Ex vivo mRNA expression of toll-like receptors during latent tuberculosis infection

BMC Immunol. 2021 Jan 28;22(1):9. doi: 10.1186/s12865-021-00400-4.

Abstract

Background: Understanding immune mechanisms, particularly the role of innate immune markers during latent TB infection remains elusive. The main objective of this study was to evaluate mRNA gene expression patterns of toll-like receptors (TLRs) as correlates of immunity during latent TB infection and further infer their roles as potential diagnostic biomarkers.

Methods: Messenger RNA (mRNA) levels were analysed in a total of 64 samples collected from apparently healthy children and adolescents latently infected with tuberculosis (n = 32) or non-infected (n = 32). Relative expression in peripheral blood of selected genes encoding TLRs (TLR-1, TLR-2, TLR-4, TLR-6 and TLR-9) was determined with a quantitative real-time polymerase chain reaction (qRT-PCR) using specific primers and florescent labelled probes and a comparative threshold cycle method to define fold change. Data were analysed using Graph-Pad Prism 7.01 for Windows and a p-value less than 0.05 was considered statistically significant.

Results: An increased mean fold change in the relative expression of TLR-2 and TLR-6 mRNA was observed in LTBI groups relative to non-LTBI groups (p < 0.05), whereas a slight fold decrease was observed for TLR-1 gene.

Conclusions: An increased mRNA expression of TLR-2 and TLR-6 was observed in latently infected individuals relative to those non-infected, possibly indicating the roles these biomarkers play in sustenance of the steady state interaction between the dormant TB bacilli and host immunity.

Keywords: Children; Latency; TLR; Tuberculosis; mRNA.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adolescent
  • Biomarkers / metabolism
  • Child
  • Early Diagnosis
  • Female
  • Humans
  • Immunity, Innate
  • Latent Tuberculosis / diagnosis
  • Latent Tuberculosis / immunology*
  • Male
  • Mycobacterium tuberculosis
  • RNA, Messenger / genetics
  • RNA, Messenger / metabolism*
  • Toll-Like Receptors / genetics*

Substances

  • Biomarkers
  • RNA, Messenger
  • Toll-Like Receptors