title: Genetics of community-acquired pneumonia.
abstract: The variable clinical presentation of community-acquired pneumonia (CAP) suggests a genetic predisposition. Specific mutations or polymorphisms in host response genes such as pattern recognition molecules (PRMs), inflammatory molecules, and the coagulation system are likely to play a role in this variable response to CAP. Mannose-binding lectin polymorphisms appear to play a more dominant role in CAP than other PRMs, such as the Toll-like receptors (TLRs). The role of tumor necrosis factor (TNF) and lymphotoxin alpha (LTA) polymorphisms remain unclear despite extensive study whereas interleukin (IL)-10 and IL-1 receptor antagonist polymorphisms appear to play an important role in the anti-inflammatory response. Coagulation gene polymorphisms are likely important as well. The real value of these genetic studies in CAP and other severe infections will be when the management of an individual patient can be optimized by therapy based on the individual's genotype for molecules important in outcome.
authors.affiliation: Division of Pulmonary and Critical Care Medicine, Northwestern University Feinberg School of Medicine, Chicago, Illinois 60611, USA. r-wunderink@northwestern.edu
authors.forename: Richard G
authors.initials: RG
authors.lastname: Wunderink
authors.forename: Grant W
authors.initials: GW
authors.lastname: Waterer
mesh_terms: D017714:Community-Acquired Infections / Q000235:genetics*; D005260:Female; D006801:Humans; D007375:Interleukin-1; D016753:Interleukin-10; D008233:Lymphotoxin-alpha; D008297:Male; D008875:Middle Aged; D009154:Mutation; D018410:Pneumonia, Bacterial / Q000235:genetics*; D011110:Polymorphism, Genetic; D018570:Risk Assessment; D012307:Risk Factors; D014409:Tumor Necrosis Factor-alpha
chemical_list: D007375:Interleukin-1; D008233:Lymphotoxin-alpha; D014409:Tumor Necrosis Factor-alpha; D016753:Interleukin-10