Cited by 101Sepsis Diagnosis and TreatmentInflammation biomarkers and pathwaysImmune Response and Inflammation

Genetic polymorphisms in sepsis

Dahmer, Mary K., Randolph, Adrienne, Vitali, Sally, Quasney, Michael W.·2005·Pediatric Critical Care Medicine

Abstract

CONTEXT: Wide variability exists in the susceptibility to and outcome from sepsis even within similar intensive care unit populations. Some of this variability in the host may be due to genetic variation in genes coding for components of the innate immune response. OBJECTIVE: To review the evidence for a genetic influence on the susceptibility to and outcome from sepsis. DESIGN: Literature review. PATIENTS: Variety of adult and pediatric patients with various critical illnesses and infections. INTERVENTIONS: None. MAIN OUTCOME MEASURES: Susceptibility to clinical symptoms of sepsis and outcome as measured by severity of disease and mortality. RESULTS: Polymorphisms in genes coding for proteins involved in the recognition of bacterial pathogens (Toll-like receptor 4, CD14, Fc(gamma)RIIa, and mannose-binding lectin) and the response to bacterial pathogens (tumor necrosis factor-alpha, interleukin (IL)-1alpha, IL-1beta, IL-1 receptor agonist, IL-6, IL-10, heat shock proteins, angiotensin I converting enzyme, plasminogen activator inhibitor-1) can influence the amount or function of the protein produced in response to bacterial stimuli. Evidence is discussed suggesting that some of these genetic polymorphisms influence the susceptibility to and outcome from sepsis. CONCLUSION: Host genetic variability in the regulatory and coding regions of genes for components of the innate immune system may influence the susceptibility to and/or outcome from sepsis. The disparate results observed in many studies of polymorphisms in sepsis emphasize the need for future studies to be larger, to include the analysis of multiple polymorphisms, and to be better designed with respect to control populations to identify the degree of influence that genetic variability has on sepsis.

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Crossref · 10.1097/01.pcc.0000161970.44470.c7

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  • Additional factors such as CAR structure and design, disease burden, and host genomic background are likely to play a part in whether cytokine storm develops in patients treated with CAR T cells or blinatumomab.

    “However, cytokine storm does not develop in all patients treated with CAR T cells or blinatumomab, so additional factors, such as CAR structure and design,51 disease burden,58 and host genomic background,59 are likely to play a part.”

    From Cytokine storm (2020) · cites this paper as [59]

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Authors
Dahmer, M. K., Randolph, A., Vitali, S., & Quasney, M. W.
Affiliations
  • University of Tennessee Health Science Center (US)
  • Harvard University (US)
Venue
Pediatric Critical Care Medicine
Published
2005-05
Volume
6
Issue
Supplement
Pages
S61-S73
ISSN
1529-7535 (ISSN-L)
OpenAlex
W1978794637
Cited by
101
References
191
Citations by year
2026: 1 · 2024: 1 · 2023: 1 · 2022: 2 · 2021: 3 · 2020: 1 · 2019: 1 · 2018: 1 · 2017: 6 · 2016: 2 · 2015: 2 · 2014: 10 · 2013: 6 · 2012: 10
FWCI
1.25
Type
journal article
Language
en
Open access
closed
Locations
  • Pediatric Critical Care Medicine (publishedVersion)
  • PubMed (publishedVersion)
Topics
  • Health Sciences › Medicine › Epidemiology › Sepsis Diagnosis and Treatment
  • Life Sciences › Immunology and Microbiology › Immunology › Inflammation biomarkers and pathways
  • Life Sciences › Immunology and Microbiology › Immunology › Immune Response and Inflammation
Keywords
sepsis, genetic polymorphism, innate immunity, TLR4, CD14, FCGR2A, mannose-binding lectin, TNF-α, interleukins, heat shock proteins, angiotensin-converting enzyme, plasminogen activator inhibitor-1, sepsis susceptibility, sepsis mortality, host genetic variation
MeSH terms
Adult, Animals, Child, Humans, Immunity, Innate, Polymorphism, Genetic, Sepsis, Genetic Predisposition to Disease

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