Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
Comment
. 2019 Jan 17;133(3):190-191.
doi: 10.1182/blood-2018-11-886259.

Resolving inflammation and pain of sickle cell

Gabrielle Fredman  1
Affiliations
Comment

Resolving inflammation and pain of sickle cell

Gabrielle Fredman. Blood. .

Abstract

In this issue of Blood, Matte et al demonstrate that sickle cell disease (SCD) disrupts inflammation-resolution programs in a mouse model of SCD, giving evidence for an entirely new way to treat this disease.

PubMed Disclaimer

Conflict of interest statement

Conflict-of-interest disclosure: The author declares no competing financial interests.

Figures

None
SPM limits inflammation in SCD in mice, which has implications for pain control. (A) SCD is characterized by heighted inflammation involving leukocytes, platelets, and endothelial cells. Sickle RBCs can obstruct the vasculature, which can lead to organ damage and pain. (B) 17R-RvD1 decreases inflammation, reactive oxygen species (ROS), vaso-occlusion, and, ultimately, tissue damage. Inflammatory cytokines, and mediators like prostaglandins (which are elevated in SCD) are directly linked to pain. High levels of proinflammatory cytokines like interleukin 6 (IL-6) activate nociceptors to initiate pain. Importantly, 17R-RvD1 decreases NF-κB activation and IL-6 in SCD mice, which implies a mechanistic link for decreasing pain in SCD. PMN, polymorphonuclear neutrophil.
See this image and copyright information in PMC

Comment on

References

    1. Matte A, Recchiuti A, Federti E, et al. . Resolution of sickle cell disease–associated inflammation and tissue damage with 17R-resolvin D1. Blood. 2019;133(3):252-265. - PMC - PubMed
    1. Zhang D, Xu C, Manwani D, Frenette PS. Neutrophils, platelets, and inflammatory pathways at the nexus of sickle cell disease pathophysiology. Blood. 2016;127(7):801-809. - PMC - PubMed
    1. Serhan CN. Pro-resolving lipid mediators are leads for resolution physiology. Nature. 2014;510(7503):92-101. - PMC - PubMed
    1. Xu ZZ, Zhang L, Liu T, et al. Resolvins RvE1 and RvD1 attenuate inflammatory pain via central and peripheral actions. Nat Med. 2010;16(5):592-597. - PMC - PubMed
    1. Fredman G, Hellmann J, Proto JD, et al. . An imbalance between specialized pro-resolving lipid mediators and pro-inflammatory leukotrienes promotes instability of atherosclerotic plaques. Nat Commun. 2016;7(1):12859. - PMC - PubMed