Genetic susceptibility to pneumonia

Grant Waterer, R.G. Wunderink

Research output: Contribution to journalArticlepeer-review

27 Citations (Scopus)


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.
Original languageEnglish
Pages (from-to)29-38
JournalClinics in Chest Medicine
Issue number1
Publication statusPublished - 2005


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