Genetic susceptibility to pneumonia

Clin Chest Med. 2005 Mar;26(1):29-38. doi: 10.1016/j.ccm.2004.10.002.


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.

Publication types

  • Review

MeSH terms

  • Cytokines / genetics
  • Genetic Predisposition to Disease
  • Humans
  • Immunocompetence / genetics*
  • Pneumonia, Bacterial / genetics*
  • Pneumonia, Bacterial / immunology*
  • Receptors, Immunologic / genetics


  • Cytokines
  • Receptors, Immunologic