

Aging is the consequence of a lifelong accumulation of stochastic damage to tissues and cellular components. Advancing age closely associates with elevated markers of innate immunity and low-grade chronic inflammation, probably reflecting steady increasing incidents of cellular and tissue damage over the life course. The DNA sensing cGAS-STING signaling pathway is activated by misplaced cytosolic self-DNA, which then initiates the innate immune responses. Here, we hypothesize that the stochastic release of various forms of DNA from the nucleus and mitochondria, e.g., because of DNA damage, altered nucleus integrity, and mitochondrial damage, can result in chronic activation of inflammatory responses that characterize the aging process. This cytosolic self-DNA-innate immunity axis may perturb tissue homeostasis and function that characterizes human aging and age-associated pathology. Proper techniques and experimental models are available to investigate this axis to develop therapeutic interventions.

scholarly journals Gut–neuroimmune interactions: the unexpected role of the immune system in brain development

2019 ◽  
Vol 41 (1) ◽  
pp. 36-41 ◽  
Author(s):  
Simon Spichak ◽  
Timothy G. Dinan ◽  
John F. Cryan
Keyword(s):  
Immune System ◽  
Brain Development ◽  
Neuronal Development ◽  
Inflammatory Responses ◽  
Later Life ◽  
Innate Immune ◽  
Brain Health ◽  
Cytokines And Chemokines ◽  
The Brain

How does the immune system impact brain development? The exciting and somewhat unexpected relationship between the immune system and the brain has become one of the most fascinating topics in neuroscience. Even though the immune system was initially implicated in resolving viral and bacterial threats, it is now becoming more evident that it also plays a role in processes in the brain, both under healthy and pathological conditions. This novel role of the immune system in brain health has been implicated in various psychopathologies where neurodevelopment, stress and mood are central. In particular, its role in healthy brain development is becoming more evident, and understanding neuroimmune communication is becoming crucial in treating neurodevelopmental and mood disorders in later life. In the brain, glia function as part of the innate immune system and are programmed to respond to pathogens and physical injury. They also play an important role in neuronal development and pruning. These cells communicate with and respond to chemical signals, such as cytokines and chemokines, which can then initiate or downregulate inflammatory responses. Finally, the trillions of microbes residing in the gut can also stimulate cytokine and chemokine responses in the periphery and play an important role in both immunity and brain development.

scholarly journals Interleukin 6 in inflammation, autoimmunity and cancer

2020 ◽  
Author(s):  
Toshio Hirano
Keyword(s):  
Chronic Inflammation ◽  
Immune Cells ◽  
Positive Feedback ◽  
Interleukin 6 ◽  
Feedback Loop ◽  
Inflammatory Responses ◽  
Virus Disease ◽  
Cytokine Storm ◽  
Necrosis Factor Alpha ◽  
Positive Feedback Loop

Abstract Interleukin 6 (IL-6) is involved both in immune responses and in inflammation, hematopoiesis, bone metabolism and embryonic development. IL-6 plays roles in chronic inflammation (closely related to chronic inflammatory diseases, autoimmune diseases and cancer) and even in the cytokine storm of corona virus disease 2019 (COVID-19). Acute inflammation during the immune response and wound healing is a well-controlled response, whereas chronic inflammation and the cytokine storm are uncontrolled inflammatory responses. Non-immune cells and immune cells, cytokines such as IL-1β, IL-6 and tumor necrosis factor alpha (TNFα) and transcription factors nuclear factor-kappa B (NF-κB) and signal transducer and activator of transcription 3 (STAT3) play central roles in inflammation. Synergistic interactions between NF-κB and STAT3 induce the hyper-activation of NF-κB followed by the production of various inflammatory cytokines. Because IL-6 is a NF-κB target, simultaneous activation of NF-κB and STAT3 in non-immune cells triggers a positive feedback loop of NF-κB activation by the IL-6–STAT3 axis. This positive feedback loop is called the IL-6 amplifier (IL-6 Amp) and is a key player in the local initiation model, which states that local initiators, such as senescence, obesity, stressors, infection, injury and smoking, trigger diseases by promoting interactions between non-immune cells and immune cells. This model counters dogma that holds that autoimmunity and oncogenesis are triggered by the breakdown of tissue-specific immune tolerance and oncogenic mutations, respectively. The IL-6 Amp is activated by a variety of local initiators, demonstrating that the IL-6–STAT3 axis is a critical target for treating diseases.

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