Therapeutic potential of IL6R blockade for the treatment of sepsis and sepsis-related death: A Mendelian randomisation study.

<h4>Background</h4>Sepsis is characterised by dysregulated, life-threatening immune responses, which are thought to be driven by cytokines such as interleukin 6 (IL-6). Genetic variants in IL6R known to down-regulate IL-6 signalling are associated with improved Coronavirus Disease 2019 (...

Full description

Saved in:
Bibliographic Details
Main Authors: Fergus W Hamilton, Matt Thomas, David Arnold, Tom Palmer, Ed Moran, Alexander J Mentzer, Nick Maskell, Kenneth Baillie, Charlotte Summers, Aroon Hingorani, Alasdair MacGowan, Golam M Khandaker, Ruth Mitchell, George Davey Smith, Peter Ghazal, Nicholas J Timpson
Format: Article
Language:English
Published: Public Library of Science (PLoS) 2023-01-01
Series:PLoS Medicine
Online Access:https://journals.plos.org/plosmedicine/article/file?id=10.1371/journal.pmed.1004174&type=printable
Tags: Add Tag
No Tags, Be the first to tag this record!
_version_ 1849331724691963904
author Fergus W Hamilton
Matt Thomas
David Arnold
Tom Palmer
Ed Moran
Alexander J Mentzer
Nick Maskell
Kenneth Baillie
Charlotte Summers
Aroon Hingorani
Alasdair MacGowan
Golam M Khandaker
Ruth Mitchell
George Davey Smith
Peter Ghazal
Nicholas J Timpson
author_facet Fergus W Hamilton
Matt Thomas
David Arnold
Tom Palmer
Ed Moran
Alexander J Mentzer
Nick Maskell
Kenneth Baillie
Charlotte Summers
Aroon Hingorani
Alasdair MacGowan
Golam M Khandaker
Ruth Mitchell
George Davey Smith
Peter Ghazal
Nicholas J Timpson
author_sort Fergus W Hamilton
collection DOAJ
description <h4>Background</h4>Sepsis is characterised by dysregulated, life-threatening immune responses, which are thought to be driven by cytokines such as interleukin 6 (IL-6). Genetic variants in IL6R known to down-regulate IL-6 signalling are associated with improved Coronavirus Disease 2019 (COVID-19) outcomes, a finding later confirmed in randomised trials of IL-6 receptor antagonists (IL6RAs). We hypothesised that blockade of IL6R could also improve outcomes in sepsis.<h4>Methods and findings</h4>We performed a Mendelian randomisation (MR) analysis using single nucleotide polymorphisms (SNPs) in and near IL6R to evaluate the likely causal effects of IL6R blockade on sepsis (primary outcome), sepsis severity, other infections, and COVID-19 (secondary outcomes). We weighted SNPs by their effect on CRP and combined results across them in inverse variance weighted meta-analysis, proxying the effect of IL6RA. Our outcomes were measured in UK Biobank, FinnGen, the COVID-19 Host Genetics Initiative (HGI), and the GenOSept and GainS consortium. We performed several sensitivity analyses to test assumptions of our methods, including utilising variants around CRP and gp130 in a similar analysis. In the UK Biobank cohort (N = 486,484, including 11,643 with sepsis), IL6R blockade was associated with a decreased risk of our primary outcome, sepsis (odds ratio (OR) = 0.80; 95% confidence interval (CI) 0.66 to 0.96, per unit of natural log-transformed CRP decrease). The size of this effect increased with severity, with larger effects on 28-day sepsis mortality (OR = 0.74; 95% CI 0.47 to 1.15); critical care admission with sepsis (OR = 0.48, 95% CI 0.30 to 0.78) and critical care death with sepsis (OR = 0.37, 95% CI 0.14 to 0.98). Similar associations were seen with severe respiratory infection: OR for pneumonia in critical care 0.69 (95% CI 0.49 to 0.97) and for sepsis survival in critical care (OR = 0.22; 95% CI 0.04 to 1.31) in the GainS and GenOSept consortium, although this result had a large degree of imprecision. We also confirm the previously reported protective effect of IL6R blockade on severe COVID-19 (OR = 0.69, 95% CI 0.57 to 0.84) in the COVID-19 HGI, which was of similar magnitude to that seen in sepsis. Sensitivity analyses did not alter our primary results. These results are subject to the limitations and assumptions of MR, which in this case reflects interpretation of these SNP effects as causally acting through blockade of IL6R, and reflect lifetime exposure to IL6R blockade, rather than the effect of therapeutic IL6R blockade.<h4>Conclusions</h4>IL6R blockade is causally associated with reduced incidence of sepsis. Similar but imprecisely estimated results supported a causal effect also on sepsis related mortality and critical care admission with sepsis. These effects are comparable in size to the effect seen in severe COVID-19, where IL-6 receptor antagonists were shown to improve survival. These data suggest that a randomised trial of IL-6 receptor antagonists in sepsis should be considered.
