Dengue fever is usually a benign acute viral infection transmitted by arthropods but may evolve to
severe clinical manifestations such as coagulation and/or hemodynamic disorders, caused mainly by
an increase of vascular permeability. Deregulated circulating immunological factors have been associated
with severity. In Brazil severe cases appeared in children only recently and we evaluated the profile
of cytokine/chemokine kinetics in 134 hospitalized young patients during the epidemic in Rio de Janeiro
in 2008. Inflammatory cytokines TNF and IFN were found elevated during the acute phase in children
as well as the anti-inflammatory IL10 and chemokines MIF and CXCL10/IP10, all last three persisting
longer during the recovery phase. Severe disease fitting the dengue hemorrhagic fever pattern (WHO,
1997) was associated with higher IL10 and CXCL10/IP10 circulating levels (peak levels at seven days with
P < 0.01 and P < 0.001 respectively as compared to DF). These factors were higher in patients pulmonary
effusion or ascites (P < 0.05 for IL10 and P < 0.01 for CXCL10/IP10). Both factors were also associated with
liver changes such as AST increase correlated with CXCL10/IP10 (r = 0.4300 with P < 0.0001) and patients
presenting painful hepatomegaly showed higher circulating levels of IL10 (P < 0.01, at 7–9 days) and of
CXCL10/IP10 (P < 0.05, 4–6 days and P < 0.001, 7–9 days) when compared to patients without apparent
liver alterations. Most cases presented a history of prior infection (93%). This is the first study demonstrating
cytokine and chemokine association with severity during dengue fever in Brazilian children. IL10
and CXCL10/IP10 play a role in the disease severity associated with induction of vascular leakage and a
novel association with changes in liver dysfunction.