Ammonia induces Treg/Th1 imbalance with triggered NF-κB pathway leading to chicken respiratory inflammation response

The Science of The Total Environment, Journal Year: 2018, Volume and Issue: 659, P. 354 - 362

Published: Dec. 26, 2018

Language: Английский

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Acquired immunodeficiencies and tuberculosis: focus on HIV/AIDS and diabetes mellitus

Immunological Reviews, Journal Year: 2015, Volume and Issue: 264(1), P. 121 - 137

Published: Feb. 20, 2015

Summary The spread of human immunodeficiency virus ( HIV ) infection within Africa led to marked increases in numbers cases tuberculosis TB ), and although the epidemic peaked 2006, there were still 1.8 million new 2013, with 29.2 prevalent cases. Half all are those co‐infection. A brief review well‐documented main immunological mechanisms ‐associated increased susceptibility is presented. However, a threat facing control, which presents itself form rapid increase number people living type II diabetes mellitus (T2 DM particularly areas that already hardest hit by epidemic. T2 threefold, burden attributable 15%. This addresses much smaller body research information available on ‐ , compared comorbidity. We discuss altered clinical presentation context comorbidity, changes innate adaptive immune responses, including lymphocyte subsets T‐cell phenotypes, effect treatment different comorbidities, biomarker expression genetic predisposition respective morbidities, other factors affecting Although significant gains have been made improving our understanding underlying susceptibility, knowledge gaps exist require urgent attention.

Language: Английский

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Diabetes and Sepsis: Risk, Recurrence, and Ruination

Frontiers in Endocrinology, Journal Year: 2017, Volume and Issue: 8

Published: Oct. 30, 2017

Sepsis develops when an infection surpasses local tissue containment. A series of dysregulated physiologic responses are generated, leading to organ dysfunction and a 10% mortality risk. When patients with sepsis demonstrate elevated serum lactates require vasopressor therapy maintain adequate blood pressure in the absence hypovolemia, they septic shock in-hospital rate greater than 40%. With improvements intensive care treatment strategies, overall has diminished approximately 20% at 30 days; however, continues steadily climb after recovery from acute event. Traditionally, it was thought that complex interplay between inflammatory anti-inflammatory led sepsis-induced mortality. However, closer examination those who die long subsides reveals many initial survivors succumb recurrent, nosocomial, secondary infections. The co-morbidly challenged, physiologically frail diabetic individuals suffer highest rates. Recent reports suggest even clinical "recovery" sepsis, persistent alterations innate adaptive immune exists resulting chronic inflammation, suppression, bacterial persistence. As sepsis-associated defects associated increased long-term, potential for modulatory improve patient outcomes. We propose diabetes causes functional deficiency directly reduces cell function. result, display bactericidal clearance, infectious complications, protracted Considering substantial expansion elderly obese population, global adoption Western diet lifestyle, multidrug resistant emergence persistence, is predicted rise dramatically over next two decades. better understanding underlying diabetic-induced persist following crucial identify therapeutic targets bolster function, prevent provide more durable survival.

Language: Английский

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T Cell Populations and Functions Are Altered in Human Obesity and Type 2 Diabetes

Current Diabetes Reports, Journal Year: 2017, Volume and Issue: 17(9)

Published: Aug. 4, 2017

Language: Английский

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Cardiomyopathy Associated with Diabetes: The Central Role of the Cardiomyocyte

International Journal of Molecular Sciences, Journal Year: 2019, Volume and Issue: 20(13), P. 3299 - 3299

Published: July 5, 2019

The term diabetic cardiomyopathy (DCM) labels an abnormal cardiac structure and performance due to intrinsic heart muscle malfunction, independently of other vascular co-morbidity. DCM, accounting for 50%-80% deaths in patients, represents a worldwide problem human health related economics. Optimal glycemic control is not sufficient prevent which derives from remodeling geometrical changes, with both consequences critical events initially occurring at the cardiomyocyte level. Cardiac cells, under hyperglycemia, very early undergo metabolic abnormalities contribute T helper (Th)-driven inflammatory perturbation, behaving as immunoactive units capable releasing biomediators, such cytokines chemokines. This paper aims focus onto role cardiomyocytes, no longer considered "passive" targets but "active" participating dialogue between local systemic counterparts underlying DCM development maintenance. Some main biomolecular/metabolic/inflammatory processes triggered within cells by high glucose are overviewed; particular attention addressed chemokines, representing potential therapeutic prompt intervention when signs or symptoms manifesting yet. clinical management still challenge further translational investigations, including studies female/male cell level, warranted.

Language: Английский

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