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Acute Inflammatory Response via Neutrophil Activation Protects Against the Development of Chronic Pain

ABSTRACT: Acute Inflammatory Response via Neutrophil Activation Protects Against the Development of Chronic Pain

PROVIDER: PRJNA736882 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR14785700_1.fastq.gz	Fastqsanger.gz
	SRR14785700_2.fastq.gz	Fastqsanger.gz
	SRR14785800_1.fastq.gz	Fastqsanger.gz
	SRR14785800_2.fastq.gz	Fastqsanger.gz
	SRR14785701_1.fastq.gz	Fastqsanger.gz

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Acute Inflammatory Response via Neutrophil Activation Protects Against the Development of Chronic Pain

Project description:We used transcriptome-wide data to investigate the molecular pathophysiological mechanisms in peripheral blood immune cells at the transcriptome-wide level that underlie the transition of acute to chronic low back pain.

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Acute inflammatory response via neutrophil activation protects against the development of chronic pain.

Project description:The transition from acute to chronic pain is critically important but not well understood. Here, we investigated the pathophysiological mechanisms underlying the transition from acute to chronic low back pain (LBP) and performed transcriptome-wide analysis in peripheral immune cells of 98 participants with acute LBP, followed for 3 months. Transcriptomic changes were compared between patients whose LBP was resolved at 3 months with those whose LBP persisted. We found thousands of dynamic transcriptional changes over 3 months in LBP participants with resolved pain but none in those with persistent pain. Transient neutrophil-driven up-regulation of inflammatory responses was protective against the transition to chronic pain. In mouse pain assays, early treatment with a steroid or nonsteroidal anti-inflammatory drug (NSAID) also led to prolonged pain despite being analgesic in the short term; such a prolongation was not observed with other analgesics. Depletion of neutrophils delayed resolution of pain in mice, whereas peripheral injection of neutrophils themselves, or S100A8/A9 proteins normally released by neutrophils, prevented the development of long-lasting pain induced by an anti-inflammatory drug. Analysis of pain trajectories of human subjects reporting acute back pain in the UK Biobank identified elevated risk of pain persistence for subjects taking NSAIDs. Thus, despite analgesic efficacy at early time points, the management of acute inflammation may be counterproductive for long-term outcomes of LBP sufferers.

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Gastrodin protects against chronic inflammatory pain by inhibiting spinal synaptic potentiation.

Project description:Tissue injury is known to produce inflammation and pain. Synaptic potentiation between peripheral nociceptors and spinal lamina I neurons has been proposed to serve as a trigger for chronic inflammatory pain. Gastrodin is a main bioactive constituent of the traditional Chinese herbal medicine Gastrodia elata Blume, which has been widely used as an analgesic since ancient times. However, its underlying cellular mechanisms have remained elusive. The present study demonstrated for the first time that gastrodin exhibits an analgesic effect at the spinal level on spontaneous pain, mechanical and thermal pain hypersensitivity induced by peripheral inflammation, which is not dependent on opioid receptors and without tolerance. This analgesia by gastrodin is at least in part mediated by depressing spinal synaptic potentiation via blockade of acid-sensing ion channels. Further studies with miniature EPSCs and paired-pulse ratio analysis revealed the presynaptic origin of the action of gastrodin, which involves a decrease in transmitter release probability. In contrast, neither basal nociception nor basal synaptic transmission was altered. This study revealed a dramatic analgesic action of gastrodin on inflammatory pain and uncovered a novel spinal mechanism that could underlie the analgesia by gastrodin, pointing the way to a new analgesic for treating chronic inflammatory pain.

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VSL#3 protects against development of visceral pain in the neonatal maternal separation model: A whole genome microarray study

Project description:Background & Aims: Irritable bowel syndrome (IBS) is a disorder characterized by chronic abdominal pain and is linked to post-inflammatory and stress-correlated factors that cause changes in the perception of visceral events. Increased evidence indicates that probiotic bacteria may be useful in treating IBS. Our aims were to evaluate the efficacy of treatment with VSL#3, a mixture of 8 probiotic bacteria strains, in the neonatal maternal separation (NMS)-induced visceral hypersensitivity rat model and to determine whether it modulates the colonic expression of pain-related genes. Methods: Male NMS pups were treated orally with placebo or VSL#3 at days 3-60, while normal, not separated rats were used as control. After 60 days from birth, perception of painful sensation induced by colorectal distension (CRD) was measured by assessing the abdominal withdrawal reflex (score 0-4). The colonic gene expression analysis was assessed by using Agilent Whole Rat Genome Oligo Microarrays. Results: NMS rats exhibited both hyperalgesia and allodynia when compared with controls. VSL#3 showed a potent analgesic effect on CRD-induced pain without modifying colorectal compliance. The microarray analysis demonstrated that NMS rats had both over- and downregulation of several genes involved in inflammatory and painful processes and VSL#3 was able to counteract these alterations. Conclusions: This study indicates that VSL#3 is effective in reducing visceral pain in an experimental model of IBS by induction or suppression of pain-modulating genes. These observations provide support for the use of VSL#3 in the treatment of painful conditions related to IBS. The dataset comprises 12 samples divided into three sample groups each representing a certain treatment condition of male rats.

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The expression profiling of the anterior cingulate cortex and hippocampus in chronic inflammatory pain mice

Project description:Chronic pain is a persistent unpleasant sensation that produces pathological synaptic plasticity in the central nervous system. Some of the studies demonstrate that the anterior cingulate cortex (ACC) is a critical area for nociceptive and chronic pain processing. Our previous study revealed that animal models of chronic pain alter excitatory and inhibitory synaptic transmission in the ACC. However, it is not clear what molecules are involved in the alterations of synaptic plasticity in the ACC of chronic pain models. To identify genes with altered expression in the ACC of a chronic pain model, whole transcriptome analysis were performed. In addition to the ACC, whole transcriptome analysis was also performed in the hippocampus, a brain region that has not been reported to be associated with chronic pain. Complete freund's adjuvant (CFA, Sigma-Aldrich, #F5881) into the left hind paw was used for induce chronic inflammatory pain in this study.

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