Results 21 to 30 of about 148,083 (310)

Nlrp6 promotes recovery after peripheral nerve injury independently of inflammasomes [PDF]

open access: yes, 2015
Background: NOD-like receptors (Nlrs) are key regulators of immune responses during infection and autoimmunity. A subset of Nlrs assembles inflammasomes, molecular platforms that are activated in response to endogenous danger and microbial ligands and ...
De Winter, Vicky   +6 more
core   +2 more sources

Targeting inflammation to reduce cardiovascular disease risk: a realistic clinical prospect? [PDF]

open access: yes, 2017
Data from basic science experiments is overwhelmingly supportive of the causal role of immune-inflammatory response(s) at the core of atherosclerosis, and therefore the theoretical potential to manipulate the inflammatory response to prevent ...
Abbas   +173 more
core   +2 more sources

Catecholamine stress alters neutrophil trafficking and impairs wound healing by β2-adrenergic receptor-mediated upregulation of IL-6. [PDF]

open access: yes, 2014
Stress-induced hormones can alter the inflammatory response to tissue injury; however, the precise mechanism by which epinephrine influences inflammatory response and wound healing is not well defined.
Byrne, Barbara A   +7 more
core   +2 more sources

Natriuretic peptide receptors regulate cytoprotective effects in a human ex vivo 3D/bioreactor model [PDF]

open access: yes, 2013
© 2013 Peake et al.; licensee BioMed Central Ltd. This is an open access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and ...
Achan, P   +8 more
core   +3 more sources

The Therapeutic Role of Interleukin-1 Inhibition in Idiopathic Recurrent Pericarditis: Current Evidence and Future Challenges

open access: yesFrontiers in Medicine, 2017
Recurrent pericarditis is a common complication of acute pericarditis (15–30%) for which, in most cases, no underlying etiology is found [idiopathic recurrent pericarditis (IRP)]. IRP is currently viewed as an autoinflammatory disease with characteristic
George Lazaros   +2 more
doaj   +1 more source

Disruption of Interleukin-1β Autocrine Signaling Rescues Complex I Activity and Improves ROS Levels in Immortalized Epithelial Cells with Impaired Cystic Fibrosis Transmembrane Conductance Regulator (CFTR) Function [PDF]

open access: yes, 2014
Patients with cystic fibrosis (CF) have elevated concentration of cytokines in sputum and a general inflammatory condition. In addition, CF cells in culture produce diverse cytokines in excess, including IL-1B. We have previously shown that IL-1B, at low
Clauzure, Mariangeles   +5 more
core   +1 more source

Intracellular Chloride Concentration Changes Modulate IL-1β Expression and Secretion in Human Bronchial Epithelial Cultured Cells [PDF]

open access: yes, 2017
Cystic fibrosis (CF) is caused by mutations in the CFTR gene, which encodes a cAMP‐regulated chloride channel. Several cellular functions are altered in CF cells. However, it is not clear how the CFTR failure induces those alterations.
Clauzure, Mariangeles   +6 more
core   +1 more source

Novel anti-tumour necrosis factor receptor-1 (TNFR1) domain antibody prevents pulmonary inflammation in experimental acute lung injury. [PDF]

open access: yes, 2018
BACKGROUND: Tumour necrosis factor alpha (TNF-α) is a pleiotropic cytokine with both injurious and protective functions, which are thought to diverge at the level of its two cell surface receptors, TNFR1 and TNFR2.

core   +2 more sources

Helicobacter pylori Seropositivity in Patients with Interleukin-1 Polymorphisms Is Significantly Associated with ST-Segment Elevation Myocardial Infarction. [PDF]

open access: yesPLoS ONE, 2016
Helicobacter pylori infection and interleukin-1 polymorphisms are associated with an increased risk of gastric cancer. We examined the prevalence of Helicobacter pylori seropositivity and interleukin-1 polymorphisms between ST-segment elevation ...
Noriaki Tabata   +15 more
doaj   +1 more source

Home - About - Disclaimer - Privacy