Sci Rep. 2026 Feb 28. doi: 10.1038/s41598-026-40464-z. Online ahead of print.
ABSTRACT
To assess the host response to mono- and co-infection of tick-borne encephalitis (TBE) virus with Borrelia burgdorferi sensu lato and Anaplasma phagocytophilum bacteria, as well as the possibility of using the analysis of the level of endocannabinoids and eicosanoids in urine for effective diagnostics. Urine of patients with Lyme disease (LD) (in the form of erythema migrans (EM) or neuroborreliosis (NB)), TBE, diagnosed by ELISA-based detection of serum and CSF anti-TBEV IgM and IgG antibodies in all cases, human granulocytic anaplasmosis (HGA), co-infection of TBEV, LD, and healthy individuals (Control Group, CG) was analyzed. A GC/LC-MS/MS platform was used to identify changes in the phospholipid metabolite profile in urine. Lipid peroxidation product levels were estimated by measuring 4-hydroxy-2-nonenal (4-HNE by GC-MS/MS and F2-isoprostanes 8-isoPGF2α by LC-MS/MS). Endocannabinoids and eicosanoids levels were assessed using LC-MS/MS. Statistically significant differences in the concentration of 8-isoP (EM, NB, TBE vs. CG) were observed in patients’ urine before treatment. However, the analysis of endocannabinoids showed significant differences in oleylethanolamide (OEA) concentration (TBE vs CG). The study of pro-inflammatory eicosanoid levels showed a difference for: prostaglandin E2 (PGE2) (TBE vs CG), leukotriene D4 LTD4 (EM vs HGA), and 5-hydroxyeicosatetraenoic acid (5-HETE) (EM vs NB), assessed before treatment. The levels of anti-inflammatory eicosanoids showed a difference for prostaglandin D2 (PGD2) (EM vs CG) and 15-hydroxyeicosatetraenoic acid (15-HETE) (TBE vs CG). However, the results in the level of phospholipid metabolites from patients after therapy did not show statistically significant differences compared to the value before treatment and between groups. Tick-borne diseases are accompanied by changes in lipid metabolism, both ROS- and enzyme-dependent, which can be identified even in urine. Urinary lipid mediators show potential as supportive markers but require validation in larger patient cohorts.
PMID:41764219 | DOI:10.1038/s41598-026-40464-z
