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      The interaction of the circadian and immune system: Desynchrony as a pathological outcome to traumatic brain injury

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          Abstract

          Traumatic brain injury (TBI) is a complex and costly worldwide phenomenon that can lead to many negative health outcomes including disrupted circadian function. There is a bidirectional relationship between the immune system and the circadian system, with mammalian coordination of physiological activities being controlled by the primary circadian pacemaker in the suprachiasmatic nucleus (SCN) of the hypothalamus. The SCN receives light information from the external environment and in turn synchronizes rhythms throughout the brain and body. The SCN is capable of endogenous self-sustained oscillatory activity through an intricate clock gene negative feedback loop. Following TBI, the response of the immune system can become prolonged and pathophysiological. This detrimental response not only occurs in the brain, but also within the periphery, where a leaky blood brain barrier can permit further infiltration of immune and inflammatory factors. The prolonged and pathological immune response that follows TBI can have deleterious effects on clock gene cycling and circadian function not only in the SCN, but also in other rhythmic areas throughout the body. This could bring about a state of circadian desynchrony where different rhythmic structures are no longer working together to promote optimal physiological function. There are many parallels between the negative symptomology associated with circadian desynchrony and TBI. This review discusses the significant contributions of an immune-disrupted circadian system on the negative symptomology following TBI. The implications of TBI symptomology as a disorder of circadian desynchrony are discussed.

          Highlights

          • •

            The immune system and circadian system interact with each other.

          • •

            During traumatic brain injury there can be a prolonged immune response.

          • •

            This immune response alters circadian rhythms in the body and brain.

          • •

            The body and brain may become desynchronized bringing about negative symptoms.

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          Estimating the global incidence of traumatic brain injury

          Michael Dewan, Abbas Rattani, Saksham Gupta … (2018)
          Traumatic brain injury (TBI)—the “silent epidemic”—contributes to worldwide death and disability more than any other traumatic insult. Yet, TBI incidence and distribution across regions and socioeconomic divides remain unknown. In an effort to promote advocacy, understanding, and targeted intervention, the authors sought to quantify the case burden of TBI across World Health Organization (WHO) regions and World Bank (WB) income groups. Open-source epidemiological data on road traffic injuries (RTIs) were used to model the incidence of TBI using literature-derived ratios. First, a systematic review on the proportion of RTIs resulting in TBI was conducted, and a meta-analysis of study-derived proportions was performed. Next, a separate systematic review identified primary source studies describing mechanisms of injury contributing to TBI, and an additional meta-analysis yielded a proportion of TBI that is secondary to the mechanism of RTI. Then, the incidence of RTI as published by the Global Burden of Disease Study 2015 was applied to these two ratios to generate the incidence and estimated case volume of TBI for each WHO region and WB income group. Relevant articles and registries were identified via systematic review; study quality was higher in the high-income countries (HICs) than in the low- and middle-income countries (LMICs). Sixty-nine million (95% CI 64–74 million) individuals worldwide are estimated to sustain a TBI each year. The proportion of TBIs resulting from road traffic collisions was greatest in Africa and Southeast Asia (both 56%) and lowest in North America (25%). The incidence of RTI was similar in Southeast Asia (1.5% of the population per year) and Europe (1.2%). The overall incidence of TBI per 100,000 people was greatest in North America (1299 cases, 95% CI 650–1947) and Europe (1012 cases, 95% CI 911–1113) and least in Africa (801 cases, 95% CI 732–871) and the Eastern Mediterranean (897 cases, 95% CI 771–1023). The LMICs experience nearly 3 times more cases of TBI proportionally than HICs. Sixty-nine million (95% CI 64–74 million) individuals are estimated to suffer TBI from all causes each year, with the Southeast Asian and Western Pacific regions experiencing the greatest overall burden of disease. Head injury following road traffic collision is more common in LMICs, and the proportion of TBIs secondary to road traffic collision is likewise greatest in these countries. Meanwhile, the estimated incidence of TBI is highest in regions with higher-quality data, specifically in North America and Europe.
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            A circadian gene expression atlas in mammals: implications for biology and medicine.

