ABSTRACT
Schistosoma mansoni [S. mansoni] is a major health problem; a large proportion of infected individuals suffer from motility-related gastrointestinal disturbances. However, the exact relationship between the gastrointestinal motility changes, the enteric nervous system neuronal excitability, and the complexity of the resulting symptoms, in both the acute and chronic phases of inflammation are still not clear. The work was designed to investigate the effect of two different intensities of S. mansoni infection on gastrointestinal transit and contractility of the colonic muscles, in both acute and chronic phases of inflammation of experimentally infected mice; and to asses the relation between gastrointestinal transit, contractility, and serum antigen and antibody levels. The study was conducted on 60 mice divided into 2 groups a control group consisting of 12 mice, and S. mansoni infected group consisting of 48 mice. The infected group was further subdivided into two subgroups, each infected by a different intensity of cercaria [50 and 200 cercaria/mouse]. Gatrointesintal transit and contractility were recorded from the colon of each group and were analyzed at the acute [8[th] week] and chronic phase [12[th] week] of inflammation. In addition, the immunological changes of the host were assessed in both infected subgroups of mice, at the same studied durations. At 8weeks postinfection, in both infected subgroups, gastrointestinal transit was significantly decreased, in concurrent with significant increase in the colonic muscle contractility, compared to the control group. At that time, the serum antigen was absent, while the serum antibody was detectable at low titre. However, at twelve weeks postinfection, there was a further statistically significant decrease in gastrointestinal transit, and increase in the colonic muscle contractility. These alterations were coinciding with absence of serum antigen and increase in the antibody titre. All changes were more pronounced in the second infected subgroup [200 cercaria/mouse] than the first infected one [50 cercaria/mouse], Indicating that the increased host immunity at the 12[th] week postinfection did not improve the motility disorder of the colon. We conclude that intestinal schistosomiasis is associated with disturbances in gastrointestinal transit and contractility, which are related to the time course and the intensity of the infection, and may be involved in the pathogenesis of the motility disorder associated with the disease. The hypercontractility in the acute phase can be explained by functional changes in the excitability of enteric nervous system neurons due to the release of mediators, and in the chronic phase due to granuloma formation leading to structural changes in the enteric nervous system. Elucidation of the mechanism whereby inflammation alters enteric nervous control of gastrointestinal function may lead to novel treatments of motility disorders of the disease