Circadian control of innate immunity in macrophages by miR-155 targeting Bmal1.

CURTIS, ANNIE; O'NEILL, LUKE; HOKAMP, KARSTEN

doi:http://dx.doi.org/10.1073/pnas.1501327112

Circadian control of innate immunity in macrophages by miR-155 targeting Bmal1.

Files

pnas.201501327.pdf (932.57 KB)

Date

2015

Authors

CURTIS, ANNIE

O'NEILL, LUKE

HOKAMP, KARSTEN

Access

openAccess

Citation

Curtis AM, Fagundes CT, Yang G, Palsson-McDermott EM, Wochal P, McGettrick AF, Foley NH, Early JO, Chen L, Zhang H, Xue C, Geiger SS, Hokamp K, Reilly MP, Coogan AN, Vigorito E, FitzGerald GA, O'Neill LA, Circadian control of innate immunity in macrophages by miR-155 targeting Bmal1., Proceedings of the National Academy of Sciences of the United States of America, 112, 23, 2015, 7231-6

Abstract

The circadian clock allows an organism to anticipate daily changes imposed by the environment. The response to LPS is altered depending on time of day; however, the molecular mechanisms underlying this are unclear. We find that the clock in myeloid cells plays a role in LPS-induced sepsis by altering NF-κB activity and the induction of the microRNA miR-155. LPS causes the repression of BMAL1 via the targeting of miR-155 to two seed sequences in the 3′-untranslated region of Bmal1. Lack of miR-155 has profound effects on circadian function and circadian induction of cytokines by LPS. Thus, the molecular clock is using miR-155 as an important regulatory component to control inflammation variably across the circadian day in myeloid cells