Abstract
Cholera, a waterborne acute diarrheal disease caused by Vibrio cholerae, remains prevalent in underdeveloped countries and is a serious health threat to those living in unsanitary conditions. The major virulence factor is cholera toxin (CT), which consists of two subunits: the A subunit (CTA) and the B subunit (CTB). CTB is a 55 kD homopentameric, non-toxic protein binding to the GM1 ganglioside on mammalian cells with high affinity. Currently, recombinantly produced CTB is used as a component of an internationally licensed oral cholera vaccine, as the protein induces potent humoral immunity that can neutralize CT in the gut. Additionally, recent studies have revealed that CTB administration leads to the induction of anti-inflammatory mechanisms in vivo. This review will cover the potential of CTB as an immunomodulatory and anti-inflammatory agent. We will also summarize various recombinant expression systems available for recombinant CTB bioproduction.
Highlights
Cholera is a highly contagious acute dehydrating diarrheal disease caused by Vibrio cholerae.There are over 200 serogroups of V. cholerae known to date; only two (O1 and 139 serotypes) are responsible for the vast majority of outbreaks [1,2]
While first being recognized for its role in the delivery of the virulence factor of V. cholerae, the works highlighted in this paper show CTB’s broad utility as a cholera vaccine immunogen, vaccine adjuvant, immune modulator and/or anti-inflammatory agent
Given that CTB appears to provide additional efficacy to killed bacteria-based cholera vaccines, development of alternative rCTB production and delivery methods may significantly contribute to cholera prevention and control
Summary
Cholera is a highly contagious acute dehydrating diarrheal disease caused by Vibrio cholerae. Symptomatic individuals can shed the organism from 2 days to 2 weeks after infection and recently shed organisms (5–24 h after shedding) have hyperinfectivity; in this state the infectious dose is 10 to 100 times lower than non-shed organisms (~106 bacteria) [4,5] This can lead to the rapid spread of cholera in densely populated areas without proper management of patients and their waste. CTA1 enters the cell cytosol and catalyzes the ADP ribosylation of adenylate cyclase, which leads to increased intracellular cAMP. This increase in intracellular cAMP results in impaired sodium uptake and increased chloride outflow, causing water secretion and diarrhea [12,17]. Images were created in Accelrys Discovery Studio Visualizer 2.5
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