Open AccessRole of interleukin‐12 in patients with dengue hemorrhagic fever
Author(s) -
Pacsa A.S,
Agarwal R,
Elbishbishi E.A,
Chaturvedi U.C,
Nagar R,
Mustafa A.S
Publication year - 2000
Publication title -
fems immunology & medical microbiology
Language(s) - English
Resource type - Journals
eISSN - 1574-695X
pISSN - 0928-8244
DOI - 10.1111/j.1574-695x.2000.tb01470.x
Subject(s) - dengue fever , pathogenesis , immunology , cytokine , peripheral blood mononuclear cell , dengue virus , interleukin , dengue hemorrhagic fever , biology , interleukin 6 , medicine , in vitro , biochemistry
Interleukin (IL)‐12 has a broad range of activities including regulation of cytokine synthesis and selective promotion of Th1‐type cell development. A shift from a Th1‐type response to Th2‐type has been suggested to be important in the pathogenesis of dengue hemorrhagic fever (DHF). This study was undertaken to investigate the possible role of IL‐12 in this shift. A total of 76 patients with various grades of dengue illness and 21 normal healthy controls were tested for IL‐12 levels in serum samples and IL‐12 mRNA in their peripheral blood mononuclear cells. The results showed that the levels of IL‐12 were the highest in patients with dengue fever (270±102 pg ml −1 ) followed by decreasing levels in the patients with DHF grade I (198±86 pg ml −1 ; P <0.05 ) and DHF grade II (84±52 pg ml −1 ; P <0.001 ). Neither IL‐12 nor its mRNA could be detected in the patients with DHF grades III and IV. The cytokine appeared and reached peak levels during the first 4 days of illness, started to decline by day 5–8 and disappeared by day 9 onwards. The absence of IL‐12 during severe illness and late phases of the disease may be responsible for the shift to a Th2‐type response and thus for the pathogenesis of DHF.