S100B protein in the gut: the evidence for enteroglial-sustained intestinal inflammation

Abstract

Glial cells in the gut represent the morphological and functional equivalent of astrocytes and microglia in the central nervous system (CNS). In recent years, the role of enteric glial cells (EGCs) has extended from that of simple nutritive support for enteric neurons to that of being pivotal participants in the regulation of inflammatory events in the gut. Similar to the CNS astrocytes, the EGCs physiologically express the S100B protein that exerts either trophic or toxic effects depending on its concentration in the extracellular milieu. In the CNS, S100B overexpression is responsible for the initiation of a gliotic reaction by the release of pro-inflammatory mediators, which may have a deleterious effect on neighboring cells. S100B-mediated pro-inflammatory effects are not limited to the brain: S100B overexpression is associated with the onset and maintenance of inflammation in the human gut too. In this review we describe the major features of EGCs and S100B protein occurring in intestinal inflammation deriving from such.

Keywords: Enteric glial cells; Intestinal diseases; Nitric oxide.

Figure 1

Changes in S100B protein expression during intestinal inflammation. A: Celiac disease[13]. Immunohistochemistry shows stronger S100B immunopositivity in the duodenal mucosa of patients affected by celiac disease, compared with healthy controls (original magnification, × 100). The graphs represent S100B protein expression (left) and release (right) in healthy controls and patients with celiac disease (^bP < 0.01); B: Ulcerative colitis[14]. Immunohistochemistry shows stronger S100B immunopositivity in the rectal submucosa of patients with ulcerative colitis, compared with healthy controls (original magnification, × 100). The graphs represent S100B protein expression (left) and release (right) in healthy controls and patients with ulcerative colitis (^dP < 0.01).