Open AccessElevated levels of interleukin‐13 and IL‐18 in patients with dengue hemorrhagic fever
Author(s) -
Mustafa A.S.,
Elbishbishi E.A.,
Agarwal R.,
Chaturvedi U.C.
Publication year - 2001
Publication title -
fems immunology & medical microbiology
Language(s) - English
Resource type - Journals
eISSN - 1574-695X
pISSN - 0928-8244
DOI - 10.1111/j.1574-695x.2001.tb01575.x
Subject(s) - dengue fever , proinflammatory cytokine , immunology , pathogenesis , dengue virus , interleukin , cytokine , dengue hemorrhagic fever , biology , medicine , inflammation
Interleukin (IL)‐13 is produced by T helper 2 (Th2)‐type cells and inhibits the production of proinflammatory cytokines by activated monocytes, while IL‐18 is a pleiotropic cytokine that induces interferon‐γ and plays an important role in the development of Th1‐type cells. Role of the shift from a Th1‐type response to Th2‐type has been suggested in the pathogenesis of dengue hemorrhagic fever (DHF). This study was undertaken to investigate the possible protective/pathogenic role of IL‐13 and IL‐18 in patients with DHF. Sera were collected from a total of 84 patients with various grades of dengue illness and 21 normal healthy controls and tested for IL‐13 and IL‐18 levels using commercial enzyme‐linked immunosorbent assay kits. The results showed that very low levels of IL‐13 (4±3 pg ml −1 ) and IL‐18 (15±4 pg ml −1 ) were detected in the sera of healthy controls. In dengue patients, the levels of IL‐13 and IL‐18 were the highest in the patients with DHF grade IV (205±103 pg ml −1 and 366±155 pg ml −1 , respectively) and the lowest in patients with dengue fever (22±12 pg ml −1 and 76±50 pg ml −1 , respectively). Both the cytokines appeared (IL‐13=20±11 pg ml −1 and IL‐18=70±45 pg ml −1 ) during the first 4 days of illness and reached peak levels (IL‐13=204±96 pg ml −1 and IL‐18=360±148 pg ml −1 ) by day 9 onwards. The presence of high levels of IL‐13 and IL‐18 during severe illness and late phases of the disease suggests that both of these cytokines may contribute to the shift from a Th1‐ to Th2‐type response and thus to the pathogenesis of DHF.