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IkappaB genetic polymorphisms and invasive pneumococcal disease.

Stephen J Chapman¹, Chiea C Khor, Fredrik O Vannberg

¹The Wellcome Trust Centre for Human Genetics, University of Oxford, and Oxford Centre for Respiratory Medicine, Churchill Hospital Site, Oxford Radcliffe Hospital, Roosevelt Drive, Oxford, OX3 7BN, UK. schapman@well.ox.ac.uk

American Journal of Respiratory and Critical Care Medicine

|April 28, 2007

Summary

Genetic variations in NFKBIA influence susceptibility to invasive pneumococcal disease (IPD). These common polymorphisms may play a role in developing infectious diseases beyond rare immunodeficiency states.

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Area of Science:

Immunology
Genetics
Infectious Diseases

Background:

Nuclear factor-kappaB (NF-kappaB) is crucial in the host response to pneumococcal infections.
The IkappaB family of inhibitors (NFKBIA, NFKBIB, NFKBIE) regulates NF-kappaB activity.
Rare NFKBIA mutations cause severe immunodeficiency, suggesting common polymorphisms might influence susceptibility to common bacterial diseases.

Purpose of the Study:

To investigate the association between polymorphisms in NFKBIA, NFKBIB, and NFKBIE genes and susceptibility to invasive pneumococcal disease (IPD) and thoracic empyema.

Main Methods:

Genotyping of 62 single-nucleotide polymorphisms (SNPs) across NFKBIA, NFKBIB, and NFKBIE in 1,060 individuals with IPD and controls.
Further analysis of significantly associated SNPs in a separate cohort of 632 individuals with thoracic empyema and controls.

Main Results:

Two NFKBIA promoter SNPs (rs3138053 and rs2233406) demonstrated a protective association against IPD in both study groups.
An NFKBIE SNP was linked to IPD susceptibility, but not thoracic empyema.
No NFKBIB SNPs showed association with IPD susceptibility.

Conclusions:

Polymorphisms in the NFKBIA gene are associated with susceptibility to invasive pneumococcal disease.
Genetic variations in NF-kappaB inhibitors may contribute to common infectious diseases, not just rare immunodeficiency states.