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Toxins
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Botulinum Toxin for Urinary Tract Disease: After a Decade from...
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Botulinum Toxin for Urinary Tract Disease: After a Decade from Approval

A special issue of Toxins (ISSN 2072-6651). This special issue belongs to the section "Bacterial Toxins".

Deadline for manuscript submissions: 31 May 2024 | Viewed by 1615

Special Issue Editor

Dr. Heinrich Schulte-Baukloh

E-Mail Website
Guest Editor
Department of Urology, and Urologic Private Practice, Charité—University Hospital Berlin, Berlin, Germany
Interests: neuro-urology; urodynamics; LUTS

Special Issue Information

Dear Colleagues,

Botulinum toxin was approved by the FDA in 2011 for neurogenic bladder and in 2013 for idiopathic overactive bladder. For this Special Issue, we would like to address the question of where we stand with this therapy a decade later: has it prevailed and been proven useful? Which techniques have become established, and how were they optimized? Are there more practical ways of distribution on the way? What obstacles/acceptance problems might there be from patients or doctors in (long-term) use? What are the risks, if any? Has the therapy gained a foothold in the outpatient sector?

Dr. Heinrich Schulte-Baukloh
Guest Editor

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a double-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Toxins is an international peer-reviewed open access monthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2700 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • urinary bladder
  • botulinum toxin
  • neurogenic bladder
  • incontinence
  • injection technique

Published Papers (1 paper)

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Research

21 pages, 4815 KiB  
Article
A Novel Catalytically Inactive Construct of Botulinum Neurotoxin A (BoNT/A) Directly Inhibits Visceral Sensory Signalling
by Hodan Ibrahim, Kevin Retailleau, Fraser Hornby, Jacquie Maignel, Matthew Beard and Donna Marie Daly
Toxins 2024, 16(1), 30; https://doi.org/10.3390/toxins16010030 - 07 Jan 2024
Viewed by 1349
Abstract
Botulinum neurotoxin A (BoNT/A) is a potent neurotoxin that silences cholinergic neurotransmission through the cleavage of the synaptic protein SNAP-25. Previous studies have shown that, in addition to its paralytic effects, BoNT/A can inhibit sensory nerve activity. The aim of this study was [...] Read more.
Botulinum neurotoxin A (BoNT/A) is a potent neurotoxin that silences cholinergic neurotransmission through the cleavage of the synaptic protein SNAP-25. Previous studies have shown that, in addition to its paralytic effects, BoNT/A can inhibit sensory nerve activity. The aim of this study was to identify how BoNT/A inhibits afferent signalling from the bladder. To investigate the role of SNAP-25 cleavage in the previously reported BoNT/A-dependent inhibition of sensory signalling, we developed a recombinant form of BoNT/A with an inactive light chain, rBoNT/A (0), unable to paralyse muscle. We also developed recombinant light chain (LC)-domain-only proteins to better understand the entry mechanisms, as the heavy chain (HC) of the protein is responsible for the internalisation of the light chain. We found that, despite a lack of catalytic activity, rBoNT/A (0) potently inhibited the afferent responses to bladder distension to a greater degree than catalytically active rBoNT/A. This was also clear from the testing of the LC-only proteins, as the inactive rLC/A (0) protein inhibited afferent responses significantly more than the active rLC/A protein. Immunohistochemistry for cleaved SNAP-25 was negative, and purinergic and nitrergic antagonists partially and totally reversed the sensory inhibition, respectively. These data suggest that the BoNT/A inhibition of sensory nerve activity in this assay is not due to the classical well-characterised ‘double-receptor’ mechanism of BoNT/A, is independent of SNAP25 cleavage and involves nitrergic and purinergic signalling mechanisms. Full article
(This article belongs to the Special Issue Botulinum Toxin for Urinary Tract Disease: After a Decade from Approval)
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