Intrathecal interleukin-1β administration induces thermal hyperalgesia by activating inducible nitric oxide synthase expression in the rat spinal cord

Sung, Chun-Sung; Wen, Zhi‐Hong; Chang, Wen-Kuei; Ho, Shung‐Tai; Tsai, Shih-Tzer; Chang, Yu‐Chan; Wong, Chih‐Shung

doi:10.1016/j.brainres.2004.04.068

Cited by 129 publications

(85 citation statements)

References 45 publications

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“…These factors are known to be involved in the sensitization of sensory nerves and contribute to the development of postinflammatory pain (8,(11)(12)(13)15). The results presented in this article also complement studies in which P2X 7 R deletion or pharmacological blockade reduced the development of hyperalgesia in models of inflammatory and neuropathic pain in response to P2X 7 R-mediated IL-1b release (21,29,30).…”

Section: Discussionsupporting

confidence: 70%

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P2X7 Receptor-Dependent Intestinal Afferent Hypersensitivity in a Mouse Model of Postinfectious Irritable Bowel Syndrome

Keating

Pelegrı́n²,

Martínez³

et al. 2011

The Journal of Immunology

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The ATP-gated P2X7 receptor (P2X7R) was shown to be an important mediator of inflammation and inflammatory pain through its regulation of IL-1β processing and release. Trichinella spiralis-infected mice develop a postinflammatory visceral hypersensitivity that is reminiscent of the clinical features associated with postinfectious irritable bowel syndrome. In this study, we used P2X7R knockout mice (P2X7R−/−) to investigate the role of P2X7R activation in the in vivo production of IL-1β and the development of postinflammatory visceral hypersensitivity in the T. spiralis-infected mouse. During acute nematode infection, IL-1β–containing cells and P2X7R expression were increased in the jejunum of wild-type (WT) mice. Peritoneal and serum IL-1β levels were also increased, which was indicative of elevated IL-1β release. However, in the P2X7R−/− animals, we found that infection had no effect upon intracellular, plasma, or peritoneal IL-1β levels. Conversely, infection augmented peritoneal TNF-α levels in both WT and P2X7R−/− animals. Infection was also associated with a P2X7R-dependent increase in extracellular peritoneal lactate dehydrogenase, and it triggered immunological changes in both strains. Jejunal afferent fiber mechanosensitivity was assessed in uninfected and postinfected WT and P2X7R−/− animals. Postinfected WT animals developed an augmented afferent fiber response to mechanical stimuli; however, this did not develop in postinfected P2X7R−/− animals. Therefore, our results demonstrated that P2X7Rs play a pivotal role in intestinal inflammation and are a trigger for the development of visceral hypersensitivity.

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Section: Discussionsupporting

confidence: 70%

“…IL-1b is pronociceptive; treatment of mice with IL-1b mediated thermal and mechanical hyperalgesia (11,12), whereas intrathecal injections of IL-1b increased the release of excitatory neurotransmitters (13). Furthermore, pharmacological blockade of IL-1b attenuated the hyperalgesia associated with microglial activation (14).…”

mentioning

confidence: 99%

P2X7 Receptor-Dependent Intestinal Afferent Hypersensitivity in a Mouse Model of Postinfectious Irritable Bowel Syndrome

Keating

Pelegrı́n²,

Martínez³

et al. 2011

The Journal of Immunology

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“…A ligação da IL1β ao receptor IL1-RI inicia uma série de eventos intracelulares, ativando fatores transcricionais, induzindo a expressão de COX-2, óxido nítrico sintetase e IL1β, a IL-6 e o TNF. Assim, a IL1β exerce ação direta e indireta nos nociceptores 48 e há aumento da síntese de IL1β na lesão de nervo periférico 49 , de modo que em camundongos há alívio da dor neuropática com empregos de anticorpos para o receptor de IL-1. A IL-6 é sintetizada pelos mastócitos, monócitos, linfócitos, neurônios e células da glia.…”

Section: Citocinasunclassified

“…O óxido nítrico, por sua vez, possui as formas endotelial e neuronal que são constitutivas, enquanto a induzida se expressa nas células do sistema imune. O óxido nítrico provoca hiperalgesia após injeção na pele e articulações 62 e está implicado na sensibilização central 48 , fortalecendo a ação da PG 2 em modelos de dor neuropática 63 .…”

Section: óXido Nítrico E Radicais Superóxidounclassified

“…Binding of IL1β to the IL1-RI receptor triggers a series of intracellular events activating transcriptional factors, inducing the expression of COX-2, nitric oxide synthase, IL1β, IL-6, and TNFα. Thus, IL1β affects nociceptors direct and indirectly 48 , in nerve damage its production is increased in peripheral nerves 49 , and in mice the administration of antibodies for the IL-1 receptor alleviates neuropathic pain. Interleukin-6 is synthesized by mast cells, monocytes, lymphocytes, neurons, and glia.…”

Section: Cytokinesmentioning

confidence: 99%

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Dor neuropática: aspectos neuroquímicos

Kraychete¹,

Gozzani²,

Kraychete³

2008

Rev. Bras. Anestesiol.

