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The Clock Gene Bmal1 Inhibits Macrophage Motility, Phagocytosis, and Impairs Defense Against Pneumonia

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The Clock Gene Bmal1 Inhibits Macrophage Motility, Phagocytosis, and Impairs Defense Against Pneumonia The clock gene Bmal1 inhibits macrophage motility, phagocytosis, and impairs defense against pneumonia Gareth B. Kitchena,b, Peter S. Cunninghama, Toryn M. Poolmanc,d, Mudassar Iqbala, Robert Maidstonec,d, Matthew Baxterc,d, James Bagnalla, Nicola Begleya, Ben Saera, Tracy Hussella, Laura C. Matthewse, David H. Dockrellf, Hannah J. Durringtona,b, Julie E. Gibbsa, John F. Blaikleya,b,1, Andrew S. Loudona,1, and David W. Rayc,d,1 aFaculty of Biology, Medicine, and Health, Manchester Academic Health Sciences Centre, University of Manchester, M13 9PT Manchester, United Kingdom; bManchester Foundation Trust, Manchester Academic Health Science Centre, M13 9WL Manchester, United Kingdom; cNational Institute for Health Research, John Radcliffe Hospital, Oxford Biomedical Research Centre, OX3 9DU Oxford, United Kingdom; dOxford Centre for Diabetes, Endocrinology and Metabolism, University of Oxford, OX37LE Oxford, United Kingdom; eLeeds Institute of Cancer and Pathology, Faculty of Medicine and Health, University of Leeds, LS9 7TF Leeds, United Kingdom; and fDepartment of Infection Medicine and Medical Research Council Centre for Inflammation Research, University of Edinburgh, EH16 4TJ Edinburgh, United Kingdom Edited by Joseph S. Takahashi, University of Texas Southwestern Medical Center, Dallas, TX, and approved December 12, 2019 (received for review September 18, 2019) The circadian clock regulates many aspects of immunity. Bacterial to regulate many aspects of physiology, including energy metab- infections are affected by time of day, but the mechanisms involved olism and immunity (6). remain undefined. Here we show that loss of the core clock protein Many cells of the innate immune system have intrinsic clocks, BMAL1 in macrophages confers protection against pneumococcal including monocytes, macrophages, neutrophils, mast cells, pneumonia. Infected mice show both reduced weight loss and eosinophils, and natural killer cells (2, 7–13). These cell-autonomous lower bacterial burden in circulating blood. In vivo studies of rhythms drive aspects of differentiated cell function, including macrophage phagocytosis reveal increased bacterial ingestion fol- cytokine production, trafficking, and phagocytosis. Within myeloid −/− lowing Bmal1 deletion, which was also seen in vitro. BMAL1 cells the core circadian gene Bmal1 exerts a broad antiinflam- macrophages exhibited marked differences in actin cytoskeletal or- matory effect, mediated to a large extent through its transcrip- ganization, a phosphoproteome enriched for cytoskeletal changes, tional regulation of Reverbα,andReverbß (3, 14, 15). Additional with reduced phosphocofilin and increased active RhoA. Further direct Bmal1 effects in macrophages have also been identified (16, CELL BIOLOGY −/− analysis of the BMAL1 macrophages identified altered cell mor- 17). For instance, specific bacterial infections show a time-of-day phology and increased motility. Mechanistically, BMAL1 regulated a dependence in outcome, including enteric Salmonella typhimurium network of cell movement genes, 148 of which were within 100 kb (18) and Streptococcus pneumoniae (5). of high-confidence BMAL1 binding sites. Links to RhoA function Infectious diseases are responsible for many deaths both in the were identified, with 29 genes impacting RhoA expression or acti- developed and developing world and, in the case of pneumonia, vation. RhoA inhibition restored the phagocytic phenotype to that are responsible for 5% of all deaths in the United Kingdom (19). seen in control macrophages. In summary, we identify a surprising The emergence of multidrug-resistant bacteria makes it essential gain of antibacterial function due to loss of BMAL1 in macrophages, associated with a RhoA-dependent cytoskeletal change, an increase in cell motility, and gain of phagocytic function. Significance circadian | Streptococcus pneumoniae | phagocytosis | The circadian clock extensively regulates physiology, with an actin cytoskeleton | RhoA emerging role in immunity. Bacterial infection development, progression, and resolution depend on the time of day, but through an unknown mechanism. Here, we show that time of he regular 24-h environmental cycle generated by the planet’s day regulates macrophage phagocytosis, and that the core clock rotation has led to the evolution of circadian rhythms in T protein BMAL1 is responsible. BMAL1 regulates RhoA-dependent virtually all life forms on Earth. These are driven by autonomous macrophage motility and bacterial engulfment, and loss of cellular biological clocks, which coordinate physiology and be- BMAL1 enhances antibacterial immunity. We identify a genetic havior over the day–night cycle. In mammals, many physiological circuit linking BMAL1 binding to motility, cytoskeletal gene ex- systems are regulated in a time-of-day–dependent manner. In- pression, and