Genetics in community-acquired pneumonia

Host defense against community-acquired pneumonia depends on an intact innate and acquired immune system. This review analyses the correlation between specific defects and polymorphisms of immunity genes with susceptibility for pneumonia.

Mutations in BTK, Bruton's tyrosine kinase, lead to X-linked agammaglobulinemia, a disease characterized by recurrent respiratory tract infections, including pneumonia. BTK inhibitors, which are used for treatment of leukemia, have pneumonia as side effect. Polymorphisms in B lymphocyte growth and differentiation factors, including IL-6 and IL-10, Fcg RIIa receptors, as well as genetic variants of ACE, angiotensin-converting enzyme, also are associated with increased susceptibility for pneumonia.

Delineation of underlying genetic defects and polymorphisms may add in diagnosis, therapy, and prognosis of community-acquired pneumonia. In case of humoral immunodeficiency, antibody replacement therapy may be indicated.