scholarly journals Systemic Inflammation Rapidly Induces Reversible Atrial Electrical Remodeling: The Role of Interleukin‐6–Mediated Changes in Connexin Expression

2019 ◽  
Vol 8 (16) ◽  
Author(s):  
Pietro Enea Lazzerini ◽  
Franco Laghi‐Pasini ◽  
Maurizio Acampa ◽  
Ujala Srivastava ◽  
Iacopo Bertolozzi ◽  
...  
Keyword(s):  
Systemic Inflammation ◽  
Interleukin 6 ◽  
Electrical Remodeling ◽  
Connexin Expression

scholarly journals THE ROLE OF INTERLEUKIN-6 SIGNALING IN DEVELOPMENT OF SYSTEMIC INFLAMMATION IN CHRONIC OBSTRUCTIVE PULMONARY DISEASE

2018 ◽  
Vol 1 (69) ◽  
pp. 97-106 ◽  
Author(s):  
Татьяна Виткина ◽  
Tatyana Vitkina ◽  
К Сидлецкая ◽  
K Sidleckaya
Keyword(s):  
Chronic Obstructive Pulmonary Disease ◽  
Pulmonary Disease ◽  
Systemic Inflammation ◽  
Interleukin 6 ◽  
Inflammatory Process ◽  
Molecular Mechanisms ◽  
Chronic Obstructive ◽  
Obstructive Pulmonary Disease ◽  
Damage Initiation

The review focuses on the role of interleukin-6 (IL-6) signaling in the development of a systemic inflammatory process in chronic obstructive pulmonary disease (COPD). In most researches the attention is paid to local inflammation in COPD. However, it is known that the pathology is characterized by a systemic inflammatory process, which is manifested in the increased levels of proinflammatory mediators in blood flow, and the study of the molecular mechanisms of its development is very important for the therapy of the disease. One of the key mediators of systemic inflammation is cytokine IL-6 which has pro- and antiinflammatory properties. Its effect on the cells is determined by the type of signaling. Nowadays three types of IL-6 signaling are identified: transsignaling, classical and cluster signaling. The review presents the known pathophysiological mechanisms of the development of systemic inflammation in COPD involving IL-6. As a proinflammatory cytokine, IL-6 performs the following functions: transmission of a signal on lung tissue damage, initiation of leukocyte migration into the inflammation site, inhibition of T-cell apoptosis into the inflammation site, influence on T helper differentiation, participation in pathophysiological reactions of development of emphysema and fibrosis. The significance of IL-6 transsignaling for the development of inflammation in COPD has been confirmed by many studies, while there are practically no works devoted to the study of classical IL-6 signaling in COPD. The data presented in the review indicate the need for further study of the role of different types of IL-6 signaling, especially classical signaling, in the regulation of systemic inflammation in COPD.

scholarly journals Harsh Parenting and Youth Systemic Inflammation_In Press

2019 ◽  
Author(s):  
Assaf Oshri ◽  
Erinn Duprey ◽  
Sihong Liu ◽  
Katherine Ehrlich
Keyword(s):  
Nervous System ◽  
Systemic Inflammation ◽  
Interleukin 6 ◽  
Family Stress ◽  
Harsh Parenting ◽  
Low Grade ◽  
C Reactive Protein ◽  
Reactive Protein ◽  
The Impact

Objective: The present study aimed to test the role of the autonomic nervous system (ANS) in modulating the impact of family stress, induced by harsh parenting, on youths’ inflammation. First, we examined the direct effect of severity of adverse parenting behaviors on two serum biomarkers of systemic inflammation (C-reactive protein and interleukin-6) among youth. Second, we tested the moderating role of ANS reactivity in response to laboratory-induced stress in the association between harsh parenting and inflammation among these youth. Methods: The sample included 101 low-income children (75.2% African-American) between 9 and 12 years of age (Mage =10.9; SDage = 1.2) who participated in a conflict task with their primary caregiver in a laboratory setting. Heart rate variability reactivity (HRV-R), skin conductance level reactivity (SCL-R), and pre-ejection period reactivity (PEPr-R) were used to index parasympathetic and sympathetic nervous system reactivity. Markers of low-grade inflammation (C-reactive protein and interleukin-6) were obtained from serum. Results: After adjusting for confounding variables, ANS activity moderated the associations between family stress and systemic inflammation. Specifically, elevated HRV-R buffered the effect of family stress on youths’ inflammation, whereas elevated PEPr-R and SCL-R exacerbated the effect. Conclusion: These findings show that self-regulatory capacity and threat sensitivity, as indicated by ANS function, may have an impact on the associations between family stress and systemic inflammation.

Role of interleukin-6 in the early and late fracture healing phase

2016 ◽  
Author(s):  
Katja Prystaz ◽  
Anna Kovtun ◽  
Kathrin Kaiser ◽  
Verena Heidler ◽  
Jochen Kroner ◽  
...  
Keyword(s):  
Fracture Healing ◽  
Interleukin 6 ◽  
Healing Phase

Non-pharmacological Strategies Against Systemic Inflammation: Molecular Basis and Clinical Evidence

2020 ◽  
Vol 26 (22) ◽  
pp. 2620-2629 ◽  
Author(s):  
Rita Del Pinto ◽  
Davide Pietropaoli ◽  
Annalisa Monaco ◽  
Giovambattista Desideri ◽  
Claudio Ferri ◽  
...  
Keyword(s):  
Human Genome ◽  
Systemic Inflammation ◽  
Clinical Evidence ◽  
Metabolic Diseases ◽  
Lifestyle Changes ◽  
Common Denominator ◽  
Active Lifestyle ◽  
Systemic Impact ◽  
Public Health Strategies

Systemic inflammation is a common denominator to a variety of cardiovascular (CV) and non-CV diseases and relative risk factors, including hypertension and its control, metabolic diseases, rheumatic disorders, and those affecting the gastrointestinal tract. Besides medications, a non-pharmacological approach encompassing lifestyle changes and other complementary measures is mentioned in several updated guidelines on the management of these conditions. We performed an updated narrative review on the mechanisms behind the systemic impact of inflammation and the role of non-pharmacological, complementary measures centered on lowering systemic phlogosis for preserving or restoring a good global health. The central role of genetics in shaping the immune response is discussed in conjunction with that of the microbiome, highlighting the interdependence and mutual influences between the human genome and microbial integrity, diversity, and functions. Several plausible strategies to modulate inflammation and restore balanced crosstalk between the human genome and the microbiome are then recapitulated, including dietary measures, active lifestyle, and other potential approaches to manipulate the resident microbial community. To date, evidence from high-quality human studies is sparse to allow the unconditioned inclusion of understudied, though plausible solutions against inflammation into public health strategies for global wellness. This gap claims further focused, well-designed research targeted at unravelling the mechanisms behind future personalized medicine.

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