title: Genetic susceptibility to pneumonia.
abstract: The persistent mortality from community-acquired pneumonia may be explained by genetic predisposition. Specific mutations or polymorphisms in host response genes that are associated with adverse outcomes from infection can be grouped into four categories: antigen recognition, proinflammatory responses, anti-inflammatory responses, and effector mechanisms. Mannose-binding lectin polymorphisms have a more dominant role in pneumonia when compared with other pattern recognition molecules such as the toll-like receptors. The roles of TNF and lymphotoxin alpha polymorphisms remain unclear despite extensive study. IL-10 and IL-1 receptor antagonist polymorphisms have an important role in the anti-inflammatory response. Specific organ dysfunction, such as ARDS or DIC, may be related to polymorphisms in specific effector genes.
authors.affiliation: School of Medicine and Pharmacology, University of Western Australia, Royal Perth Hospital, GP0 Box X2213, Perth, Western Australia.
authors.forename: Grant W
authors.initials: GW
authors.lastname: Waterer
authors.forename: Richard G
authors.initials: RG
authors.lastname: Wunderink
mesh_terms: D016207:Cytokines / Q000235:genetics; D020022:Genetic Predisposition to Disease; D006801:Humans; D007121:Immunocompetence / Q000235:genetics*; D018410:Pneumonia, Bacterial / Q000235:genetics* / Q000276:immunology*; D011971:Receptors, Immunologic / Q000235:genetics
chemical_list: D016207:Cytokines; D011971:Receptors, Immunologic