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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

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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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APOE Protects Against Severe Infection with Mycobacterium tuberculosis by Restraining Production of Neutrophil Extracellular Traps

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Project description:Background. Inter- and intra-individual fluctuations in pain intensity pose a major challenge to treatment efficacy, with a majority perceiving their pain relief as inadequate. Recent preclinical studies have identified circadian rhythmicity as a potential contributor to these fluctuations and therapeutic target. Methods. We therefore sought to determine the impact of these rhythms in people with chronic low back pain (CLBP) through a detailed characterization, including questionnaires to evaluate biopsychosocial characteristics, ecological momentary assessment (7-day e-diaries at 8:00/14:00/20:00) to assess pain fluctuations, and intra-day blood transcriptomics (8:00/20:00) to identify genes/pathways of interest. Results. While most individuals displayed constant or variable/mixed pain phenotypes, a distinct subset had daily fluctuations of increasing pain scores (>30% change in intensity over 12-hours in ≥4/7 days). This population had no opioid users, better biopsychosocial profiles, and differentially expressed transcripts relative to other pain phenotypes. The circadian-governed neutrophil degranulation pathway was particularly enriched among arhythmic individuals; the link between neutrophil degranulation and opioid use was further confirmed in a separate CLBP cohort. Conclusion. Our findings identify pain rhythmicity and the circadian expression of neutrophil degranulation pathways as indicators of CLBP outcomes, which may help provide a personalized approach to phenotyping biopsychosocial characteristics and medication use. This highlights the need to better understand the impact of circadian rhythmicity across chronic pain conditions.

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