Abstract:
Cholera is an acute diarrhoeal illness that poses serious public health problems in developing countries. The causative agent of this disease is Vibrio cholerae, a distinct curved, rod-shaped Gram-negative bacterium. It is well acknowledged that naturally occurring biofilms are composed of multispecies communities. However, little is known about the interactions of V. cholerae with other bacterial species in biofilm development. In a preliminary in vitro study, high coaggregation activity between V. cholerae with human commensals, namely Escherichia coli and Enterobacter cloacae were established. Building upon the result, in this study, the effect of coaggregation on the pathogenicity of V. cholerae was evaluated using an adult BALB/c mouse model. Based on the results obtained, no significant differences in mortality and fluid accumulation ratio (FA ratio) were detected between treatment groups infected with V. cholerae alone and those infected with coaggregation partnership (V. cholerae + E. coli and V. cholerae + E. cloacae). However, the presence of V. cholerae microcolonies and mild inflammation in the intestinal tissue of the co-infected mice are thought to explain, at least in part of the successful establishment of cholera mouse model. Interestingly, elevated numbers of V. cholerae were recovered from faecal samples of mice co-infected with E. coli and V. cholerae at 24 hours post infection, suggesting potential growth promoting effect of E. coli. This partnership also induced slightly higher interleukin-5 (IL-5) and interleukin-10 (IL-10), when compared to other co-infection groups. Nonetheless, the involvement of autoinducer-2 (AI-2) quorum sensing system is not evident in this case. In summary, our findings suggest a potential role of human commensals particularly E. coli in V. cholerae disease development.
