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000282965 1001_ $$aOlde Heuvel, Florian$$b0
000282965 245__ $$aBasophils activate splenic B cells and dendritic cells via IL-13 signaling in acute traumatic brain injury.
000282965 260__ $$aLondon$$bBioMed Central$$c2025
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000282965 520__ $$aPeripheral consequences following traumatic brain injury (TBI) are characterized by both systemic inflammatory responses and autonomic dysregulation. One of the main immune regulatory organs, the spleen, shows high interaction with the brain which is controlled by both circulating mediators as well as autonomic fibers targeting splenic immune cells. The brain-spleen axis does not function as a one-way street, it also shows reciprocal effects where the spleen affects neuroinflammatory and cognitive functions post injury. To date, systemic and splenic inflammatory responses are measured by cells or mediators located in circulation. Nevertheless, most of the signaling and inflammation post injury takes place in the organs.We set out to investigate the early (3 h) signaling landscape in the spleen following a moderate severity closed head injury model to wild-type animals aged p60-90. Using phospho-proteomic signaling approaches, immunofluorescence stainings, Enzyme-Linked Immunosorbent Assay (ELISA), super-resolution microscopy and single mRNA in situ hybridization we investigated novel molecular and cellular players in the spleen involved in immune modulation after a head injury.Based on the signaling signature, we found a rapid influx of basophil granulocytes towards the spleen, via a recruitment mechanism that includes CXCL1 expressed by B-cells and dendritic cells (DCs). The basophils in turn seem to activate B cells and dendritic cells via the IL-13/IL-13Ra1 signaling pathway and enhance protein translation through the long non-coding RNA NORAD. The early recruitment of basophils and subsequent activation of B cells and DCs, is short lived and sets at 3dpi. Interestingly, the rapid recruitment of basophils is inhibited by ethanol intoxication in TBI, with a subsequent prevention of IL-13Ra phosphorylation and NORAD increase in B-cells and DCs.Basophils recruitment to the spleen may serve as an early mediator of systemic inflammatory responses to TBI with potential implications for research on biomarkers and therapeutic targets.
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000282965 650_7 $$2Other$$aB-cell
000282965 650_7 $$2Other$$aBasophil
000282965 650_7 $$2Other$$aDendritic cell
000282965 650_7 $$2Other$$aIL-13
000282965 650_7 $$2Other$$aSpleen
000282965 650_7 $$2Other$$aTraumatic brain injury
000282965 650_7 $$2NLM Chemicals$$aInterleukin-13
000282965 650_2 $$2MeSH$$aAnimals
000282965 650_2 $$2MeSH$$aBrain Injuries, Traumatic: immunology
000282965 650_2 $$2MeSH$$aBrain Injuries, Traumatic: metabolism
000282965 650_2 $$2MeSH$$aBrain Injuries, Traumatic: pathology
000282965 650_2 $$2MeSH$$aMice
000282965 650_2 $$2MeSH$$aSpleen: immunology
000282965 650_2 $$2MeSH$$aSpleen: metabolism
000282965 650_2 $$2MeSH$$aSpleen: pathology
000282965 650_2 $$2MeSH$$aSignal Transduction: physiology
000282965 650_2 $$2MeSH$$aB-Lymphocytes: metabolism
000282965 650_2 $$2MeSH$$aB-Lymphocytes: immunology
000282965 650_2 $$2MeSH$$aInterleukin-13: metabolism
000282965 650_2 $$2MeSH$$aInterleukin-13: immunology
000282965 650_2 $$2MeSH$$aBasophils: metabolism
000282965 650_2 $$2MeSH$$aBasophils: immunology
000282965 650_2 $$2MeSH$$aMice, Inbred C57BL
000282965 650_2 $$2MeSH$$aDendritic Cells: metabolism
000282965 650_2 $$2MeSH$$aDendritic Cells: immunology
000282965 650_2 $$2MeSH$$aMale
000282965 7001_ $$aZhang, Jin$$b1
000282965 7001_ $$aSun, Fan$$b2
000282965 7001_ $$aKrishnamurthy, Sruthi Sankari$$b3
000282965 7001_ $$0P:(DE-2719)9001770$$aYartas, Gizem$$b4$$udzne
000282965 7001_ $$aÖzkan, Burak$$b5
000282965 7001_ $$aPagliarini, Marica$$b6
000282965 7001_ $$aVoehringer, David$$b7
000282965 7001_ $$aO'Meara, Caitlin C$$b8
000282965 7001_ $$aSchäfer, Michael K E$$b9
000282965 7001_ $$aHuber-Lang, Markus$$b10
000282965 7001_ $$0P:(DE-2719)2812851$$aRoselli, Francesco$$b11$$eLast author$$udzne
000282965 773__ $$0PERI:(DE-600)2156455-3$$a10.1186/s12974-025-03621-1$$gVol. 22, no. 1, p. 290$$n1$$p290$$tJournal of neuroinflammation$$v22$$x1742-2094$$y2025
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