format Article
id doaj-art-2608ebec05cb45ed9c68e5978c195d71
institution Kabale University
issn 1549-1277
1549-1676
language English
publishDate 2023-01-01
publisher Public Library of Science (PLoS)
record_format Article
series PLoS Medicine
spelling doaj-art-2608ebec05cb45ed9c68e5978c195d712025-08-20T03:46:25ZengPublic Library of Science (PLoS)PLoS Medicine1549-12771549-16762023-01-01201e100417410.1371/journal.pmed.1004174Therapeutic potential of IL6R blockade for the treatment of sepsis and sepsis-related death: A Mendelian randomisation study.Fergus W HamiltonMatt ThomasDavid ArnoldTom PalmerEd MoranAlexander J MentzerNick MaskellKenneth BaillieCharlotte SummersAroon HingoraniAlasdair MacGowanGolam M KhandakerRuth MitchellGeorge Davey SmithPeter GhazalNicholas J Timpson<h4>Background</h4>Sepsis is characterised by dysregulated, life-threatening immune responses, which are thought to be driven by cytokines such as interleukin 6 (IL-6). Genetic variants in IL6R known to down-regulate IL-6 signalling are associated with improved Coronavirus Disease 2019 (COVID-19) outcomes, a finding later confirmed in randomised trials of IL-6 receptor antagonists (IL6RAs). We hypothesised that blockade of IL6R could also improve outcomes in sepsis.<h4>Methods and findings</h4>We performed a Mendelian randomisation (MR) analysis using single nucleotide polymorphisms (SNPs) in and near IL6R to evaluate the likely causal effects of IL6R blockade on sepsis (primary outcome), sepsis severity, other infections, and COVID-19 (secondary outcomes). We weighted SNPs by their effect on CRP and combined results across them in inverse variance weighted meta-analysis, proxying the effect of IL6RA. Our outcomes were measured in UK Biobank, FinnGen, the COVID-19 Host Genetics Initiative (HGI), and the GenOSept and GainS consortium. We performed several sensitivity analyses to test assumptions of our methods, including utilising variants around CRP and gp130 in a similar analysis. In the UK Biobank cohort (N = 486,484, including 11,643 with sepsis), IL6R blockade was associated with a decreased risk of our primary outcome, sepsis (odds ratio (OR) = 0.80; 95% confidence interval (CI) 0.66 to 0.96, per unit of natural log-transformed CRP decrease). The size of this effect increased with severity, with larger effects on 28-day sepsis mortality (OR = 0.74; 95% CI 0.47 to 1.15); critical care admission with sepsis (OR = 0.48, 95% CI 0.30 to 0.78) and critical care death with sepsis (OR = 0.37, 95% CI 0.14 to 0.98). Similar associations were seen with severe respiratory infection: OR for pneumonia in critical care 0.69 (95% CI 0.49 to 0.97) and for sepsis survival in critical care (OR = 0.22; 95% CI 0.04 to 1.31) in the GainS and GenOSept consortium, although this result had a large degree of imprecision. We also confirm the previously reported protective effect of IL6R blockade on severe COVID-19 (OR = 0.69, 95% CI 0.57 to 0.84) in the COVID-19 HGI, which was of similar magnitude to that seen in sepsis. Sensitivity analyses did not alter our primary results. These results are subject to the limitations and assumptions of MR, which in this case reflects interpretation of these SNP effects as causally acting through blockade of IL6R, and reflect lifetime exposure to IL6R blockade, rather than the effect of therapeutic IL6R blockade.<h4>Conclusions</h4>IL6R blockade is causally associated with reduced incidence of sepsis. Similar but imprecisely estimated results supported a causal effect also on sepsis related mortality and critical care admission with sepsis. These effects are comparable in size to the effect seen in severe COVID-19, where IL-6 receptor antagonists were shown to improve survival. These data suggest that a randomised trial of IL-6 receptor antagonists in sepsis should be considered.https://journals.plos.org/plosmedicine/article/file?id=10.1371/journal.pmed.1004174&type=printable
spellingShingle Fergus W Hamilton
Matt Thomas
David Arnold
Tom Palmer
Ed Moran
Alexander J Mentzer
Nick Maskell
Kenneth Baillie
Charlotte Summers
Aroon Hingorani
Alasdair MacGowan
Golam M Khandaker
Ruth Mitchell
George Davey Smith
Peter Ghazal
Nicholas J Timpson
Therapeutic potential of IL6R blockade for the treatment of sepsis and sepsis-related death: A Mendelian randomisation study.
