Abstract
Myenteric plexus alterations hamper gastrointestinal motor function during intestinal inflammation. Hyaluronan (HA), an extracellular matrix glycosaminoglycan involved in inflammatory responses, may play a role in this process. In the colon of control rats, HA-binding protein (HABP), was detected in myenteric neuron soma, perineuronal space and ganglia surfaces. Prominent hyaluronan synthase 2 (HAS2) staining was found in myenteric neuron cytoplasm, suggesting that myenteric neurons produce HA. In the myenteric plexus of rats with 2, 4-dinitrobenzene sulfonic (DNBS)-induced colitis HABP staining was altered in the perineuronal space, while both HABP staining and HA levels increased in the muscularis propria. HAS2 immunopositive myenteric neurons and HAS2 mRNA and protein levels also increased. Overall, these observations suggest that inflammation alters HA distribution and levels in the gut neuromuscular compartment. Such changes may contribute to alterations in the myenteric plexus.
Highlights
Myenteric plexus alterations hamper gastrointestinal motor function during intestinal inflammation
Our findings are the first demonstration that a glycosaminoglycan (GAG) component of the extracellular matrix (ECM) may participate in the formation of a pericellular coat of condensed matrix surrounding myenteric neurons, similar to the perineuronal net associated with some classes of neurons within the central nervous system (CNS)[14]
HA levels significantly increase in the muscularis propria containing the myenteric plexus suggesting that the GAG may participate to colonic neuromuscular derangement during inflammation
Summary
Myenteric plexus alterations hamper gastrointestinal motor function during intestinal inflammation. In the myenteric plexus of rats with 2, 4-dinitrobenzene sulfonic (DNBS)-induced colitis HABP staining was altered in the perineuronal space, while both HABP staining and HA levels increased in the muscularis propria. HAS2 immunopositive myenteric neurons and HAS2 mRNA and protein levels increased Overall, these observations suggest that inflammation alters HA distribution and levels in the gut neuromuscular compartment. These observations suggest that inflammation alters HA distribution and levels in the gut neuromuscular compartment Such changes may contribute to alterations in the myenteric plexus. The mechanism/s underlying derangement of myenteric neuronal circuitries during gut inflammation have not been completely unraveled yet In this context, it is important to unveil possible modulators of pro-inflammatory states, in order to prevent the incidence of more evident inflammatory conditions. The expression of hyaluronan synthase 2 (HAS2), the more abundant of HA synthase isoforms, has been analyzed
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