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Articles, Neurobiology of Disease

Peripheral Role of Cathepsin S in Th1 Cell-Dependent Transition of Nerve Injury-Induced Acute Pain to a Chronic Pain State

Xinwen Zhang, Zhou Wu, Yoshinori Hayashi, Ryo Okada and Hiroshi Nakanishi
Journal of Neuroscience 19 February 2014, 34 (8) 3013-3022; DOI: https://doi.org/10.1523/JNEUROSCI.3681-13.2014
Xinwen Zhang
1Department of Aging Science and Pharmacology, Faculty of Dental Science, Kyushu University, Fukuoka 812-8582, Japan, and
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Zhou Wu
1Department of Aging Science and Pharmacology, Faculty of Dental Science, Kyushu University, Fukuoka 812-8582, Japan, and
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Yoshinori Hayashi
1Department of Aging Science and Pharmacology, Faculty of Dental Science, Kyushu University, Fukuoka 812-8582, Japan, and
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Ryo Okada
1Department of Aging Science and Pharmacology, Faculty of Dental Science, Kyushu University, Fukuoka 812-8582, Japan, and
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Hiroshi Nakanishi
1Department of Aging Science and Pharmacology, Faculty of Dental Science, Kyushu University, Fukuoka 812-8582, Japan, and
2Japan Science and Technology Agency, CREST, Tokyo, 102-0075, Japan
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Jump to comment:

  • Comment on "Peripheral role of cathepsin S in Th1 cell-dependent transition of nerve injury-induced acute pain to a chronic pain state"
    Marzia Malcangio
    Submitted on: 04 March 2014
  • Submitted on: (4 March 2014)
    Page navigation anchor for Comment on "Peripheral role of cathepsin S in Th1 cell-dependent transition of nerve injury-induced acute pain to a chronic pain state"
    Comment on "Peripheral role of cathepsin S in Th1 cell-dependent transition of nerve injury-induced acute pain to a chronic pain state"
    • Marzia Malcangio
    • Other Contributors:
      • Anna K Clark

    We have read with interest this article by the Nakanishi group, which provides evidence for a role of peripheral Cathepsin S in the generation of neuropathic pain. We are pleased to note that this study confirmed our observations as indeed we were the first authors to report on the therapeutic potential of peripheral and central CatS inhibition for the treatment of neuropathic pain (Barclay et al., 2007; Clark et al., 20...

    Show More

    We have read with interest this article by the Nakanishi group, which provides evidence for a role of peripheral Cathepsin S in the generation of neuropathic pain. We are pleased to note that this study confirmed our observations as indeed we were the first authors to report on the therapeutic potential of peripheral and central CatS inhibition for the treatment of neuropathic pain (Barclay et al., 2007; Clark et al., 2007; Irie et al., 2008). We provided evidence for an extracellular role of CatS located in macrophages (periphery) and microglia (centrally) in the maintenance of neuropathic pain. This article supports our suggestion that CatS is critical for neuropathic pain maintenance, because in figure 1a of Zhang and colleagues article, CatS knockout mice develop the same degree of allodynia as wild-type mice 1 and 2 days after injury. Likewise, in figure 1b when the CatS antagonist ZFL is administered by daily injections commencing on day 0 after injury a total of 5 days are required to start reversing allodynia, which is in line with a lack of participation in the initiation of neuropathic pain that we have previously demonstrated.

    We are surprised that our work is discussed as being in contrast with this study and that reference to our study on peripheral CatS in macrophages is missed. Nevertheless, in addition to the role of extracellular CatS during neuropathic pain demonstrated by our group, this elegant study demonstrates yet another site of action for CatS inhibitors in the periphery: that intracellular CatS in the dendritic cells of the spleen contribute to neuropathic pain via the classical role for CatS in antigen presentation.

    References

    Barclay J, Clark AK, Ganju P, Gentry C, Patel S, Wotherspoon G, Buxton F, Song C, Ullah J, Winter J, Fox A, Bevan S, Malcangio M. Role of the cysteine protease cathepsin S in neuropathic hyperalgesia. Pain, 130:225-234, 2007.

    Clark AK, Yip P, Grist J, Gentry C, Staniland AA, Marchand F, Dehvari M, Wotherspoon G, Winter J, Ullah J, Bevan SB, Malcangio M. Inhibition of spinal microglial cathepsin S for the reversal of neuropathic pain. Proc. Natl. Acad. Sci. USA, 104:10655-10660, 2007. Please note that this paper is discussed in the Zhang article.

    Irie O, Kosaka T, Ehara T, Yokokawa F, Kanazawa T, Hirao H, Iwasaki A, Sakaki J, Teno N, Hitomi Y, Iwasaki G, Fukaya H, Nonomura K, Tanabe K, Koizumi S, Uchiyama N, Bevan SJ, Malcangio M, Gentry C, Fox AJ, Yaqoob M, Culshaw AJ, Hallett A.Discovery of Orally Bioavailable Cathepsin S Inhibitors for the Reversal of Neuropathic Pain. J. Med .Chem. 51: 5502-5505,2008.

