
Clostridium botulinum is a gram-positive anaerobic rod that forms endospores. This bacterium produces large molecular toxin complexes, namely botulinum toxin complexes (progenitor toxins). It (L toxin complex) is composed of a single neurotoxin molecule (BoNT with a molecular weight of 150 kDa), a single nontoxic nonhemagglutinin molecule (NTNHA), and a hemagglutinin complex (HA). On food-borne botulism, nontoxic components have the roles of protecting toxin protein from the degeneration and degradation action of acids and proteases existing in the gastrointestinal tract. The HA facilitates transport when progenitor toxins cross the intestinal epithelial barrier to enter the systemic circulation. BoNT disassociates from the toxin complexes in the systemic circulation. BoNT is immunologically classified into 7 serotypes, A to G. Serotypes A, B, E, and F are the causative agents of human botulism. The active BoNT molecules are composed of 2 chains that are termed the heavy chain (c. 100 kDa) and the light chain (c. 50 kDa); these are covalently connected by a disulfide bond. The light chains have a tetrahedral zinc binding motif conteining a consensus HExxH amino acid sequence, and exhibit metalloprotease activity. After BoNTs reach the neuromuscular junction (the peripheral nerve ending), these are endocytosed in lipid vesicles (synaptic vesicles), and the light chain is released into the cytosol of a nerve cell via a translocation event through the phospholipid vesicle membrane. The light chains of BoNTs (zinc endopeptidases) cleave core proteins involved in the trafficking and release of neurotransmitters (acetylcholine), including synaptobrevin, SNAP-25, and syntaxin. These proteins comprise the synaptic members of the SNARE complex (soluble NSF (N-ethylmaleimide-sensitive fusionprotein) attachment protein) that have a central role in membrane fusion events. The selective proteolysis of these SNARE proteins inhibits neurotransmitter release from neurons. Botulism occurs via a series of processes that cause muscular paralysis in human and animals.
Botulinum Toxins, Clostridium botulinum, Neuromuscular Junction, Animals, Humans
Botulinum Toxins, Clostridium botulinum, Neuromuscular Junction, Animals, Humans
| selected citations These citations are derived from selected sources. This is an alternative to the "Influence" indicator, which also reflects the overall/total impact of an article in the research community at large, based on the underlying citation network (diachronically). | 0 | |
| popularity This indicator reflects the "current" impact/attention (the "hype") of an article in the research community at large, based on the underlying citation network. | Average | |
| influence This indicator reflects the overall/total impact of an article in the research community at large, based on the underlying citation network (diachronically). | Average | |
| impulse This indicator reflects the initial momentum of an article directly after its publication, based on the underlying citation network. | Average |
