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Background: Community-acquired pneumonia (CAP) is an acute disease conditionwith a high risk of rapid deteriorations. We analysed the influence of geneticson cytokine regulation to obtain a better understanding of patient'sheterogeneity. Methods: For up to N=389 genotyped participants of the PROGRESSstudy of hospitalised CAP patients, we performed a genome-wide associationstudy of ten cytokines IL-1b, IL-6, IL-8, IL-10, IL-12, MCP-1 (MCAF), MIP-1a(CCL3), VEGF, VCAM-1, and ICAM-1. Consecutive secondary analyses were performedto identify independent hits and corresponding causal variants. Results: 102SNPs from 14 loci showed genome-wide significant associations with five of thecytokines. The most interesting associations were found at 6p21.1 for VEGF(p=1.58x10E-20), at 17q21.32 (p=1.51x10E-9) and at 10p12.1 (p=2.76x10E-9) forIL-1b, at 10p13 for MIP-1a (CCL3) (p=2.28x10E-9), and at 9q34.12 for IL-10(p=4.52x10E-8). Functionally plausible genes could be assigned to the majorityof loci including genes involved in cytokine secretion, granulocyte function,and cilial kinetics. Conclusions: This is the first context-specific geneticassociation study of blood cytokine concentrations in CAP patients revealingnumerous biologically plausible candidate genes. Two of the loci were alsoassociated with atherosclerosis with probable common or consecutivepathomechanisms.

Genetic Regulation of Cytokine Response in Patients with Acute Community-acquired Pneumonia