            Ray Zhang, Nicholas Lahens, Heather I Ballance … (2014)
            To characterize the role of the circadian clock in mouse physiology and behavior, we used RNA-seq and DNA arrays to quantify the transcriptomes of 12 mouse organs over time. We found 43% of all protein coding genes showed circadian rhythms in transcription somewhere in the body, largely in an organ-specific manner. In most organs, we noticed the expression of many oscillating genes peaked during transcriptional "rush hours" preceding dawn and dusk. Looking at the genomic landscape of rhythmic genes, we saw that they clustered together, were longer, and had more spliceforms than nonoscillating genes. Systems-level analysis revealed intricate rhythmic orchestration of gene pathways throughout the body. We also found oscillations in the expression of more than 1,000 known and novel noncoding RNAs (ncRNAs). Supporting their potential role in mediating clock function, ncRNAs conserved between mouse and human showed rhythmic expression in similar proportions as protein coding genes. Importantly, we also found that the majority of best-selling drugs and World Health Organization essential medicines directly target the products of rhythmic genes. Many of these drugs have short half-lives and may benefit from timed dosage. In sum, this study highlights critical, systemic, and surprising roles of the mammalian circadian clock and provides a blueprint for advancement in chronotherapy.
            Article 0 comments Cited 519 times – based on 0 reviews     Review now
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              Dynamic mapping of human cortical development during childhood through early adulthood.

              Nitin Gogtay, Jay Giedd, Leslie Lusk … (2004)
              We report the dynamic anatomical sequence of human cortical gray matter development between the age of 4-21 years using quantitative four-dimensional maps and time-lapse sequences. Thirteen healthy children for whom anatomic brain MRI scans were obtained every 2 years, for 8-10 years, were studied. By using models of the cortical surface and sulcal landmarks and a statistical model for gray matter density, human cortical development could be visualized across the age range in a spatiotemporally detailed time-lapse sequence. The resulting time-lapse "movies" reveal that (i) higher-order association cortices mature only after lower-order somatosensory and visual cortices, the functions of which they integrate, are developed, and (ii) phylogenetically older brain areas mature earlier than newer ones. Direct comparison with normal cortical development may help understanding of some neurodevelopmental disorders such as childhood-onset schizophrenia or autism.
              Article 0 comments Cited 501 times – based on 0 reviews     Review now
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                Author and article information

                Contributors
                G.R. Yamakawa
                Journal
                Journal ID (nlm-ta): Neurobiol Sleep Circadian Rhythms
                Journal ID (iso-abbrev): Neurobiol Sleep Circadian Rhythms
                Title: Neurobiology of Sleep and Circadian Rhythms
                Publisher: Elsevier
                ISSN (Electronic): 2451-9944
                Publication date PMC-release: 10 October 2020
                Publication date Collection: November 2020
                Publication date (Electronic): 10 October 2020
                Volume: 9
                Electronic Location Identifier: 100058
                Affiliations
                [a ]Department of Neuroscience, Central Clinical School, Monash University, Melbourne, Australia
                [b ]Department of Medicine, University of Melbourne, Parkville, Australia
                [c ]Department of Physiology, Anatomy and Microbiology, La Trobe University, Melbourne, Australia
                Author notes
                [∗ ]Corresponding author. Department of Neuroscience, Central Clinical School, Monash University The Alfred Centre, Level 6 99 Commercial Road, Melbourne, VIC, 3004, Australia. glenn.yamakawa@ 123456monash.edu
                Article
                Publisher Item ID: S2451-9944(20)30010-9 Publisher ID: 100058
                DOI: 10.1016/j.nbscr.2020.100058
                PMC ID: 7752723
                PubMed ID: 33364525
                SO-VID: ad824994-f01b-47ce-b77a-7c3a32fa8985
                Copyright © © 2020 The Authors
                License:

                This is an open access article under the CC BY license (http://creativecommons.org/licenses/by/4.0/).

                History
                Date received : 30 June 2020
                Date revision received : 11 September 2020
                Date accepted : 7 October 2020
                Categories
                Subject: Review Article

                Keywords: concussion,clock genes,cytokines,suprachiasmatic nucleus,neuroinflammation
                Data availability:
                Keywords: concussion, clock genes, cytokines, suprachiasmatic nucleus, neuroinflammation

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