Pineda Maria Ruth B*, Ramos and John A Donnie
Allergy is highly prevalent in well-developed countries; hygiene hypothesis suggests that this is due to exposure to previous bacterial infection eliciting Th1-response that suppresses Th2-mediated responses. Aside from Th2 suppressing Th1-responses, Th2-mediated infections such as parasitism, appear to lower the risk of developing allergy. This study investigates the effects of Ascaris suum infection in Dermatophagoides pteronyssinus-induced allergic BALB/c mice. Ninety BALB/c mice divided into three trials were randomly grouped into: normal control (1), A. suum infected mice (2), D. pteronyssinus exposed mice (3), A. suum infected mice and then exposed to D. pteronyssinus (4), D. pteronyssinus exposed mice and then infected with A. suum (5), and mice exposed and infected with D. pteronyssinus and A. suum, simultaneously (6). Blood and fecal samples were collected at days 0, 36, and 72 for the measurement of cytokines and immunoglobulins through ELISA, and for fecal analysis. Results showed that A. suum infection suppressed D. pteronyssinus-induced allergy morphologically and histologically and downregulated the production of D. pteronyssinus-specific IgE. A. suum and D. pteronyssinus upregulated the production of IL-4 and IL-5, and only A. suum eggs enhanced the production of IL-10. D. pteronyssinus enhanced production of both D. pteronyssinus-specific and A. suum-specific IgE and IgG and may be accounted to crossreacting antigens present in D. pteronyssinus and A. suum. IL-10 is upregulated in mice with A. suum infection and appears to protect mice against D. pteronyssinus-induced allergy. The possible role of IL-10 production in response to A. suum infection and against D. pteronyssinus-induced allergy needs further investigation.