Necrotizing Enterocolitis Migration and the Pathogenesis of Autophagy in the Regulation of Enterocyte A Critical Role for TLR4 Induction of

Necrotizing enterocolitis report of 20 cases

Necrotizing enterocolitis is a disease of unknown origin. Epidemiological observations emphasize the potential roles of  infection, enteric feeding and local vascular compromise of the Gastrointestinal tract in the pathogenesis of this disease. Clinical findings include signs of sepsis , plus abdominal distention , vomiting, bloody stool and occasionally , signs of intestinal perforation and pe...

Innate Immune Signaling in the Pathogenesis of Necrotizing Enterocolitis

Necrotizing enterocolitis (NEC) is a challenging disease to treat, and caring for patients afflicted by it remains both frustrating and difficult. While NEC may develop quickly and without warning, it may also develop slowly, insidiously, and appear to take the caregiver by surprise. In seeking to understand the molecular and cellular processes that lead to NEC development, we have identified a...

Fecal Calprotectin Level in Neonates with Necrotizing Enterocolitis

Background: Necrotizing enterocolitis (NEC) is a disease with high mortality. It is more present in premature infants and can also happen in term and late preterm neonates. It may affect any segment of the small intestine or colon. However, most commonly influences the terminal ileum and proximal ascending colon. This disease might damage the entire bowel, which can be...

Intestinal Injury and Repair of Necrotizing Enterocolitis by Modulating A Critical Role for TLR4 in the Pathogenesis

Nitric oxide inhibits enterocyte migration through activation of RhoA-GTPase in a SHP-2-dependent manner.

Diseases of intestinal inflammation like necrotizing enterocolitis (NEC) are associated with impaired epithelial barrier integrity and the sustained release of intestinal nitric oxide (NO). NO modifies the cytoskeletal regulator RhoA-GTPase, suggesting that NO could affect barrier healing by inhibiting intestinal restitution. We now hypothesize that NO inhibits enterocyte migration through RhoA...