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Exotoxin
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=== Type III: intracellular === Type III exotoxins can be classified by their mode of entry into the cell, or by their mechanism once inside. ==== By mode of entry ==== Intracellular toxins must be able to gain access to the cytoplasm of the target cell to exert their effects. * Some bacteria deliver toxins directly from their cytoplasm to the cytoplasm of the target cell through a needle-like structure. The effector proteins injected by the type III [[secretion]] apparatus of ''[[Yersinia]]'' into target cells are one example. * Another group of intracellular toxins is the [[AB toxin]]s. The 'B'-subunit ('''''b'''inding'') attaches to target regions on cell membranes, the 'A'-subunit ('''''a'''ctive'') enters through the membrane and possesses [[enzymatic]] function that affects internal cellular bio-mechanisms. A common example of this A-subunit activity is called [[ADP-ribosylation]] in which the A-subunit catalyzes the addition of an ADP-ribose group onto specific residues on a protein. The structure of these toxins allows for the development of specific [[vaccine]]s and treatments. Certain compounds can be attached to the B unit, which is not, in general, harmful, which the body learns to recognize, and which elicits an [[immunity (medical)|immune response]]. This allows the body to detect the harmful toxin if it is encountered later, and to eliminate it before it can cause harm to the host. Toxins of this type include [[cholera toxin]], [[pertussis toxin]], [[Shiga toxin]] and heat-labile [[enterotoxin]] from ''E. coli''. ==== By mechanism ==== Once in the cell, many of the exotoxins act at the eukaryotic [[ribosome]]s (especially [[60S]]), as [[protein synthesis inhibitor]]s. (Ribosome structure is one of the most important differences between eukaryotes and prokaryotes, and, in a sense, these exotoxins are the bacterial equivalent of antibiotics such as [[clindamycin]].) * Some exotoxins act directly at the ribosome to inhibit protein synthesis. An example is [[Shiga toxin]]. * Other toxins act at [[elongation factor-2]]. In the case of the [[diphtheria toxin]], EF2 is ADP-ribosylated and becomes unable to participate in protein elongation, and, so, the cell dies. [[Pseudomonas exotoxin]] has a similar action. Other intracellular toxins do not directly inhibit protein synthesis. * For example, [[Cholera toxin]] ADP-ribosylates, thereby activating tissue adenylate cyclase to increase the concentration of cAMP, which causes the movement of massive amounts of fluid and electrolytes from the lining of the small intestine and results in life-threatening diarrhea. * Another example is [[Pertussis toxin]].
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