Trigeminal ganglionic neuronal death in a case positive for the botulinum neurotoxin B
نویسندگان
چکیده
Botulinum neurotoxin B (BoNT-B) is a well known lethal agent in humans. In the last years botulinum neurotoxins have been used as therapeutic agents in pain management; their intimate effects on the peripheral nervous ganglia were however not thoroughly described. We present here a rare case of a BoNT-B serologically positive human adult in which trigeminal ganglia were found immunopositive for caspases 3 and 9. Thus the intrinsic apoptotic pathway was proposed as the cell death mechanism involving primary trigeminal neurons. Scavengers such as macrophages and resident satellite glial cells, with a CD68 immunopositivity were also identified, presumably being in the process of eliminating apoptotic remnants. Taking into account that the downregulation of metalloproteinases leads to inactivation of neuronal caspase 3, exogenous metalloproteinases, such as BoNT, may lead to apoptosis. If this causal relation, neurotoxin-to-apoptosis is valid, similar apoptotic processes can be presumed to occur in various ganglia, sensory and autonomic, involved in vital functions of the body. In conclusion, further morphological and experimental studies are needed to extensively evaluate the apoptotic effect of BoNT within the peripheral nervous ganglia in botulinum infections and BoNT treatments.
منابع مشابه
Characterization of Clostridium botulinum spores and its toxin in honey
Botulism is a serious paralytic disease caused by Clostridium botulinum toxin in foods. There are seven recognized serotypes of botulinum neurotoxins among which the principal prevalent types in humans include A, B and E. Infant botulism results from intestinal colonization and toxin production by C. botulinum spores in babies less than 1 year old. Honey is the most important food discriminated...
متن کاملActivation of TRPV1 mediates calcitonin gene-related peptide release, which excites trigeminal sensory neurons and is attenuated by a retargeted botulinum toxin with anti-nociceptive potential.
Excessive release of inflammatory/pain mediators from peripheral sensory afferents renders nerve endings hyper-responsive, causing central sensitization and chronic pain. Herein, the basal release of proinflammatory calcitonin gene-related peptide (CGRP) was shown to increase the excitability of trigeminal sensory neurons in brainstem slices via CGRP1 receptors because the effect was negated by...
متن کاملExpression and Purification of Neurotoxin-Associated Protein HA-33/A from Clostridium botulinum and Evaluation of Its Antigenicity
Background: Botulinum neurotoxin (BoNT) complexes consist of neurotoxin and neurotoxin-associated proteins. Hemagglutinin-33 (HA-33) is a member of BoNT type A (BoNT/A) complex. Considering the protective role of HA-33 in preservation of BoNT/A in gastrointestinal harsh conditions and also its adjuvant role, recombinant production of this protein is favorable. Thus in this study, HA-33 was expr...
متن کاملImmunogenic and Protective Potentials of Recombinant Receptor Binding Domain and a C-Terminal Fragment of Clostridium botulinum Neurotoxin Type E
Clostridium Botulinum Type E neurotoxin heavy chain consists of two domains: the translocation domain asthe N-terminal half and the binding domain as the Cterminal half (Hc). One effective way to neutralize botulinum neurotoxin is to inhibit binding of this toxin to neuromuscular synapses with antibodies against binding domain. Two synthetic genes, coding for Hc (the full length binding d...
متن کاملBotulinum neurotoxin type C protease induces apoptosis in differentiated human neuroblastoma cells
Neuroblastomas constitute a major cause of cancer-related deaths in young children. In recent years, a number of translation-inhibiting enzymes have been evaluated for killing neuroblastoma cells. Here we investigated the potential vulnerability of human neuroblastoma cells to protease activity derived from botulinum neurotoxin type C. We show that following retinoic acid treatment, human neuro...
متن کاملذخیره در منابع من
با ذخیره ی این منبع در منابع من، دسترسی به آن را برای استفاده های بعدی آسان تر کنید
عنوان ژورنال:
دوره شماره
صفحات -
تاریخ انتشار 2012