| Literature DB >> 35636458 |
Wolfram C Poller1,2, Jeffrey Downey3,4,5,6,7, Agnes A Mooslechner4, Nargis Khan5,6,7, Long Li8, Christopher T Chan3,4, Cameron S McAlpine3,4,8, Chunliang Xu9, Florian Kahles4, Shun He4, Henrike Janssen3,4, John E Mindur4, Sumnima Singh3,4, Máté G Kiss3,4, Laura Alonso-Herranz4, Yoshiko Iwamoto4, Rainer H Kohler4, Lai Ping Wong10,11, Kashish Chetal10,11, Scott J Russo8, Ruslan I Sadreyev10,11, Ralph Weissleder4,12, Matthias Nahrendorf4, Paul S Frenette9, Maziar Divangahi5,6,7, Filip K Swirski13,14.
Abstract
The nervous and immune systems are intricately linked1. Although psychological stress is known to modulate immune function, mechanistic pathways linking stress networks in the brain to peripheral leukocytes remain poorly understood2. Here we show that distinct brain regions shape leukocyte distribution and function throughout the body during acute stress in mice. Using optogenetics and chemogenetics, we demonstrate that motor circuits induce rapid neutrophil mobilization from the bone marrow to peripheral tissues through skeletal-muscle-derived neutrophil-attracting chemokines. Conversely, the paraventricular hypothalamus controls monocyte and lymphocyte egress from secondary lymphoid organs and blood to the bone marrow through direct, cell-intrinsic glucocorticoid signalling. These stress-induced, counter-directional, population-wide leukocyte shifts are associated with altered disease susceptibility. On the one hand, acute stress changes innate immunity by reprogramming neutrophils and directing their recruitment to sites of injury. On the other hand, corticotropin-releasing hormone neuron-mediated leukocyte shifts protect against the acquisition of autoimmunity, but impair immunity to SARS-CoV-2 and influenza infection. Collectively, these data show that distinct brain regions differentially and rapidly tailor the leukocyte landscape during psychological stress, therefore calibrating the ability of the immune system to respond to physical threats.Entities:
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Year: 2022 PMID: 35636458 DOI: 10.1038/s41586-022-04890-z
Source DB: PubMed Journal: Nature ISSN: 0028-0836 Impact factor: 69.504