Vasoactive intestinal peptide and substance P immunoreactive nerve fibres in the myenteric plexus of mouse colon during the chronic phase of Trypanosoma cruzi infection

Abstract

The distribution of a tachykinin (substance P) and vasoactive intestinal peptide (VIP) and the number and morphology of the large granular vesicles (LGV) in the myenteric plexus of the colons of mice were investigated. Six of the 12 young, male, Swiss mice studied had been inoculated with the Y strain of Trypanosoma cruzi 2 months previously whereas the others were uninfected controls. Substance P (SP) and VIP were localized by light microscopy, using an immunohistochemical method, and LGV were counted in sections studied by electron microscopy. There were far fewer LGV and less intensely staining varicose VIP- and SP-positive nerve fibres in the infected mice than in the controls. Denervation of the myenteric plexus may decrease the content of tachykinins (TK) and VIP in animals infected with T. cruzi. Such reduction in TK and VIP activity could be related to the disturbances in intestinal motility observed in the chronic phase of Chagas disease.

Immunohistochemical study on the neuroendocrine system of the digestive tract of turbot, Scophthalmus maximus (L.), infected by Enteromyxum scophthalmi (Myxozoa)

“…In the current study, the number of both VIP-immunoreactive endocrine cells and nerve cell bodies and fibres were significantly lower in infected turbots than in controls. Similar findings were reported in humans with ulcerative colitis [64] and in mice infected with Trypanosoma cruzi [65]. Contrary to this, an increase in the number of nerve cell bodies and nerve fibres immunoreactive to the VIP antiserum was observed by Dezfuli et al [16] and Bosi et al [20] in fishes parasitized with helminths.…”

The role of selenium in intestinal motility and morphology in a murine model of Typanosoma cruzi infection

“…Several substances identified in the enteric nervous system of mammals can be released and participate in the control of gastrointestinal motility by acting directly on the gastrointestinal smooth muscle, or indirectly by modulating the release of inhibitory or excitatory mediators (Matsuda and Dantas 2008). Since Se supplementation prevented the delayed evacuation time in infected mice, it would be worthy to explore the effect of Se on factors related to disturbances in intestinal motility, in addition to those caused by T. cruzi infection, such as decreased levels of tachykinins and vasoactive intestinal peptide (Maifrino et al 1999), decreased somatostatin (Maifrino et al 2005), and reduced number of interstitial cells of Cajal (Hagger et al 2000). …”

Targeting tachykinin receptors for the treatment of functional gastrointestinal disorders with a focus on irritable bowel syndrome

“…Many studies, mainly in animals, have suggested that TKs are also implicated in modulation of inflammation and of inflammation‐induced alteration of motility and secretion in pathological gut conditions. Table reports the results of these studies …”