In a recent study the author writes "enteric neurons are supported by glial cells, the ENS counterparts of astrocytes of the CNS, that can modulate enteric neuron function. Enteric neurons are known to control virtually all GI functions, including motility, secretion, blood flow, mucosal growth and aspects of the local immune system. Consequently, permanent or even transient structural alterations in the ENS, as occur in IBD, disrupt normal GI function. Structural changes in the ENS are predictive of disease evolution suggesting that neuroprotection would decrease disease severity and may play a role in recurrence in CD." Further he continues that under conditions of experimental trichinosis infection in the murine "that in this animal model of colitis, there was a significant loss of nitric oxide synthase- (NOS-) immunoreactive neurons in the myenteric plexus of infected rats. Moreover, the selective loss of NOS-positive neurons appears to underlie changes in motility." (Lakhan) Recent reports also suggest that hormones such as serotonin influences gut regulation and may activate inflammatory cytokines in the intestine leading to alterations in gut function. (Khan) Inflammatory activity such as Tnf-a in the periphery such as the gut may influence production of cytokines and changes in gene expression in the brain that change behavior and have other unexpected health effects.
Khan, W. I. and Ghia, J. E. (2010). Gut hormones: emerging role in immune activation and inflammation. Clinical and experimental immunology, 161(1):19-27.
http://www.citeulike.org/user/HEIRS/article/7323747
Lakhan, S. E. and Kirchgessner, A. (2010). Neuroinflammation in inflammatory bowel disease. Journal of neuroinflammation, 7:37+.
http://www.citeulike.org/user/HEIRS/article/7471133
Health research blog is for those people who secure their better quality life. From the recent study the loss of neurons causes in the inflammation and changes in the intestinal function.
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