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Intravascular danger signals guide neutrophils to sites of sterile inflammation

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Tags: etiology, classics, inflammation, biology, chronic pain, arthritis, tendinosis, pro, pain problems, aging, overuse injury, injury

Three articles on PainSci cite McDonald 2010: (576) 34 Surprising Causes of Pain(577) Tissue Provocation Therapies

PainSci summary of 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 at the bottom of the page, as often as 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!

~ Paul Ingraham

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.

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