Chemotherapy-induced peripheral neuropathy: part 1—current state of knowledge and perspectives for pharmacotherapy

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Abstract

Background

Despite the increasing knowledge of the etiology of neuropathic pain, this type of chronic pain is resistant to available analgesics in approximately 50% of patients and therefore is continuously a subject of considerable interest for physiologists, neurologists, medicinal chemists, pharmacologists and others searching for more effective treatment options for this debilitating condition.

Materials and methods

The present review article is the first of the two articles focused on chemotherapy-induced peripheral neuropathy (CIPN).

Results

CIPN is regarded as one of the most common drug-induced neuropathies and is highly pharmacoresistant. The lack of efficacious pharmacological methods for treating CIPN and preventing its development makes CIPN-related neuropathic pain a serious therapeutic gap in current medicine and pharmacotherapy. In this paper, the most recent advances in the field of studies on CIPN caused by platinum compounds (namely oxaliplatin and cisplatin), taxanes, vinca alkaloids and bortezomib are summarized.

Conclusions

The prevalence of CIPN, potential causes, risk factors, symptoms and molecular mechanisms underlying this pharmacoresistant condition are discussed.

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Most cited references 164

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Different immune cells mediate mechanical pain hypersensitivity in male and female mice.

Simon Beggs, Sarah Taves, Jessica K Alexander … (2015)

A large and rapidly increasing body of evidence indicates that microglia-to-neuron signaling is essential for chronic pain hypersensitivity. Using multiple approaches, we found that microglia are not required for mechanical pain hypersensitivity in female mice; female mice achieved similar levels of pain hypersensitivity using adaptive immune cells, likely T lymphocytes. This sexual dimorphism suggests that male mice cannot be used as proxies for females in pain research.

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Akkermansia muciniphila Adheres to Enterocytes and Strengthens the Integrity of the Epithelial Cell Layer.

Justus Reunanen, Veera Kainulainen, Laura Huuskonen … (2015)

Akkermansia muciniphila is a Gram-negative mucin-degrading bacterium that resides in the gastrointestinal tracts of humans and animals. A. muciniphila has been linked with intestinal health and improved metabolic status in obese and type 2 diabetic subjects. Specifically, A. muciniphila has been shown to reduce high-fat-diet-induced endotoxemia, which develops as a result of an impaired gut barrier. Despite the accumulating evidence of the health-promoting effects of A. muciniphila, the mechanisms of interaction of the bacterium with the host have received little attention. In this study, we used several in vitro models to investigate the adhesion of A. muciniphila to the intestinal epithelium and its interaction with the host mucosa. We found that A. muciniphila adheres strongly to the Caco-2 and HT-29 human colonic cell lines but not to human colonic mucus. In addition, A. muciniphila showed binding to the extracellular matrix protein laminin but not to collagen I or IV, fibronectin, or fetuin. Importantly, A. muciniphila improved enterocyte monolayer integrity, as shown by a significant increase in the transepithelial electrical resistance (TER) of cocultures of Caco-2 cells with the bacterium. Further, A. muciniphila induced interleukin 8 (IL-8) production by enterocytes at cell concentrations 100-fold higher than those for Escherichia coli, suggesting a very low level of proinflammatory activity in the epithelium. In conclusion, our results demonstrate that A. muciniphila adheres to the intestinal epithelium and strengthens enterocyte monolayer integrity in vitro, suggesting an ability to fortify an impaired gut barrier. These results support earlier associative in vivo studies and provide insights into the interaction of A. muciniphila with the host.

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Spinal cord Toll-like receptor 4 mediates inflammatory and neuropathic hypersensitivity in male but not female mice.

Amy C. Graham, Jean-Sebastien Austin, Glade L Topham … (2011)

The innate immune system is increasingly appreciated to play an important role in the mediation of chronic pain, and one molecule implicated in this process is the Toll-like receptor 4 (TLR4). Here, using pharmacological and genetic manipulations, we found that activating TLR4 in the spinal cord, with the agonist lipopolysaccharide (LPS), causes robust mechanical allodynia but only in male mice. Spinal LPS had no pain-producing effect in female mice. TLR4 also has a sex-specific role in inflammatory (complete Freund's adjuvant) and neuropathic (spared nerve injury) pain: pain behaviors were TLR4 dependent in males but TLR4 independent in females. The sex differences appear to be specific to the spinal cord, as LPS administered to the brain or the hindpaw produces equivalent allodynia in both sexes, and specific to pain, as intrathecal LPS produces equivalent hypothermia in both sexes. The involvement of TLR4 in pain behaviors in male mice is dependent on testosterone, as shown by gonadectomy and hormone replacement. We found no sex differences in spinal Tlr4 gene expression at baseline or after LPS, suggesting the existence of parallel spinal pain-processing circuitry in female mice not involving TLR4.

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Author and article information

Contributors

Kinga Sałat: kinga.salat@uj.edu.pl

Journal

Journal ID (nlm-ta): Pharmacol Rep

Journal ID (iso-abbrev): Pharmacol Rep

Title: Pharmacological Reports

Publisher: Springer International Publishing (Cham )

ISSN (Print): 1734-1140

ISSN (Electronic): 2299-5684

Publication date (Electronic): 11 May 2020

Publication date PMC-release: 11 May 2020

Publication date (Print): 2020

Volume: 72

Issue: 3

Pages: 486-507

Affiliations

GRID grid.5522.0, ISNI 0000 0001 2162 9631, Department of Pharmacodynamics, Chair of Pharmacodynamics, , Jagiellonian University Medical College, ; 9 Medyczna St., 30-688 Krakow, Poland

Article

Publisher ID: 109

DOI: 10.1007/s43440-020-00109-y

PMC ID: 7329796

PubMed ID: 32394362

SO-VID: f71c5b77-466a-4cce-bb1e-39620b939afc

License:

Open AccessThis article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/.

History

Date received : 18 February 2020

Date revision received : 20 April 2020

Date accepted : 28 April 2020

Funding

Funded by: FundRef http://dx.doi.org/10.13039/501100004281, Narodowe Centrum Nauki;

Award ID: UMO-2015/17/B/NZ7/02937

Award Recipient : Kinga Sałat

Custom metadata

Keywords: chemotherapy-induced peripheral neuropathy,neuronal hyperexcitability,platinum derivatives,paclitaxel,vinca alkaloids,bortezomib

Data availability:

Keywords: chemotherapy-induced peripheral neuropathy, neuronal hyperexcitability, platinum derivatives, paclitaxel, vinca alkaloids, bortezomib

Chemotherapy-induced peripheral neuropathy: part 1—current state of knowledge and perspectives for pharmacotherapy

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Abstract

Background

Materials and methods

Results

Conclusions

Graphic abstract

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Most cited references 164

Different immune cells mediate mechanical pain hypersensitivity in male and female mice.

Akkermansia muciniphila Adheres to Enterocytes and Strengthens the Integrity of the Epithelial Cell Layer.

Spinal cord Toll-like receptor 4 mediates inflammatory and neuropathic hypersensitivity in male but not female mice.

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