Genetic polymorphisms in sepsis.
BACKGROUND
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.


METHODS
Literature review.


METHODS
Variety of adult and pediatric patients with various critical illnesses and infections.


METHODS
None.


METHODS
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.


CONCLUSIONS
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.
Dahmer
Mary K
MK
Department of Molecular Sciences, University of Tennessee Health Science Center, Memphis, TN, USA.
Randolph
Adrienne
A
Vitali
Sally
S
Quasney
Michael W
MW
D000328:Adult; D000818:Animals; D002648:Child; D020022:Genetic Predisposition to Disease; D006801:Humans; D007113:Immunity, Innate; D011110:Polymorphism, Genetic; D018805:Sepsis / Q000235:genetics* / Q000276:immunology / Q000378:metabolism