NLRP2 Is Overexpressed in Spinal Astrocytes at the Peak of Mechanical Pain Sensitivity during Complete Freund Adjuvant-Induced Persistent Pain

Our earlier findings revealed that interleukin-1 receptor type-1 (IL-1R1) was overexpressed in spinal neurons, and IL-1R1-deficient mice showed significant attenuation of thermal and mechanical allodynia during the course of the Complete Freund adjuvant (CFA)-induced persistent pain model. In the pr...

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Autores principales:	László Ducza, Péter Szücs, Krisztina Hegedűs, Erzsébet Bakk, Andrea Gajtkó, Ildikó Wéber, Krisztina Holló
Formato:	article
Lenguaje:	EN
Publicado:	MDPI AG 2021
Materias:	interleukin-1β NLRP2 astrocyte persistent pain spinal cord CFA-induced pain Biology (General) QH301-705.5 Chemistry QD1-999
Acceso en línea:	https://doaj.org/article/0972b4475540444a9db62909573ac717
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spelling	oai:doaj.org-article:0972b4475540444a9db62909573ac7172021-11-11T16:52:56ZNLRP2 Is Overexpressed in Spinal Astrocytes at the Peak of Mechanical Pain Sensitivity during Complete Freund Adjuvant-Induced Persistent Pain10.3390/ijms2221114081422-00671661-6596https://doaj.org/article/0972b4475540444a9db62909573ac7172021-10-01T00:00:00Zhttps://www.mdpi.com/1422-0067/22/21/11408https://doaj.org/toc/1661-6596https://doaj.org/toc/1422-0067Our earlier findings revealed that interleukin-1 receptor type-1 (IL-1R1) was overexpressed in spinal neurons, and IL-1R1-deficient mice showed significant attenuation of thermal and mechanical allodynia during the course of the Complete Freund adjuvant (CFA)-induced persistent pain model. In the present study, we found that a ligand of IL-1R1, termed interleukin-1β (IL-1β), is also significantly overexpressed at the peak of mechanical pain sensitivity in the CFA-evoked pain model. Analysis of cellular distribution and modeling using IMARIS software showed that in the lumbar spinal dorsal horn, IL-1β is significantly elevated by astrocytic expression. Maturation of IL-1β to its active form is facilitated by the formation of the multiprotein complex called inflammasome; thus, we tested the expression of NOD-like receptor proteins (NLRPs) in astrocytes. At the peak of mechanical allodynia, we found expression of the NLRP2 inflammasome sensor and its significantly elevated co-localization with the GFAP astrocytic marker, while NLRP3 was moderately present and NLRP1 showed total segregation from the astrocytic profiles. Our results indicate that peripheral CFA injection induces NLRP2 inflammasome and IL-1β expression in spinal astrocytes. The release of mature IL-1β can contribute to the maintenance of persistent pain by acting on its neuronally expressed receptor, which can lead to altered neuronal excitability.László DuczaPéter SzücsKrisztina HegedűsErzsébet BakkAndrea GajtkóIldikó WéberKrisztina HollóMDPI AGarticleinterleukin-1βNLRP2astrocytepersistent painspinal cordCFA-induced painBiology (General)QH301-705.5ChemistryQD1-999ENInternational Journal of Molecular Sciences, Vol 22, Iss 11408, p 11408 (2021)
institution	DOAJ
collection	DOAJ
language	EN
topic	interleukin-1β NLRP2 astrocyte persistent pain spinal cord CFA-induced pain Biology (General) QH301-705.5 Chemistry QD1-999
spellingShingle	interleukin-1β NLRP2 astrocyte persistent pain spinal cord CFA-induced pain Biology (General) QH301-705.5 Chemistry QD1-999 László Ducza Péter Szücs Krisztina Hegedűs Erzsébet Bakk Andrea Gajtkó Ildikó Wéber Krisztina Holló NLRP2 Is Overexpressed in Spinal Astrocytes at the Peak of Mechanical Pain Sensitivity during Complete Freund Adjuvant-Induced Persistent Pain
description	Our earlier findings revealed that interleukin-1 receptor type-1 (IL-1R1) was overexpressed in spinal neurons, and IL-1R1-deficient mice showed significant attenuation of thermal and mechanical allodynia during the course of the Complete Freund adjuvant (CFA)-induced persistent pain model. In the present study, we found that a ligand of IL-1R1, termed interleukin-1β (IL-1β), is also significantly overexpressed at the peak of mechanical pain sensitivity in the CFA-evoked pain model. Analysis of cellular distribution and modeling using IMARIS software showed that in the lumbar spinal dorsal horn, IL-1β is significantly elevated by astrocytic expression. Maturation of IL-1β to its active form is facilitated by the formation of the multiprotein complex called inflammasome; thus, we tested the expression of NOD-like receptor proteins (NLRPs) in astrocytes. At the peak of mechanical allodynia, we found expression of the NLRP2 inflammasome sensor and its significantly elevated co-localization with the GFAP astrocytic marker, while NLRP3 was moderately present and NLRP1 showed total segregation from the astrocytic profiles. Our results indicate that peripheral CFA injection induces NLRP2 inflammasome and IL-1β expression in spinal astrocytes. The release of mature IL-1β can contribute to the maintenance of persistent pain by acting on its neuronally expressed receptor, which can lead to altered neuronal excitability.
format	article
author	László Ducza Péter Szücs Krisztina Hegedűs Erzsébet Bakk Andrea Gajtkó Ildikó Wéber Krisztina Holló
author_facet	László Ducza Péter Szücs Krisztina Hegedűs Erzsébet Bakk Andrea Gajtkó Ildikó Wéber Krisztina Holló
author_sort	László Ducza
title	NLRP2 Is Overexpressed in Spinal Astrocytes at the Peak of Mechanical Pain Sensitivity during Complete Freund Adjuvant-Induced Persistent Pain
title_short	NLRP2 Is Overexpressed in Spinal Astrocytes at the Peak of Mechanical Pain Sensitivity during Complete Freund Adjuvant-Induced Persistent Pain
title_full	NLRP2 Is Overexpressed in Spinal Astrocytes at the Peak of Mechanical Pain Sensitivity during Complete Freund Adjuvant-Induced Persistent Pain
title_fullStr	NLRP2 Is Overexpressed in Spinal Astrocytes at the Peak of Mechanical Pain Sensitivity during Complete Freund Adjuvant-Induced Persistent Pain
title_full_unstemmed	NLRP2 Is Overexpressed in Spinal Astrocytes at the Peak of Mechanical Pain Sensitivity during Complete Freund Adjuvant-Induced Persistent Pain
title_sort	nlrp2 is overexpressed in spinal astrocytes at the peak of mechanical pain sensitivity during complete freund adjuvant-induced persistent pain
publisher	MDPI AG
publishDate	2021
url	https://doaj.org/article/0972b4475540444a9db62909573ac717
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NLRP2 Is Overexpressed in Spinal Astrocytes at the Peak of Mechanical Pain Sensitivity during Complete Freund Adjuvant-Induced Persistent Pain

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