Effects of inflammation on cell proliferation in the myenteric plexus of the guinea-pig ileum

Abstract

This study was undertaken to investigate the occurrence and identity of dividing cells within the myenteric plexus of the guinea-pig ileum and to analyze the effects of inflammation induced by trinitrobenzene sulfonic acid. The incorporation of 5-bromo-2-deoxyuridine, or BrdU, into replicating DNA was used to label proliferative cells, and immunohistochemistry was used to assess the occurrence of BrdU in specific cells of the myenteric plexus. Compared to normal tissue, inflammation is associated with increased BrdU labelling in the crypts and in the substantially thickened muscle layers. In longitudinal muscle/myenteric plexus whole-mounts, there was a significant increase in BrdU labelling of the myenteric plexus after induced inflammation. No BrdU-labelled neurons were detected in tissue double labelled with neuron-specific antibodies. Fluorescein isothiocyanate/dextran-labelled macrophages were rare or absent from the ganglia, and none were double labelled with BrdU in the muscle layers. CD3-immunoreactive T cells were substantially increased in the inflamed longitudinal muscle, but still rare or absent within the enteric ganglia. Some BrdU-labelled T cells were observed in the longitudinal muscle but not in the myenteric ganglia. Lastly, in tissues double labelled with anti-BrdU and anti-S-100, many BrdU-containing cells within the myenteric ganglia were found to be S-100-immunoreactive glial cells. We conclude that inflammation does not stimulate the appearance of new myenteric neurons but does stimulate mitosis in myenteric glia.

Endogenous Prion Protein Attenuates Experimentally Induced Colitis

“…In the gut, we and others have observed that the cells of the enteric nervous system, the proliferation of which increases during intestinal inflammation, 50 express high levels of immunoreactive PrP C . 11 In view of the ability of enteric glial cells to produce IL-6, 51 these cells may have provided an additional source of this cytokine.…”

Vagal nerve stimulation protects against burn-induced intestinal injury through activation of enteric glia cells

“…It has been hypothesized that a subpopulation of enteric glia cells can rapidly upregulate GFAP expression in response to inflammation, whereas other glia cells respond more slowly and require proliferation and GFAP synthesis (4,24). The CNS may signal the ENS via the vagus nerve to increase enteric glial cell GFAP synthesis in response to injury.…”

Role of enteric glial cells in inflammatory bowel disease

“…Using a model of inflammatory bowel disease (IBD) in the guinea pig, Bradley et al (1997) demonstrated that EGCs incorporate BrdU during inflammatory conditions. Whether this proliferative response represents a phenomenon comparable to the neuroprotective astrogliosis observed in the CNS is not known at present since this observation could also result from EGC renewal in response to injury and death.…”