Ontology highlight
ABSTRACT: Background
Toll-like receptors (TLRs) play an important role in activation of innate and adaptive immune responses.Aim
We aimed to detect the association between TLR2 rs5743708 G>A and TLR9 rs5743836 C>T variants and COVID-19 disease susceptibility, severity, and thrombosis by using neutrophil extracellular traps (NETs).Subjects and methods
We included 100 adult COVID-19 patients as well as 100 age- and gender-matched normal controls. Participants were genotyped for TLR2 rs5743708 and TLR9 rs5743836. Citrullinated Histone (H3) was detected as an indicator of NETs.Results
The mutant (G/A and C/C) genotypes and (A and C) alleles of TLR2 rs5743708 and TLR9 rs5743836, respectively, have been significantly related to a higher risk of COVID-19 infection, representing a significant risk factor for the severity of COVID-19. There was no significant association between the two variants and citrullinated histone (H3).Conclusion
TLR2 rs5743708 and TLR9 rs5743836 variants have been significantly related to a higher risk and severity of COVID-19 infection but had no effect on thrombus formation.
SUBMITTER: Alhabibi AM
PROVIDER: S-EPMC9942505 | biostudies-literature | 2023
REPOSITORIES: biostudies-literature
Alhabibi Alshaymaa M AM Hassan Asmaa S AS Abd Elbaky Nashwa Mohamed NM Eid Hoda Asaad HA Khalifa Mohie Aldeen Abd Alzaher MAAA Wahab Maisa A MA Althoqapy Azza Ali AA Abdou Aml E AE Zakaria Doaa Mohammed DM Nassef Eman Mostafa EM Kasim Sammar Ahmed SA Saleh Ola I OI Elsheikh Asmaa Abdelghany AA Lotfy Mahmoud M Sayed Alaa A
Journal of inflammation research 20230217
<h4>Background</h4>Toll-like receptors (TLRs) play an important role in activation of innate and adaptive immune responses.<h4>Aim</h4>We aimed to detect the association between TLR2 rs5743708 G>A and TLR9 rs5743836 C>T variants and COVID-19 disease susceptibility, severity, and thrombosis by using neutrophil extracellular traps (NETs).<h4>Subjects and methods</h4>We included 100 adult COVID-19 patients as well as 100 age- and gender-matched normal controls. Participants were genotyped for TLR2 ...[more]