The intestinal mucosa is a rich source of interferon (INF)-gamma, and INF-y receptors are restricted to the basolateral membrane of epithelial cells. Activation of this receptor decreases epithelial barrier function, decreases epithelial ion transport, induces proinflammatory surface markers and regulates polymorphonuclear leukocyte trafficking across the intestinal epithelium. During hypoxia, there is release of TNF-a, which potentiates the effect of INF-y on the epithelial barrier function. Thus, during hypoxia, epithelium-derived mediators such as TNF-a have the potential to regulate permeability through autocrine pathways. Fast and reliable shopping for drugs – to get safe shopping atmosphere.
In contrast to necrosis, apoptosis is an active process of gene-directed cellular self destruction. Apoptosis is characterized by morphological changes such as cell shrinkage, condensation of chromatin and nuclear fragmentation. Apoptosis occurs during intestinal ischemia by a process that is independent of ornithine decarboxylase (ODC) activity. Disruption of the epithelial cell-matrix interaction plays a part in the induction of apoptosis in detached ischemic cells. Modulation of a genetic regulatory and biochemical effector machinery of apoptosis might be an important therapeutic target to treat or to prevent I/R injury. Another approach to accelerate the repair of the mucosa during reperfusion after ischemic injury is to administer oral solutions containing a polyamine precursor such as ornithine alpha-ketoglutarate.
Clinical learning point: Novel approaches to the treatment of intestinal ischemia include the use of TNF-a-modifying gene-directed cellular self-destruction (apoptosis), or the use of polyamines or polyamine precursors.