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γδT cells but not αβT cells contribute to sepsis-induced white matter injury and motor abnormalities in mice

Journal article
Authors Xiaoli Zhang
Eridan Rocha-Ferreira
Tao Li
Regina Vontell
Darakhshan Jabin
Sha Hua
Kai Zhou
Arshed Nazmi
Anna-Maj Albertsson
Kristina Sobotka
C. Joakim Ek
Claire Thornton
Henrik Hagberg
Carina Mallard
Jianmei W. Leavenworth
Changlian Zhu
Xiaoyang Wang
Published in Journal of Neuroinflammation
Volume 14
Issue 1
ISSN 1742-2094
Publication year 2017
Published at Institute of Neuroscience and Physiology, Department of Health and Rehabilitation
Institute of Neuroscience and Physiology
Institute of Neuroscience and Physiology, Department of Physiology
Institute of Clinical Sciences, Department of Obstetrics and Gynecology
Language en
Links https://doi.org/10.1186/s12974-017-...
Subject categories Pediatrics

Abstract

Background Infection and sepsis are associated with brain white matter injury in preterm infants and the subsequent development of cerebral palsy. Methods In the present study, we used a neonatal mouse sepsis-induced white matter injury model to determine the contribution of different T cell subsets (αβT cells and γδT cells) to white matter injury and consequent behavioral changes. C57BL/6J wild-type (WT), T cell receptor (TCR) δ-deficient (Tcrd −/−, lacking γδT cells), and TCRα-deficient (Tcra −/−, lacking αβT cells) mice were administered with lipopolysaccharide (LPS) at postnatal day (PND) 2. Brain myelination was examined at PNDs 12, 26, and 60. Motor function and anxiety-like behavior were evaluated at PND 26 or 30 using DigiGait analysis and an elevated plus maze. Results White matter development was normal in Tcrd −/− and Tcrα −/− compared to WT mice. LPS exposure induced reductions in white matter tissue volume in WT and Tcrα −/− mice, but not in the Tcrd −/− mice, compared with the saline-treated groups. Neither LPS administration nor the T cell deficiency affected anxiety behavior in these mice as determined with the elevated plus maze. DigiGait analysis revealed motor function deficiency after LPS-induced sepsis in both WT and Tcrα −/− mice, but no such effect was observed in Tcrd −/− mice. Conclusions Our results suggest that γδT cells but not αβT cells contribute to sepsis-induced white matter injury and subsequent motor function abnormalities in early life. Modulating the activity of γδT cells in the early stages of preterm white matter injury might represent a novel therapeutic strategy for the treatment of perinatal brain injury.

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