PLoS Medicine
title Therapeutic potential of IL6R blockade for the treatment of sepsis and sepsis-related death: A Mendelian randomisation study.
title_full Therapeutic potential of IL6R blockade for the treatment of sepsis and sepsis-related death: A Mendelian randomisation study.
title_fullStr Therapeutic potential of IL6R blockade for the treatment of sepsis and sepsis-related death: A Mendelian randomisation study.
title_full_unstemmed Therapeutic potential of IL6R blockade for the treatment of sepsis and sepsis-related death: A Mendelian randomisation study.
title_short Therapeutic potential of IL6R blockade for the treatment of sepsis and sepsis-related death: A Mendelian randomisation study.
title_sort therapeutic potential of il6r blockade for the treatment of sepsis and sepsis related death a mendelian randomisation study
url https://journals.plos.org/plosmedicine/article/file?id=10.1371/journal.pmed.1004174&type=printable
work_keys_str_mv AT ferguswhamilton therapeuticpotentialofil6rblockadeforthetreatmentofsepsisandsepsisrelateddeathamendelianrandomisationstudy
AT mattthomas therapeuticpotentialofil6rblockadeforthetreatmentofsepsisandsepsisrelateddeathamendelianrandomisationstudy
AT davidarnold therapeuticpotentialofil6rblockadeforthetreatmentofsepsisandsepsisrelateddeathamendelianrandomisationstudy
AT tompalmer therapeuticpotentialofil6rblockadeforthetreatmentofsepsisandsepsisrelateddeathamendelianrandomisationstudy
AT edmoran therapeuticpotentialofil6rblockadeforthetreatmentofsepsisandsepsisrelateddeathamendelianrandomisationstudy
AT alexanderjmentzer therapeuticpotentialofil6rblockadeforthetreatmentofsepsisandsepsisrelateddeathamendelianrandomisationstudy
AT nickmaskell therapeuticpotentialofil6rblockadeforthetreatmentofsepsisandsepsisrelateddeathamendelianrandomisationstudy
AT kennethbaillie therapeuticpotentialofil6rblockadeforthetreatmentofsepsisandsepsisrelateddeathamendelianrandomisationstudy
AT charlottesummers therapeuticpotentialofil6rblockadeforthetreatmentofsepsisandsepsisrelateddeathamendelianrandomisationstudy
AT aroonhingorani therapeuticpotentialofil6rblockadeforthetreatmentofsepsisandsepsisrelateddeathamendelianrandomisationstudy
AT alasdairmacgowan therapeuticpotentialofil6rblockadeforthetreatmentofsepsisandsepsisrelateddeathamendelianrandomisationstudy
AT golammkhandaker therapeuticpotentialofil6rblockadeforthetreatmentofsepsisandsepsisrelateddeathamendelianrandomisationstudy
AT ruthmitchell therapeuticpotentialofil6rblockadeforthetreatmentofsepsisandsepsisrelateddeathamendelianrandomisationstudy
AT georgedaveysmith therapeuticpotentialofil6rblockadeforthetreatmentofsepsisandsepsisrelateddeathamendelianrandomisationstudy
AT peterghazal therapeuticpotentialofil6rblockadeforthetreatmentofsepsisandsepsisrelateddeathamendelianrandomisationstudy
AT nicholasjtimpson therapeuticpotentialofil6rblockadeforthetreatmentofsepsisandsepsisrelateddeathamendelianrandomisationstudy