When a person with gluten sensitivity eats gluten (not just wheat, but gliadin, glutenin, and transglutaminase proteins in other grains), the immune system jumps into action, releasing
pro-inflammatory signaling cells.
Not exact matches
Hypertonic Saline Primes Activation of the p53 — p21
Signaling Axis in Human Small Airway Epithelial
Cells That Prevents Inflammation Induced by
Pro-inflammatory Cytokines.
Likewise, many of the same small molecules used by
cells to
signal to each other as they rout microbes are the ones that whip up unhealthy inflammatory responses, chief among them
pro-inflammatory cytokines of the TNF family, which activate T
cells and prolong their response.
Josin researchers made two major findings: They identified the mechanisms by which GLP - 1 can induce protective actions on the glomerular (renal) endothelial
cells by inhibiting the
signaling pathway of Ang II and its
pro-inflammatory effect; and demonstrated a dual
signaling mechanism by which hyperglycemia, via PKCβ activation, can increase Ang II action and inhibit GLP - 1's protective effects by reducing the expression of GLP - 1 receptors in the glomerular endothelial
cells.
Signaling through the CXCR3 - mediated, MyD88 - dependent pathway generates a Th1 - dominant,
pro-inflammatory cytokine milieu that recruits mononuclear
cells into the submucosa (Fasano, 2011).
Piperine also interferes with inflammatory
signaling mechanisms and inhibits
pro-inflammatory cytokines, which are small proteins secreted by some
cells and linked with a number of degenerative diseases.
Moreover, the idea that the brain was isolated from immune reactions was challenged long ago by insights about microglia
cells, a type of macrophage which resides in the brain, engulfs antigens, and produces
pro-inflammatory signaling molecules called cytokines.
This accelerates
cell senescence, which leads to increased
pro-inflammatory and pro-oxidant
signaling by the senescence associated secretory phenotype (SASP) response, and induction of mitochondrial dysfunction, thereby propagating DNA damage and senescence to bystander
cells.
Most of the proposed mechanisms of actions in these studies involve changes in
cell signaling and decreased production of
pro-inflammatory cytokines.
The current results suggest that better understanding the way in which mononuclear white blood
cell signaling processes are altered, net of effects on individual differences in
cell type composition, is promising as a mechanism by which protective parenting influences young adult
pro-inflammatory tendencies among African American youth.