The research demonstrated that following injury, there is increased migration of
inflammatory cells from blood to the liver, increasing IFNL3 secretion and liver damage.
Not exact matches
Another key finding of the research was that the impact of vitamin D on
inflammatory disease can not be predicted using
cells from healthy individuals or even
from the
blood of patients with inflammation as
cells from the disease tissue are very different.
«
Inflammatory arthritis is caused when immune
cells are recruited
from the
blood into the joint in a highly regulated process controlled by chemoattractants and adhesion receptors,» says Andrew Luster, MD, PhD, chief of the MGH Division of Rheumatology, Allergy and Immunology, director of the CIID and senior author of the report.
Dr Mohamed Elrayess,
from ADLQ, said: «In this study we have shown that the impaired ability of fat stem
cells to store excess fat was partially due to increased levels of the
inflammatory marker interleukin - 6 in the
blood.
Instead of responding to viruses or other foreign invaders in the body, the activated CD8 + T
cells launch an
inflammatory response to fat, and to bacterial components that migrate to the liver
from the gut through the
blood.
Using
cells from mice and human livers, Toronto General Hospital Research Institute researchers demonstrated for the first time how under specific conditions, such as obesity, liver CD8 + T
cells, white
blood cells which play an important role in the control of viral infections, become highly activated and
inflammatory, reprogramming themselves into disease - driving
cells.
In patients with
inflammatory bowel diseases, microbiota - reactive CD4 + T
cells were reduced in the
blood compared with intestine; T -
cell responses that we detected had an increased frequency of interleukin 17A production compared with responses of T
cells from blood or intestinal tissues of controls.
Methods: We collected samples of peripheral
blood mononuclear
cells and intestinal tissues
from healthy individuals (controls, n = 13 - 30) and patients with
inflammatory bowel diseases (n = 119; 59 with ulcerative colitis and 60 with Crohn's disease).
GABA Regulates Release of
Inflammatory Cytokines
From Peripheral
Blood Mononuclear
Cells and CD4 + T
Cells and Is Immunosuppressive in Type 1 Diabetes.
Conclusions: In an analysis of peripheral
blood mononuclear
cells and intestinal tissues
from patients with
inflammatory bowel diseases vs controls, we found that reactivity to intestinal bacteria is a normal property of the human CD4 + T -
cell repertoire, and does not necessarily indicate disrupted interactions between immune
cells and the commensal microbiota.
Diet - induced
inflammatory reactions cause mediator release (cytokines, histamine, leukotrienes, prostaglandins, etc.)
from various white
blood cells (lymphocytes, neutrophils, monocytes, eosinophils).
The release of pro-
inflammatory and pro-algesic mediators (cytokines, histamine, leukotrienes, prostaglandins)
from white
blood cells (neutrophils, monocytes, eosinophils and lymphocytes) is a common component of all diet - induced
inflammatory reactions.
Forty extracts were therefore prepared
from twenty - seven foodstuffs common to the Western diet, and the capacity of each to induce the secretion of IL - 6 and TNF - α
from human monocytes was measured and compared» The capacity of these foods to cause white
blood cells to secrete
inflammatory signals was measured.
One of the earliest events in the development of atherosclerosis is the recruitment of
inflammatory white
blood cells from the
blood to the arterial wall by vascular
cell adhesion molecules (42).