Intravascular danger signals guide neutrophils to sites of sterile inflammation
Three articles on PainSci cite McDonald 2010: 1. 35 Surprising Causes of Pain 2. Tissue Provocation Therapies
PainSci commentary on McDonald 2010: ?This page is one of thousands in the PainScience.com bibliography. It is not a general article: it is focused on a single scientific paper, and it may provide only just enough context for the summary to make sense. Links to other papers and more general information are provided wherever possible.
Researchers at the University of Calgary Faculty of Medicine are using an innovative new imaging technique to study how white blood cells (called neutrophils) respond to inflammation, and have revealed new targets to inhibit the response. Basically this research explains why neutrophils unnecessarily “swarm” sterile injury sites, causing damage and pain with no direct benefit — a biological glitch with profound implications. Collateral damage!
original abstract †Abstracts here may not perfectly match originals, for a variety of technical and practical reasons. Some abstacts are truncated for my purposes here, if they are particularly long-winded and unhelpful. I occasionally add clarifying notes. And I make some minor corrections.
Neutrophils are recruited from the blood to sites of sterile inflammation, where they contribute to wound healing but may also cause tissue damage. By using spinning disk confocal intravital microscopy, we examined the kinetics and molecular mechanisms of neutrophil recruitment to sites of focal hepatic necrosis in vivo. Adenosine triphosphate released from necrotic cells activated the Nlrp3 inflammasome to generate an inflammatory microenvironment that alerted circulating neutrophils to adhere within liver sinusoids. Subsequently, generation of an intravascular chemokine gradient directed neutrophil migration through healthy tissue toward foci of damage. Lastly, formyl-peptide signals released from necrotic cells guided neutrophils through nonperfused sinusoids into the injury. Thus, dynamic in vivo imaging revealed a multistep hierarchy of directional cues that guide neutrophil localization to sites of sterile inflammation.
related content
Specifically regarding McDonald 2010:
- Why Does Pain Hurt? — How an evolutionary wrong turn led to a biological glitch that condemned the animal kingdom — you included — to much louder, longer pain
- “Images shed new light on inflammation,” Braedon McDonald and Paul Kubes, Faculty of Medicine (University of Calgary).
“Immune Collateral Damage: An interview with Paul Kubes” an audio recording from Quirks & Quarks (CBC Radio One).
This page is part of the PainScience BIBLIOGRAPHY, which contains plain language summaries of thousands of scientific papers & others sources. It’s like a highly specialized blog. A few highlights:
- Association of Lumbar MRI Findings with Current and Future Back Pain in a Population-based Cohort Study. Kasch 2022 Spine (Phila Pa 1976).
- A double-blinded randomised controlled study of the value of sequential intravenous and oral magnesium therapy in patients with chronic low back pain with a neuropathic component. Yousef 2013 Anaesthesia.
- Is Neck Posture Subgroup in Late Adolescence a Risk Factor for Persistent Neck Pain in Young Adults? A Prospective Study. Richards 2021 Phys Ther.
- Sudden amnesia resulting in pain relief: the relationship between memory and pain. Choi 2007 Pain.
- Photobiomodulation therapy is not better than placebo in patients with chronic nonspecific low back pain: a randomised placebo-controlled trial. Guimarães 2021 Pain.