{"database":"GEO","file_versions":[{"headers":{"Content-Type":["application/json"]},"body":{"files":{"Other":["ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE319nnn/GSE319702/"]},"type":"primary"},"statusCode":"OK","statusCodeValue":200}],"scores":null,"additional":{"omics_type":["Transcriptomics"],"species":["Homo sapiens"],"gds_type":["Expression profiling by high throughput sequencing"],"full_dataset_link":["https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE319702"],"repository":["GEO"],"entry_type":["GSE"],"additional_accession":[]},"is_claimable":false,"name":"Loss of O-Antigen Due to wbbL Mutations is Common and Associated with Increased Mortality in Escherichia coli Bloodstream Infections","description":"Escherichia coli bloodstream infections are common and associated with high mortality. A key feature of E. coli is the lipopolysaccharide (LPS) O-antigen, which contributes to immune evasion during invasive infection. We analyzed serial E. coli isolates from patients with relapsed bacteremia and identified frequent disruption of O-antigen synthesis due to mutations in wbbL, resulting in a rough LPS (R-LPS) phenotype. E. coli with rough LPS isolates were more serum sensitive and less pathogenic in mice. Despite this apparent attenuation, 11 of 66 (18%) E. coli sequence type 131 bloodstream isolates in our cohort lacked O-antigen and were associated with significantly worse clinical outcomes, including septic shock and mortality. Using a recurrent bacteremia model, we show that R-LPS isolates partially evade protective immunity generated against smooth-LPS E. coli, highlighting the importance of host immune context in invasive disease.","dates":{"publication":"2026/05/18"},"accession":"GSE319702","cross_references":{"GSM":["GSM9524099","GSM9524098","GSM9524100","GSM9524095","GSM9524094","GSM9524097","GSM9524096","GSM9524093","GSM9524092"],"GPL":["34284"],"GSE":["319702"],"taxon":["Homo sapiens"]}}