The following is a summary of “Cytokines CXCL10 and CCL2 and the Kynurenine Metabolite Anthranilic Acid Accurately Predict Patients at Risk of Developing Dengue With Warning Signs” published in the December 2022 issue of Infectious Disease by Jusof et al.
The patient’s immune response during the crucial period determines whether the dengue infection will clear up or get worse. Immune cells generate more cytokines when dengue infections become more severe. The degree to which the kynurenine pathway (KP) is activated as a result of cytokines then determines the severity of the illness.
Plasma samples from individuals with dengue infection (dengue without warning signs [DWS–], dengue with warning signs [DWS+], or severe dengue) were examined for KP metabolites and cytokines. Cytokines (interferon gamma [IFN-ɣ], tumor necrosis factor, interleukin 6, CXCL10/interferon-inducile protein 10 [IP-10], interleukin 18 [IL-18], CCL2/monocyte chemoattractant protein-1 [MCP-1], & CCL4/macrophage inflammatory protein-1beta [MIP-1β]) and KP metabolites (tryptophan, kynurenine, anthranilic acid [AA], picolinic acid, & quinolinic acid) were assessed by ultra-high-performance liquid chromatography & Gas Chromatography Mass Spectrophotometry [GCMS] assays.
When the kynurenine-tryptophan ratio, anthranilic acid, and picolinic acid were high, the KP was more activated in patients with DWS+. In addition, these individuals’ levels of the cytokines IFN-ɣ, CXCL10, CCL4, and IL-18 were greater than those of those with DWS–. Three prognostic biomarker candidates—CXCL10, CCL2, and AA—were discovered using further receiver operating characteristic analysis, and they accurately indicated individuals who were more likely to develop DWS+, with an accuracy of 97%.
The information points to a distinctive metabolic profile in DWS+ patients. Potential prognostic biomarkers include CXCL10, CCL2, and AA, which can identify individuals at increased risk of developing DWS+ at earlier stages of infection.
Reference: academic.oup.com/jid/article-abstract/226/11/1964/6619611?redirectedFrom=fulltext