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Rev Bras AnestesiolARTIGO DE REVISÃO 2008; 58: 5: 492-505 REVIEW ARTICLE RESUMO Kraychete DC, Gozzani JL, Kraychete AC -Dor Neuropática -Aspectos Neuroquímicos. JUSTIFICATIVA E OBJETIVOS:A dor neuropática é causada por lesão ou inflamação do sistema nervoso. É síndrome complexa, com mecanismos biológicos pouco esclarecidos, envolvendo teorias inflamatórias e imunes. O objetivo desta revisão foi descrever os principais fatores biológicos relacionados com a dor neuropática, associando de forma lógica as hipóteses sugeridas pela literatura. CONTEÚDO:Foram descritos os principais neuromediadores, canais iônicos e células, incluindo as do sistema imune envolvidos na excitabilidade neuronal, assim como enfatizada possível seqüência de ativação ou interação desses agentes na alteração neuroplástica decorrente da agressão ao nervo.CONCLUSÕES: Do estudo, foi possível concluir que os avanços no conhecimento da fisiopatologia da dor neuropática podem determinar novos alvos para abordagem farmacológica dessa síndrome.Unitermos: DOR: neuropática; FISIOLOGIA: neurotransmissores. SUMMARYKraychete DC, Gozzani JL, Kraychete AC -Neuropathic PainNeurochemical Aspects. BACKGROUND AND OBJECTIVES:Neuropathic pain is caused by damage or inflammation of the nervous system. It is a complex syndrome and its biological mechanisms, involving inflammatory and immunologic theories, are not clear. The objective of this review was to describe the main biologic factors associated with neuropathic pain, making a logical association between hypotheses suggested in the literature. CONTENTS:The main neuromediators, ion channels, and cells, including cells in the nervous system involved in neuronal excitation are described, and the possible activation sequence or interaction among those agents in the neoplastic change secondary to nerve damage are emphasized. CONCLUSIONS:It was possible to conclude that the advances on the knowledge of the pathophysiology of neuropathic pain can determine new pharmacologic approaches for this syndrome.

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NAMPT/NAD⁺/PARP1 Pathway Regulates CFA‐Induced Inflammatory Pain via NF‐κB Signaling in Rodents

Dai,

Lin,

Chen

et al. 2024

Advanced Biology

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Emerging evidence has implicated nicotinamide adenine dinucleotide (NAD+) metabolism in various inflammatory diseases. In the study, the role of NAD+ metabolism in Complete Freund's Adjuvant (CFA)‐evoked inflammatory pain and the underlying mechanisms are investigated. The study demonstrated that CFA induced upregulation of nicotinamide phosphoribosyltransferase (NAMPT) in dorsal root ganglia (DRG) without significant changes in the spinal cord. Inhibition of NAMPT expression by intrathecal injection of NAMPT siRNA alleviated CFA‐induced pain‐like behavior, decreased NAD+ contents in DRG, and lowered poly‐(ADP‐ribose) polymerase 1 (PARP1) activity levels. These effects are all reversed by the supplement of nicotinamide mononucleotide (NMN). Inhibition of PARP1 expression by intrathecal injection of PARP1 siRNA alleviated CFA‐induced pain‐like behavior, while elevated NAD+ levels of DRG. The analgesic effect of inhibiting NAMPT/NAD+/PARP1 axis can be attributed to the downregulation of the NF‐κB/IL‐1β inflammatory pathway. Double immunofluorescence staining showed that the expression of NAMPT/NAD+/PARP1 axis is restricted to DRG neurons. In conclusion, PARP1 activation in response to CFA stimulation, fueled by NAMPT‐derived NAD+, mediates CFA‐induced inflammatory pain through NF‐κB/IL‐1β inflammatory pathway.

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Intrathecal interleukin-1β administration induces thermal hyperalgesia by activating inducible nitric oxide synthase expression in the rat spinal cord

Cited by 129 publications

References 45 publications

P2X7 Receptor-Dependent Intestinal Afferent Hypersensitivity in a Mouse Model of Postinfectious Irritable Bowel Syndrome

P2X7 Receptor-Dependent Intestinal Afferent Hypersensitivity in a Mouse Model of Postinfectious Irritable Bowel Syndrome

Dor neuropática: aspectos neuroquímicos

NAMPT/NAD⁺/PARP1 Pathway Regulates CFA‐Induced Inflammatory Pain via NF‐κB Signaling in Rodents

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Intrathecal interleukin-1β administration induces thermal hyperalgesia by activating inducible nitric oxide synthase expression in the rat spinal cord

Cited by 129 publications

References 45 publications

P2X7 Receptor-Dependent Intestinal Afferent Hypersensitivity in a Mouse Model of Postinfectious Irritable Bowel Syndrome

P2X7 Receptor-Dependent Intestinal Afferent Hypersensitivity in a Mouse Model of Postinfectious Irritable Bowel Syndrome

Dor neuropática: aspectos neuroquímicos

NAMPT/NAD+/PARP1 Pathway Regulates CFA‐Induced Inflammatory Pain via NF‐κB Signaling in Rodents

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Resources

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NAMPT/NAD⁺/PARP1 Pathway Regulates CFA‐Induced Inflammatory Pain via NF‐κB Signaling in Rodents