Immune system disorders in the early post-injury period in patients after severe brain injury from the perspective of the severity of the injury

Mrlian, Andrej; Smrčka, Martin; Juráň, Vilém; Navrátil, Ondřej; Neuman, Eduard; Ďuriš, Kamil

doi:10.1007/s10072-022-06482-1

Cited by 1 publication

(1 citation statement)

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“…Specifically, our results outlined that TBI alters the systemic levels of T cells and age affects their ability to become activated and to differentiate. Although the lower viability of PBMC from TBI patients could have induced a bias on the analyzed cells, we showed a significant reduction in the frequencies of T cells in agreement with literature [ 12 – 15 , 29 , 49 ]. This T cell decrease was observed in both young and elderly patients.…”

Section: Discussionsupporting

confidence: 92%

Systemic immune response in young and elderly patients after traumatic brain injury

Magatti,

Pischiutta,

Ortolano

et al. 2023

Immun Ageing

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Background Traumatic brain injury (TBI) is a leading cause of death and long-term disability worldwide. In addition to primary brain damage, systemic immune alterations occur, with evidence for dysregulated immune responses in aggravating TBI outcome and complications. However, immune dysfunction following TBI has been only partially understood, especially in the elderly who represent a substantial proportion of TBI patients and worst outcome. Therefore, we aimed to conduct an in-depth immunological characterization of TBI patients, by evaluating both adaptive (T and B lymphocytes) and innate (NK and monocytes) immune cells of peripheral blood mononuclear cells (PBMC) collected acutely (< 48 h) after TBI in young (18–45 yo) and elderly (> 65 yo) patients, compared to age-matched controls, and also the levels of inflammatory biomarkers. Results Our data show that young respond differently than elderly to TBI, highlighting the immune unfavourable status of elderly compared to young patients. While in young only CD4 T lymphocytes are activated by TBI, in elderly both CD4 and CD8 T cells are affected, and are induced to differentiate into subtypes with low cytotoxic activity, such as central memory CD4 T cells and memory precursor effector CD8 T cells. Moreover, TBI enhances the frequency of subsets that have not been previously investigated in TBI, namely the double negative CD27- IgD- and CD38-CD24- B lymphocytes, and CD56dim CD16- NK cells, both in young and elderly patients. TBI reduces the production of pro-inflammatory cytokines TNF-α and IL-6, and the expression of HLA-DM, HLA-DR, CD86/B7-2 in monocytes, suggesting a compromised ability to drive a pro-inflammatory response and to efficiently act as antigen presenting cells. Conclusions We described the acute immunological response induced by TBI and its relation with injury severity, which could contribute to pathologic evolution and possibly outcome. The focus on age-related immunological differences could help design specific therapeutic interventions based on patients’ characteristics.

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Section: Discussionsupporting

confidence: 92%