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Challenges in understanding host genetics and severity of community-acquired pneumonia.

ABSTRACT: This study found no association of the top two associated FER variants with severity of community-acquired pneumonia. Precise characterisation of phenotypes may be required in order to unravel the genetic mechanisms predisposing to poor outcome in sepsis. https://bit.ly/3jc9SmR.

SUBMITTER: Sole-Violan J

PROVIDER: S-EPMC7836604 | biostudies-literature | 2021 Jan

REPOSITORIES: biostudies-literature

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Challenges in understanding host genetics and severity of community-acquired pneumonia.

Solé-Violán Jordi J Hernández-Brito Elisa E Valencia-Gallardo José Manuel JM Herrera-Ramos Estefanía E Borderías Luis L Briones M Luisa ML Rajas Olga O Freixinet Jorge J Lorente Leonardo L Payeras Antoni A Ferreres José J Carbonell Nieves N González-Quevedo Nereida N González-Martín Jesús M JM Rodríguez de Castro Felipe F Rodríguez-Gallego Carlos C

ERJ open research 20210125 1

<b>This study found no association of the top two associated <i>FER</i> variants with severity of community-acquired pneumonia. Precise characterisation of phenotypes may be required in order to unravel the genetic mechanisms predisposing to poor outcome in sepsis.</b> https://bit.ly/3jc9SmR. ...[more]

PMID: 33532473

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Project description:BackgroundCommunity-acquired pneumonia (CAP) can be caused by a variety of pathogens, of which Streptococcus pneumoniae, Influenza and currently SARS-CoV-2 are the most common. We sought to identify shared and pathogen-specific host response features by directly comparing different aetiologies of CAP.MethodsWe measured 72 plasma biomarkers in a cohort of 265 patients hospitalized for CAP, all sampled within 48 hours of admission, and 28 age-and sex matched non-infectious controls. We stratified the biomarkers into several pathophysiological domains- antiviral response, vascular response and function, coagulation, systemic inflammation, and immune checkpoint markers. We directly compared CAP caused by SARS-CoV-2 (COVID-19, n=39), Streptococcus pneumoniae (CAP-strep, n=27), Influenza (CAP-flu, n=22) and other or unknown pathogens (CAP-other, n=177). We adjusted the comparisons for age, sex and disease severity scores.FindingsBiomarkers reflective of a stronger cell-mediated antiviral response clearly separated COVID-19 from other CAPs (most notably granzyme B). Biomarkers reflecting activation and function of the vasculature showed endothelial barrier integrity was least affected in COVID-19, while glycocalyx degradation and angiogenesis were enhanced relative to other CAPs. Notably, markers of coagulation activation, including D-dimer, were not different between the CAP groups. Ferritin was most increased in COVID-19, while other systemic inflammation biomarkers such as IL-6 and procalcitonin were highest in CAP-strep. Immune checkpoint markers showed distinctive patterns in viral and non-viral CAP, with highly elevated levels of Galectin-9 in COVID-19.InterpretationOur investigation provides insight into shared and distinct pathophysiological mechanisms in different aetiologies of CAP, which may help guide new pathogen-specific therapeutic strategies.FundingThis study was financially supported by the Dutch Research Council, the European Commission and the Netherlands Organization for Health Research and Development.

Dataset Information

Challenges in understanding host genetics and severity of community-acquired pneumonia.

Publications

Challenges in understanding host genetics and severity of community-acquired pneumonia.

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