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The combination of these proinflammatory factors reflects a devastating problem as opioids have high abuse liability and continue to be prescribed for certain patients experiencing HIV-1-related pain. \nMETHODS: Here, we examined the impact of chronic (3-month) HIV-1 transactivator of transcription (Tat) exposure to short-term (8-day), escalating morphine in HIV-1 Tat transgenic mice that express the HIV-1 Tat protein in a GFAP promoter-regulated, doxycycline (DOX)-inducible manner. In addition to assessing morphine-induced tolerance in nociceptive responses organized at spinal (i.e., tail-flick) and supraspinal (i.e., hot-plate) levels, we evaluated neuroinflammation via positron emission tomography (PET) imaging using the [¹⁸F]-PBR111 ligand, immunohistochemistry, and cytokine analyses. Further, we examined endocannabinoid (eCB) levels, related non-eCB lipids, and amino acids via mass spectrometry. \nRESULTS: Tat-expressing [Tat(+)] transgenic mice displayed antinociceptive tolerance in the tail withdrawal and hot-plate assays compared to control mice lacking Tat [Tat(-)]. This tolerance was accompanied by morphine-dependent increases in Iba-1 +/- 3-nitrotryosine immunoreactive microglia, and alterations in pro- and anti-inflammatory cytokines, and chemokines in the spinal cord and striatum, while increases in neuroinflammation were absent by PET imaging of [¹⁸F]-PBR111 uptake. Tat and morphine exposure differentially affected eCB levels, non-eCB lipids, and specific amino acids in a region-dependent manner. In the striatum, non-eCB lipids were significantly increased by short-term, escalating morphine exposure, including peroxisome proliferator activator receptor alpha (PPAR-alpha) ligands N-oleoyl ethanolamide (OEA) and N-palmitoyl ethanolamide (PEA), as well as the amino acids phenylalanine and proline. In the spinal cord, Tat exposure increased amino acids leucine and valine, while morphine decreased levels of tyrosine and valine but did not affect eCBs or non-eCB lipids. \nCONCLUSION: Overall results demonstrate that 3 months of Tat exposure increased morphine tolerance and potentially innate immune tolerance evidenced by reductions in specific cytokines (e.g., IL-1alpha, IL-12p40) and microglial reactivity. 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Escalating morphine dosing in HIV-1 Tat transgenic mice with sustained Tat exposure reveals an allostatic shift in neuroinflammatory regulation accompanied by increased neuroprotective non-endocannabinoid lipid signaling molecules and amino acids
https://oist.repo.nii.ac.jp/records/1841
https://oist.repo.nii.ac.jp/records/18418b9dc3c6-4855-4d81-8c24-6710759a45b2
名前 / ファイル | ライセンス | アクション |
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Hermes-2020-Escalating morphine dosing in HIV- (6.1 MB)
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Creative Commons Attribution 4.0 International(https://creativecommons.org/licenses/by/4.0/)
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Item type | 学術雑誌論文 / Journal Article(1) | |||||
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公開日 | 2020-12-09 | |||||
タイトル | ||||||
言語 | en | |||||
タイトル | Escalating morphine dosing in HIV-1 Tat transgenic mice with sustained Tat exposure reveals an allostatic shift in neuroinflammatory regulation accompanied by increased neuroprotective non-endocannabinoid lipid signaling molecules and amino acids | |||||
言語 | ||||||
言語 | eng | |||||
キーワード | ||||||
言語 | en | |||||
主題Scheme | Other | |||||
主題 | Opioid drug abuse | |||||
キーワード | ||||||
言語 | en | |||||
主題Scheme | Other | |||||
主題 | [¹⁸F]-PBR111 PET imaging | |||||
キーワード | ||||||
言語 | en | |||||
主題Scheme | Other | |||||
主題 | Endocannabinoids | |||||
キーワード | ||||||
言語 | en | |||||
主題Scheme | Other | |||||
主題 | Peroxisome proliferator activator receptor α (PPAR-α) agonists | |||||
キーワード | ||||||
言語 | en | |||||
主題Scheme | Other | |||||
主題 | Microgliosis | |||||
キーワード | ||||||
言語 | en | |||||
主題Scheme | Other | |||||
主題 | Cytokines | |||||
キーワード | ||||||
言語 | en | |||||
主題Scheme | Other | |||||
主題 | Chemokines | |||||
キーワード | ||||||
言語 | en | |||||
主題Scheme | Other | |||||
主題 | Anti-inflammation | |||||
キーワード | ||||||
言語 | en | |||||
主題Scheme | Other | |||||
主題 | Proinflammation | |||||
キーワード | ||||||
言語 | en | |||||
主題Scheme | Other | |||||
主題 | Phenylalanine | |||||
キーワード | ||||||
言語 | en | |||||
主題Scheme | Other | |||||
主題 | Aliphatic side-chain amino acids | |||||
資源タイプ | ||||||
資源タイプ識別子 | http://purl.org/coar/resource_type/c_6501 | |||||
資源タイプ | journal article | |||||
著者(英) |
Hermes, Douglas J.
