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Shorter leukocyte telomere length (LTL) may causally increase sepsis risk. This Mendelian randomization study found genetically predicted shorter LTL is linked to higher sepsis susceptibility, but sepsis does not affect LTL.

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Area of Science:

  • Genetics and Genomics
  • Infectious Diseases
  • Epidemiology

Background:

  • Observational studies suggest a link between leukocyte telomere length (LTL) and sepsis.
  • The causal relationship between LTL and sepsis remains unclear.

Purpose of the Study:

  • To investigate the causal effect of leukocyte telomere length (LTL) on sepsis.
  • To examine the potential reverse causality of sepsis on LTL using a bidirectional Mendelian randomization approach.

Main Methods:

  • Utilized a bidirectional Mendelian randomization (MR) design.
  • Selected single nucleotide polymorphisms (SNPs) associated with LTL and various sepsis phenotypes from genome-wide association studies (GWAS).
  • Employed the inverse variance weighted (IVW) method and conducted sensitivity analyses to assess causality and pleiotropy.

Main Results:

  • Forward MR analysis indicated a potential causal relationship between genetically predicted shorter LTL and increased susceptibility to sepsis (OR=1.161, p=0.008).
  • Reverse MR analysis found no evidence that sepsis causally influences LTL.
  • Sensitivity analyses supported the primary findings, suggesting a robust association.

Conclusions:

  • Genetically determined shorter leukocyte telomere length may increase the risk of developing sepsis.
  • These findings highlight LTL as a potential risk factor for sepsis and may inform novel diagnostic and therapeutic strategies.