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TLRs1-10 Protein Expression in Circulating Human White Blood Cells during Bacterial and COVID-19 Infections

Authors :
Louise Chomel
Mathieu Vogt
Julien Demiselle
Pierrick Le Borgne
Marine Tschirhart
Valentin Morandeau
Hamid Merdji
Laurent Miguet
Julie Helms
Ferhat Meziani
Laurent Mauvieux
Source :
Journal of Innate Immunity, Pp 1-1 (2024)
Publication Year :
2024
Publisher :
Karger Publishers, 2024.

Abstract

Introduction: Toll-like receptors play crucial roles in the sepsis-induced systemic inflammatory response. Septic shock mortality correlates with overexpression of neutrophilic TLR2 and TLR9, while the role of TLR4 overexpression remains a debate. In addition, TLRs are involved in the pathogenesis of viral infections such as COVID-19, where the single-stranded RNA of SARS-CoV-2 is recognized by TLR7 and TLR8, and the spike protein activates TLR4. Methods: In this study, we conducted a comprehensive analysis of TLRs 1–10 expressions in white blood cells from 71 patients with bacterial and viral infections. Patients were divided into 4 groups based on disease type and severity (sepsis, septic shock, moderate, and severe COVID-19) and compared to 7 healthy volunteers. Results: We observed a significant reduction in the expression of TLR4 and its co-receptor CD14 in septic shock neutrophils compared to the control group (p < 0.001). Severe COVID-19 patients exhibited a significant increase in TLR3 and TLR7 levels in neutrophils compared to controls (p < 0.05). Septic shock patients also showed a similar increase in TLR7 in neutrophils along with elevated intermediate monocytes (CD14+CD16+) compared to the control group (p < 0.005 and p < 0.001, respectively). However, TLR expression remained unchanged in lymphocytes. Conclusion: This study provides further insights into the mechanisms of TLR activation in various infectious conditions. Additional analysis is needed to assess their correlation with patient outcome and to evaluate the impact of TLR-pathway modulation during septic shock and severe COVID-19.

Details

Language :
English
ISSN :
16628128
Database :
Directory of Open Access Journals
Journal :
Journal of Innate Immunity
Publication Type :
Academic Journal
Accession number :
edsdoj.84cf3857ea24c17a4a735af9dbbd1ab
Document Type :
article
Full Text :
https://doi.org/10.1159/000536593