× Hermes, Douglas J.× Jacobs, Ian R.× Key, Megan C.× League, Alexis F.× Yadav-Samudrala, Barkha J.× Xu, Changqing× McLane, Virginia D.× Nass, Sara R.× Jiang, Wei× Meeker, Rick B.× Ignatowska-Jankowska, Bogna M.× Lichtman, Aron H.× Li, Zibo× Wu, Zhanhong× Yuan, Hong× Knapp, Pamela E.× Hauser, Kurt F.× Fitting, Sylvia |
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書誌情報 |
en : Journal of Neuroinflammation 巻 17, 号 1, p. 345, 発行日 2020-11-18 |
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抄録 | ||||||
内容記述タイプ | Other | |||||
内容記述 | BACKGROUND: Human immunodeficiency virus type-1 (HIV-1) and opiates cause long-term inflammatory insult to the central nervous system (CNS) and worsen disease progression and HIV-1-related neuropathology. The combination of these proinflammatory factors reflects a devastating problem as opioids have high abuse liability and continue to be prescribed for certain patients experiencing HIV-1-related pain. METHODS: Here, we examined the impact of chronic (3-month) HIV-1 transactivator of transcription (Tat) exposure to short-term (8-day), escalating morphine in HIV-1 Tat transgenic mice that express the HIV-1 Tat protein in a GFAP promoter-regulated, doxycycline (DOX)-inducible manner. In addition to assessing morphine-induced tolerance in nociceptive responses organized at spinal (i.e., tail-flick) and supraspinal (i.e., hot-plate) levels, we evaluated neuroinflammation via positron emission tomography (PET) imaging using the [¹⁸F]-PBR111 ligand, immunohistochemistry, and cytokine analyses. Further, we examined endocannabinoid (eCB) levels, related non-eCB lipids, and amino acids via mass spectrometry. RESULTS: Tat-expressing [Tat(+)] transgenic mice displayed antinociceptive tolerance in the tail withdrawal and hot-plate assays compared to control mice lacking Tat [Tat(-)]. This tolerance was accompanied by morphine-dependent increases in Iba-1 +/- 3-nitrotryosine immunoreactive microglia, and alterations in pro- and anti-inflammatory cytokines, and chemokines in the spinal cord and striatum, while increases in neuroinflammation were absent by PET imaging of [¹⁸F]-PBR111 uptake. Tat and morphine exposure differentially affected eCB levels, non-eCB lipids, and specific amino acids in a region-dependent manner. In the striatum, non-eCB lipids were significantly increased by short-term, escalating morphine exposure, including peroxisome proliferator activator receptor alpha (PPAR-alpha) ligands N-oleoyl ethanolamide (OEA) and N-palmitoyl ethanolamide (PEA), as well as the amino acids phenylalanine and proline. In the spinal cord, Tat exposure increased amino acids leucine and valine, while morphine decreased levels of tyrosine and valine but did not affect eCBs or non-eCB lipids. CONCLUSION: Overall results demonstrate that 3 months of Tat exposure increased morphine tolerance and potentially innate immune tolerance evidenced by reductions in specific cytokines (e.g., IL-1alpha, IL-12p40) and microglial reactivity. In contrast, short-term, escalating morphine exposure acted as a secondary stressor revealing an allostatic shift in CNS baseline inflammatory responsiveness from sustained Tat exposure. |
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出版者 | ||||||
出版者 | BMC Part of Springer Nature | |||||
ISSN | ||||||
収録物識別子タイプ | ISSN | |||||
収録物識別子 | 1742-2094 | |||||
PubMed番号 | ||||||
関連タイプ | isIdenticalTo | |||||
識別子タイプ | PMID | |||||
関連識別子 | info:pmid/33208151 | |||||
DOI | ||||||
関連タイプ | isIdenticalTo | |||||
識別子タイプ | DOI | |||||
関連識別子 | info:doi/10.1186/s12974-020-01971-6 | |||||
権利 | ||||||
権利情報 | © 2020 The Author(s). | |||||
関連サイト | ||||||
識別子タイプ | URI | |||||
関連識別子 | https://jneuroinflammation.biomedcentral.com/articles/10.1186/s12974-020-01971-6 | |||||
著者版フラグ | ||||||
出版タイプ | VoR | |||||
出版タイプResource | http://purl.org/coar/version/c_970fb48d4fbd8a85 |