which are used to compromise the host, with the most important of these being cholera toxin (CT) itself. B subunit of CT binds to GM1 ganglioside receptor on enterocyte surface, facilitating CT uptake into the cells (28). Inside the intestinal epithelial cells, CT retrogrades into endoplasmic reticulum and hijacks Endoplasmic Reticulum Associated Protein Degradation (ERAD) pathway for transporting its enzymatic A chain into cytosol. The A chain perturbs cellular homeostasis by irreversibly ADP-ribosylating Gsα subunit, leading to constitutive activation of adenylate cyclase and massive cAMP production. Intracellular cAMP elevation subsequently activates PKA, which then phosphorylates the regulatory domain of CFTR (29). The accessory cholera toxin from V. cholerae elicits diarrhea by increasing intracellular Ca2+ leading to CaCC stimulation. In addition to increased Cl- secretion, intracellular cAMP elevation also inhibits sodium absorption process by