Table 1.
Description of discovery (168 white individuals with SAB from Duke University Hospital) and replication (240 white individuals with SAB from Danish DANSAB study group) samples.
Table 2.
Top results (p<1 x 10−4) from SKAT-O gene-based association analysis in the discovery sample, overall (adjusted for age, sex, and bacterial clonal complex) and stratified by bacterial clonal complex (adjusted for age and sex).
Fig 1.
Regional association plot surrounding GLS2 in the overall replication sample.
The–log10 p-values for individual SNV association tests are plotted against chromosomal position. The strongest association is at intronic variant rs2657878 (purple diamond). The next strongest result is at rs937115 (blue circle), an intronic variant in modest linkage disequilibrium (r2<0.2) with rs2657878 in the 1000 Genomes November 2014 European sample. Three additional variants (red circles), including missense variant rs2657879, are in strong linkage disequilibrium (r2>0.8) with rs2657878.
Table 3.
Top results (p<1 x 10−2) from SKAT-O gene-based association analysis in the replication sample, overall (adjusted for age, sex, and bacterial clonal complex) and restricted to bacterial clonal complex CC5 or CC30 (adjusted for age and sex).
Fig 2.
GLS2 transcript is suppressed in (A) patients with S. aureus or E. coli blood stream infection and in (B) RAW 264.7 macrophages challenged with S. aureus. Data represent two independent experiments each with six biological replicates.
Fig 3.
(A) Knockdown of Gls2 decreased IL-1β mRNA and (B) enhanced NO production in RAW 264.7 macrophages challenged with S. aureus. Data represent two independent experiments, with six biological replicates for IL-1β (A) and three biological replicates for NO production (B).