Evaluation of Advanced Immune Markers (TLR4 and sTREM-1) among three Strains of Escherichia coli

These Escherichia coli strains (Uropathogenic - UPEC, Enteroaggregative – EAEC and Enterotoxigenic ETEC) are major pathogens involved in urinary tract infections, diarrhea diseases and systemic infections. They become pathogenic through adhesion factors, toxin synthesis and tissue colonization, inducing strong innate immune reactions. Toll-like receptor 4 (TLR4) and soluble triggering receptor expressed on myeloid cells-1 (sTREM-1) are important immune mediators representing both host recognition of bacterial moieties and further amplification of inflammation. In the present study we aimed to assess serum concentrations of TLR4 as well as sTREM-1 in patients infected with three distinct E. coli serotypes in comparison to healthy controls. Patients and methods A total of 65-cases (confirmed cases due to E. coli) were included at Hilla Teaching Hospital, Babylon/Iraq, over the period from March to September 2025 in addition to 50 apparently healthy subjects as controls. Exclusion criteria were recent antibiotic or anti-inflammatory treatment, chronic systemic diseases, pregnancy and lactation. Peripheral venous blood samples were obtained, the serum TLR4 and sTREM-1 levels in both groups were determined by ELISA. Results Serum levels of TLR4 (mean ≈ 5.8 ng/mL) and sTREM-1 (mean ≈ 152 pg/mL) were significantly raised in infected patients as compared to the controls (p < 0.05). Within strains, UPEC-infected patients had the greatest while EAEC- and ETEC-infected patients had lower responses; these findings suggest strain-specific differences in host immune activation. There were no important differences in experimental factors by sex or residence. These findings demonstrate that TLR4 and sTREM-1 are strong markers of innate immunity activation in E. coli infection, which could be used as additional biomarkers to assess host inflammatory response, follow disease activity and potentially differentiate between strain dependent pathogenic profiles.