Publications by authors named "I Grants"
Article Synopsis
- ET-1 signaling plays a role in regulating intestinal motility and inflammation, primarily through the involvement of enteric glial cells, which influence neural-motor pathways.* -
- The study involved various experimental methods, including the use of ET-related drugs and genetically modified mice, to uncover how ET-1 and its receptors affect calcium responses and motor contractions in the intestines.* -
- Key findings suggest that glial ET signaling inhibits intestinal contractions and peristalsis, especially during inflammation, and that targeted blocking of ET receptors could alleviate intestinal inflammation in specific conditions.*
Article Synopsis
- Enteric glial cells (EGCs) play a critical role in gut health by regulating motility, maintaining balance, and contributing to inflammation in intestinal diseases; however, the mechanisms behind their activation, especially after injury, are not fully understood.
- Research suggests that surgical trauma during intestinal surgery releases ATP, which activates a specific signaling pathway (p38-dependent MAPK), leading to enteric gliosis and inflammation, resulting in impaired gut motility known as postoperative ileus (POI).
- The study identified the P2X2 receptor as a key target in this process and discovered that ambroxol, a drug that blocks this receptor, can prevent gliosis and inflammation in both mice and human intestines, suggesting it may
Histamine-dependent interactions between mast cells, glia, and neurons are altered following early-life adversity in mice and humans.
Am J Physiol Gastrointest Liver Physiol
December 2020
Article Synopsis
- Early-life adversity, such as neonatal maternal separation in mice, is linked to changes in the relationship between mast cells and enteric glia, which may lead to bowel disorders later in life.
- The study found that stress increases mast cell numbers near myenteric ganglia and enhances histamine production, affecting how glia respond to these cells.
- Importantly, while stress modifies glial responses and protein expression, it does not lead to neurodegeneration, suggesting that altered mast cell-glial signaling could be a key factor in how early-life stress impacts gut health.
Mechanisms resulting in abdominal pain include altered neuro-immune interactions in the gastrointestinal tract, but the signaling processes that link immune activation with visceral hypersensitivity are unresolved. We hypothesized that enteric glia link the neural and immune systems of the gut and that communication between enteric glia and immune cells modulates the development of visceral hypersensitivity. To this end, we manipulated a major mechanism of glial intercellular communication that requires connexin-43 and assessed the effects on acute and chronic inflammation, visceral hypersensitivity, and immune responses.
View Article and Find Full Text PDFBackground: Clopidogrel is an irreversible antagonist of P2Y receptors (P2YRs) used as an antiplatelet drug to reduce risk of thrombosis. P2YRs are expressed in gastrointestinal (GI) tract where they might regulate GI function.
Aim: To evaluate if blockade of P2YRs by clopidogrel is associated with higher incidence of GI symptoms in patients with irritable bowel syndrome (IBS).