Genetics of community-acquired pneumonia

Richard G. Wunderink*, Grant W. Waterer

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

13 Scopus citations


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.

Original languageEnglish (US)
Pages (from-to)553-562
Number of pages10
JournalSeminars in Respiratory and Critical Care Medicine
Issue number6
StatePublished - Dec 2005


  • Community-acquired pneumonia
  • Genetics
  • Lymphotoxin alpha
  • Polymorphism
  • Tumor necrosis factor

ASJC Scopus subject areas

  • Pulmonary and Respiratory Medicine
  • Critical Care and Intensive Care Medicine


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