Gut Inflammation in Chronic Fatigue Syndrome

Shaheen E Lakhan; Annette Kirchgessner

Disclosures

Nutr Metab. 2010;7(1) 

In This Article

Effects of Inflammation on the Gut

Patients with CFS manifest symptoms suggestive of disturbed gut function, such as abdominal pain, diarrhea and/or constipation.[9] Under both physiological and pathological conditions, the ENS, the intrinsic innervation of the bowel, regulates intestinal mucosal function and coordinates the activity of the GI tract. The ENS is a component of the autonomic nervous system with the unique ability to function independently from the CNS (for review, see [67]). Enteric ganglia are organized into two major ganglionated plexuses, namely the myenteric (Auerbach's) and submucosal (Meissner's) plexus, and contain a variety of functionally distinct neurons, including primary afferent neurons, interneurons, and motor neurons, synaptically linked to each other in microcircuits.

While the myenteric plexus mainly regulates intestinal motility, the submucosal plexus together with nerve fibers in the lamina propria are involved in regulating epithelial transport. These nerves form networks within the lamina propria of both crypts and villi with the terminal axons in close contact with the basal lamina, an ideal position not only to affect epithelial cell functions but also to detect absorbed nutrients and antigens. These substances or released mediators from epithelial cells may act on the nerve terminals to change the properties of enteric neurons and cause peripheral sensitization. Consequently, permanent or even transient structural alterations in the ENS disrupt normal GI function. Since the ENS controls the motility and secretion of the bowel these abnormalities indicate the impact of inflammation on neural signaling in the ENS.

Several studies have demonstrated ENS structural changes associated with gut inflammation. For example, damage to axons has been observed in the inflamed human intestine in episodes of IBD.[68–70] Other changes that occur in the ENS during inflammation include altered neurotransmitter synthesis, content, and release, changes in glial cell numbers and a myenteric ganglionitis associated with infiltrates of lymphocytes, plasma cells and mast cells.[71,72] In fact, consequences of intestinal inflammation, even if mild, persist for weeks beyond the point at which detectable inflammation has subsided (for review see [73]). Thus, persistent changes in GI nerve function, resulting in dysmotility, pain, and gut dysfunction long after the resolution of the initiating inflammatory event could contribute to GI disorders observed in CFS.

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