Genetic risk of acute pulmonary infections and sepsis.
The focus of this review is the genetic influence on pneumonia and sepsis. A large number of polymorphisms in a diverse collection of genes have been identified as potential candidates to explain the genetic variability in susceptibility to acute pulmonary infection and its adverse outcomes. Unfortunately, apart from polymorphisms in mannose-binding lectin, CD14 and the IgG2 receptor, there is little consensus on which polymorphisms are truly important. As well as discussing some of the major published findings, this review will focus on the reasons for failure to make more progress. We will also address the issues for future research, particularly the need to address the limitations of past studies, including the grouping of patients with different pathogens, as the relationship between genotype and phenotype may be highly pathogen dependent. Finally, our approach to reporting genetic studies needs to change to minimize the number of publications of spurious findings.
Waterer
Grant W
GW
School of Medicine and Pharmacology, University of Western Australia, Level 4 MRF Building, Royal Perth Hospital, GPO Box X2213, Perth 6847, Australia. grant.waterer@uwa.edu.au
Bruns
Anke H W
AH
D000208:Acute Disease; D020022:Genetic Predisposition to Disease; D014644:Genetic Variation; D006801:Humans; D007074:Immunoglobulin G / Q000235:genetics; D015810:Linkage Disequilibrium; D018950:Lipopolysaccharide Receptors / Q000235:genetics; D037601:Mannose-Binding Lectin / Q000235:genetics; D011014:Pneumonia / Q000235:genetics*; D011110:Polymorphism, Genetic; D012307:Risk Factors; D018805:Sepsis / Q000235:genetics*
D007074:Immunoglobulin G; D018950:Lipopolysaccharide Receptors; D037601:Mannose-Binding Lectin