RhoA activation. With the rise in antimicrobial re- cluded in this, mammalian immunity is strongly regulated by the sistance, finding new ways to enhance immunity, by targeting circadian clockwork, driving the magnitude and nature of both clock components, offers new therapeutic opportunities. innate and acquired responses (1). Macrophages, in particular, have a strong endogenous circadian clock, which drives inflam- Author contributions: G.B.K., T.H., L.C.M., D.H.D., H.J.D., J.F.B., A.S.L., and D.W.R. de- matory function (2–4). We have previously identified a role for signed research; G.B.K., P.S.C., T.M.P., M.B., J.B., N.B., B.S., and J.F.B. performed research; the circadian clock in regulation of time-of-day variation in J.E.G., J.F.B., A.S.L., and D.W.R. contributed new reagents/analytic tools; G.B.K., T.M.P., outcomes following pneumococcal infection (5), but the mech- M.I., R.M., J.B., J.F.B., and D.W.R. analyzed data; and G.B.K., M.I., D.H.D., H.J.D., J.E.G., J.F.B., A.S.L., and D.W.R. wrote the paper. anisms responsible remain unknown. The core cellular circadian pacemaker in mammals, oscillates The authors declare no competing interest. with a 24-h period, and consists of a positive arm, comprising This article is a PNAS Direct Submission. BMAL1/CLOCK heterodimeric transcription factors, which drive This open access article is distributed under Creative Commons Attribution License 4.0 transcription of the repressor genes period and cryptochrome.As (CC BY). PERIOD and CRYPTOCHROME proteins accumulate, they Data deposition: RNA-Seq data that support the findings of this study have been deposited in ArrayExpress, https://www.ebi.ac.uk/arrayexpress/ (accession code then inhibit BMAL1/CLOCK transactivation function. In addi- E-MTAB-8411). tion, BMAL1/CLOCK drive expression of a second repressor 1To whom correspondence may be addressed. Email: [email protected], circuit consisting of the orphan nuclear receptors REVERBα,and [email protected], or [email protected]. REVERBβ. These, in turn, repress Bmal1 gene expression. Beyond This article contains supporting information online at https://www.pnas.org/lookup/suppl/ the core circadian transcription–translation feedback loop the core doi:10.1073/pnas.1915932117/-/DCSupplemental. clock transcription factors act through clock-controlled genes First published January 3, 2020. www.pnas.org/cgi/doi/10.1073/pnas.1915932117 PNAS | January 21, 2020 | vol. 117 | no. 3 | 1543–1551 Downloaded by guest on September 27, 2021 that we gain a better understanding of the mechanisms behind A LysM-Bmal1-/- B CX3CR1-Bmal1-/- infection, to identify new therapeutic strategies. The role of Lung Blood Lung Blood circadian biology in bacterial pathogenesis has yet to be fully 10 10 10 10 * * * explored. This is important, as several compounds now exist 8 8 8 8 which can alter key circadian pathways as well as repress or ac- 6 6 6 6 centuate circadian amplitudes. One of the key pathways gov- 4 erning the pathogenicity of an organism is phagocytosis. Log CFUs 4 4 4 Phagocytosis is the process of ingestion of large particles by 2 2 2 2 cells, based on rearrangement of the actin microfilament cyto- 0 0 0 0 skeleton. Macrophages and neutrophils are typical cells that fulfill WT KO WT KO WT KO WT KO this function in mammals and are beneficial for host defense LysM-Bmal1-/- C2.0 Neutrophils6 AMs 20 IMs D Weight Loss against bacterial pathogens. Engulfment of the particle, through 6 * cell-surface receptors for immunoglobulins, or complement, acti- 100 1.5 vates small GTP binding proteins of the Rho family, with speci- 4 10 ficity of downstream coupling. As an example RhoA is activated 1.0 90 γ by the complement receptor, but not the Fc R receptor. In its 5 2 weight in % 0.5 active, GTP bound state, RhoA interacts with further downstream 80 effectors to drive F-actin reorganization. Previous work suggests Cells per mouse x 10 – 0 0 0 that ex vivo synchronized macrophages show time-of-day WT KO WT KO WT KO WT KO dependent changes in S. typhimurium phagocytosis and bacterial killing (20). However, the role of the circadian clock and its E F WT KO 3 components in regulating phagocytosis, and the impact this has on bacterial responses in vivo remains undefined. Here we identify a P significant gain in pneumococcal immunity resulting from loss of B 2 the core clock protein BMAL1 in macrophages. This was accom- S P panied by an increase in macrophage movement, and phagocytosis, 10 Log but not by a change in immune cell infiltration to the infected lung. The most striking change was protection from bacteraemia (ex- S 1 tension of the infection to the bloodstream). Further analysis P identified a gain in RhoA, and cofilin activity, accompanied by a N major reorganization in the actin cytoskeleton. This macrophage 0 Total = 248 genes gain-of-function phenotype was reversed by low concentrations of −5.0 −2.5 0.0 2.5 5.0 Log2 fold change (KO-WT) the specific RhoA inhibitor CT04. G MCP-1 IL-1b MIP-1a IL-10 IL-3 * * Results 6000 0.036 0.052 10000 0.054 80 0.036 0.053 100 8000 40 Bmal1 Deletion Increases Resistance to Pneumococcal Pneumonia.
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