@Article{ecn.2017.0392,
AUTHOR = {Juan Sun, Wei Guo, Xingguang Du},
TITLE = {Buprenorphine differentially affects M1- and M2-polarized macrophages from human umbilical cord blood},
JOURNAL = {European Cytokine Network},
VOLUME = {28},
YEAR = {2017},
NUMBER = {2},
PAGES = {85--92},
URL = {http://www.techscience.com/ECN/v28n2/65522},
ISSN = {1952-4005},
ABSTRACT = {Background: As a partial μ-opioid receptor agonist with long half-life time, buprenorphine has been
widely used to relieve chronic cancer and nonmalignant pain. The maintenance of chronic pain involves inflammation;
however whether buprenorphine has anti-inflammation property remains unclear. Methods: Macrophages,
the immune cells that initiate and maintain inflammation, were isolated from human umbilical cord blood, and were
polarized into M1 or M2 macrophages with IFN-γ in the presence of lipopolysaccharide (LPS) or IL-4, respectively.
Quantitative PCR, ELISA, Western blotting analysis, and chromatin immunoprecipitation assays were employed to
characterize M1 and M2 macrophages. Results: 1) Buprenorphine did not change not only the apoptosis, survival,
and morphology of resting macrophages, but also the antigen-presenting function of macrophages. 2) Buprenorphine
inhibited the levels of mRNA and protein of several cytokines in M1 macrophages, and enhanced the expression of
Ym1 and Fizz1 in M2 macrophages. 3) Buprenorphine did not affect the modulation of NF-κB and MAPK cascades
by LPS in M1 macrophages. 4) Buprenorphine inhibited the expression of IRF5 and reduced binding of DNA to
IRF5. Conclusion: Buprenorphine may downregulate IRF5 pathway and limit M1 macrophage phenotype. These
effects may contribute to its therapeutic benefit for chronic neuropathic pain.},
DOI = {10.1684/ecn.2017.0392}
}