ABSTRACT
Patients with bancroftian filariasis show a wide spectrum of clinical presentations often related to their immune responsiveness. The present study was designed to determine the role of host immune response and intensity of infection in the pathogenesis of bancroftian filariasis. In this study , 130 individuals seropositive for circulating filarial antigen [CFA] from endemic area for bancroftian filariasis with age ranged from 20- 60 years were subjected to, complete history taking , thorough clinical examination, midnight blood film and modified knott method for detection of microfilariae, then they were classified into the following groups. Group [I], 24 asymptomatic microfilaraemic patients, group [II] comprised 76 patients with chronic filariasis, all of them are amicrofilaraemic and group [III], 30 patients with symptomatic microfilaraemia presented with signs of acute filariasis. In addition to them 10 subjects from endemic area were included as endemic control group and 10 healthy subjects from non-filarial area were included as non-endemic control group. Circulating filarial antigen and anti-filarial specific IgG1 and IgG4 were quantitatively assessed by ELISA, Interleukin -2 [IL-2], interleukin - 4 [IL- 4] and tumor necrosis factor- alpha [TNF- alpha] were assessed in all groups by ELISA technique . The intensity of infection expressed in units of CFA/ml correlated positively with specific IgG1 and negatively with IgG4. Significant increase of CFA levels were encountered among group II and group III [2254.7 and 1985.8 respectively], than among group I and endemic control group [973.6 and 1349.2 respectively]. IL-2 significantly elevated in groups II and III in comparison to group I and endemic control. IL-4 was not significantly different among the three patients groups examined and TNF- alpha was significantly elevated in patients with acute filariasis [group III] only
Conclusion: as it is known that IgG1 is mainly controlled by cytokines Th1 response and IgG4 by Th2 response, the present study concluded that the antigen excess may have polarized Th0 response towards Th1 with consequent increase in its inflammatory cytokines that may have developed the recorded pathology