TRPV1 and the MCP-1/CCR2 Axis Modulate Post-UTI Chronic Pain

Abstract The etiology of chronic pelvic pain syndromes remains unknown. In a murine urinary tract infection (UTI) model, lipopolysaccharide of uropathogenic E. coli and its receptor TLR4 are required for post-UTI chronic pain development. However, downstream mechanisms of post-UTI chronic pelvic pai...

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Autores principales:	John M. Rosen, Ryan E. Yaggie, Patrick J. Woida, Richard. J. Miller, Anthony J. Schaeffer, David J. Klumpp
Formato:	article
Lenguaje:	EN
Publicado:	Nature Portfolio 2018
Materias:	Medicine R Science Q
Acceso en línea:	https://doaj.org/article/331784aac4b342c2ac644d5fddea1a20
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spelling	oai:doaj.org-article:331784aac4b342c2ac644d5fddea1a202021-12-02T16:07:52ZTRPV1 and the MCP-1/CCR2 Axis Modulate Post-UTI Chronic Pain10.1038/s41598-018-24056-02045-2322https://doaj.org/article/331784aac4b342c2ac644d5fddea1a202018-05-01T00:00:00Zhttps://doi.org/10.1038/s41598-018-24056-0https://doaj.org/toc/2045-2322Abstract The etiology of chronic pelvic pain syndromes remains unknown. In a murine urinary tract infection (UTI) model, lipopolysaccharide of uropathogenic E. coli and its receptor TLR4 are required for post-UTI chronic pain development. However, downstream mechanisms of post-UTI chronic pelvic pain remain unclear. Because the TRPV1 and MCP-1/CCR2 pathways are implicated in chronic neuropathic pain, we explored their role in post-UTI chronic pain. Mice were infected with the E. coli strain SΦ874, known to produce chronic allodynia, and treated with the TRPV1 antagonist capsazepine. Mice treated with capsazepine at the time of SΦ874 infection failed to develop chronic allodynia, whereas capsazepine treatment of mice at two weeks following SΦ874 infection did not reduce chronic allodynia. TRPV1-deficient mice did not develop chronic allodynia either. Similar results were found using novelty-suppressed feeding (NSF) to assess depressive behavior associated with neuropathic pain. Imaging of reporter mice also revealed induction of MCP-1 and CCR2 expression in sacral dorsal root ganglia following SΦ874 infection. Treatment with a CCR2 receptor antagonist at two weeks post-infection reduced chronic allodynia. Taken together, these results suggest that TRPV1 has a role in the establishment of post-UTI chronic pain, and CCR2 has a role in maintenance of post-UTI chronic pain.John M. RosenRyan E. YaggiePatrick J. WoidaRichard. J. MillerAnthony J. SchaefferDavid J. KlumppNature PortfolioarticleMedicineRScienceQENScientific Reports, Vol 8, Iss 1, Pp 1-7 (2018)
institution	DOAJ
collection	DOAJ
language	EN
topic	Medicine R Science Q
spellingShingle	Medicine R Science Q John M. Rosen Ryan E. Yaggie Patrick J. Woida Richard. J. Miller Anthony J. Schaeffer David J. Klumpp TRPV1 and the MCP-1/CCR2 Axis Modulate Post-UTI Chronic Pain
description	Abstract The etiology of chronic pelvic pain syndromes remains unknown. In a murine urinary tract infection (UTI) model, lipopolysaccharide of uropathogenic E. coli and its receptor TLR4 are required for post-UTI chronic pain development. However, downstream mechanisms of post-UTI chronic pelvic pain remain unclear. Because the TRPV1 and MCP-1/CCR2 pathways are implicated in chronic neuropathic pain, we explored their role in post-UTI chronic pain. Mice were infected with the E. coli strain SΦ874, known to produce chronic allodynia, and treated with the TRPV1 antagonist capsazepine. Mice treated with capsazepine at the time of SΦ874 infection failed to develop chronic allodynia, whereas capsazepine treatment of mice at two weeks following SΦ874 infection did not reduce chronic allodynia. TRPV1-deficient mice did not develop chronic allodynia either. Similar results were found using novelty-suppressed feeding (NSF) to assess depressive behavior associated with neuropathic pain. Imaging of reporter mice also revealed induction of MCP-1 and CCR2 expression in sacral dorsal root ganglia following SΦ874 infection. Treatment with a CCR2 receptor antagonist at two weeks post-infection reduced chronic allodynia. Taken together, these results suggest that TRPV1 has a role in the establishment of post-UTI chronic pain, and CCR2 has a role in maintenance of post-UTI chronic pain.
format	article
author	John M. Rosen Ryan E. Yaggie Patrick J. Woida Richard. J. Miller Anthony J. Schaeffer David J. Klumpp
author_facet	John M. Rosen Ryan E. Yaggie Patrick J. Woida Richard. J. Miller Anthony J. Schaeffer David J. Klumpp
author_sort	John M. Rosen
title	TRPV1 and the MCP-1/CCR2 Axis Modulate Post-UTI Chronic Pain
title_short	TRPV1 and the MCP-1/CCR2 Axis Modulate Post-UTI Chronic Pain
title_full	TRPV1 and the MCP-1/CCR2 Axis Modulate Post-UTI Chronic Pain
title_fullStr	TRPV1 and the MCP-1/CCR2 Axis Modulate Post-UTI Chronic Pain
title_full_unstemmed	TRPV1 and the MCP-1/CCR2 Axis Modulate Post-UTI Chronic Pain
title_sort	trpv1 and the mcp-1/ccr2 axis modulate post-uti chronic pain
publisher	Nature Portfolio
publishDate	2018
url	https://doaj.org/article/331784aac4b342c2ac644d5fddea1a20
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TRPV1 and the MCP-1/CCR2 Axis Modulate Post-UTI Chronic Pain

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