    Conflict of Interest:

    None declared

    Show Less
    Competing Interests: None declared.
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The Journal of Neuroscience: 34 (8)
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19 Feb 2014
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Peripheral Role of Cathepsin S in Th1 Cell-Dependent Transition of Nerve Injury-Induced Acute Pain to a Chronic Pain State
Xinwen Zhang, Zhou Wu, Yoshinori Hayashi, Ryo Okada, Hiroshi Nakanishi
Journal of Neuroscience 19 February 2014, 34 (8) 3013-3022; DOI: 10.1523/JNEUROSCI.3681-13.2014

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Peripheral Role of Cathepsin S in Th1 Cell-Dependent Transition of Nerve Injury-Induced Acute Pain to a Chronic Pain State
Xinwen Zhang, Zhou Wu, Yoshinori Hayashi, Ryo Okada, Hiroshi Nakanishi
Journal of Neuroscience 19 February 2014, 34 (8) 3013-3022; DOI: 10.1523/JNEUROSCI.3681-13.2014
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Keywords

  • cathepsin S
  • dendritic cells
  • interferon-ganmma
  • microglia
  • neuropathic pain
  • Th1 cells

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Jump to comment:

  • Comment on "Peripheral role of cathepsin S in Th1 cell-dependent transition of nerve injury-induced acute pain to a chronic pain state"
    Marzia Malcangio
    Published on: 04 March 2014
  • Published on: (4 March 2014)
    Page navigation anchor for Comment on "Peripheral role of cathepsin S in Th1 cell-dependent transition of nerve injury-induced acute pain to a chronic pain state"
    Comment on "Peripheral role of cathepsin S in Th1 cell-dependent transition of nerve injury-induced acute pain to a chronic pain state"
    • Marzia Malcangio
    • Other Contributors:
      • Anna K Clark

    We have read with interest this article by the Nakanishi group, which provides evidence for a role of peripheral Cathepsin S in the generation of neuropathic pain. We are pleased to note that this study confirmed our observations as indeed we were the first authors to report on the therapeutic potential of peripheral and central CatS inhibition for the treatment of neuropathic pain (Barclay et al., 2007; Clark et al., 20...

    Show More

    We have read with interest this article by the Nakanishi group, which provides evidence for a role of peripheral Cathepsin S in the generation of neuropathic pain. We are pleased to note that this study confirmed our observations as indeed we were the first authors to report on the therapeutic potential of peripheral and central CatS inhibition for the treatment of neuropathic pain (Barclay et al., 2007; Clark et al., 2007; Irie et al., 2008). We provided evidence for an extracellular role of CatS located in macrophages (periphery) and microglia (centrally) in the maintenance of neuropathic pain. This article supports our suggestion that CatS is critical for neuropathic pain maintenance, because in figure 1a of Zhang and colleagues article, CatS knockout mice develop the same degree of allodynia as wild-type mice 1 and 2 days after injury. Likewise, in figure 1b when the CatS antagonist ZFL is administered by daily injections commencing on day 0 after injury a total of 5 days are required to start reversing allodynia, which is in line with a lack of participation in the initiation of neuropathic pain that we have previously demonstrated.

    We are surprised that our work is discussed as being in contrast with this study and that reference to our study on peripheral CatS in macrophages is missed. Nevertheless, in addition to the role of extracellular CatS during neuropathic pain demonstrated by our group, this elegant study demonstrates yet another site of action for CatS inhibitors in the periphery: that intracellular CatS in the dendritic cells of the spleen contribute to neuropathic pain via the classical role for CatS in antigen presentation.

    References

    Barclay J, Clark AK, Ganju P, Gentry C, Patel S, Wotherspoon G, Buxton F, Song C, Ullah J, Winter J, Fox A, Bevan S, Malcangio M. Role of the cysteine protease cathepsin S in neuropathic hyperalgesia. Pain, 130:225-234, 2007.

    Clark AK, Yip P, Grist J, Gentry C, Staniland AA, Marchand F, Dehvari M, Wotherspoon G, Winter J, Ullah J, Bevan SB, Malcangio M. Inhibition of spinal microglial cathepsin S for the reversal of neuropathic pain. Proc. Natl. Acad. Sci. USA, 104:10655-10660, 2007. Please note that this paper is discussed in the Zhang article.

    Irie O, Kosaka T, Ehara T, Yokokawa F, Kanazawa T, Hirao H, Iwasaki A, Sakaki J, Teno N, Hitomi Y, Iwasaki G, Fukaya H, Nonomura K, Tanabe K, Koizumi S, Uchiyama N, Bevan SJ, Malcangio M, Gentry C, Fox AJ, Yaqoob M, Culshaw AJ, Hallett A.Discovery of Orally Bioavailable Cathepsin S Inhibitors for the Reversal of Neuropathic Pain. J. Med .Chem. 51: 5502-5505,2008.

    Conflict of Interest:

    None declared

    Show Less
    Competing Interests: None declared.

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