Modulation of immune responses to helminth infections by concurrent protozoan pathogens has been shown in many human epidemiological studies. We established a murine model of coinfection with an intracellular apicomplexan, E. falcifomis, and the gastrointestinal helminth N. brasiliensis. The role of Stat 6 (signal transducers and activators of transcription) and Stat4 in the recruitment of eosinophils during coinfection with both parasites was investigated. Results of this study demonstrated that eosinophil responses occur in a Stat6-dependent manner in mice infected with the intestinal nematode, N. brasiliensis. Prominent blood eosinophilia was induced in wild type Balb/c mice, whereas in Stat6 ^-/- mice eosinophil responses were considerably reduced. Reversal of blood eosinophil profile was noted in N. brasiliensis-infected Stat4-deficient mice. Oral infection with E. falciformis of Stat6^-/-, Stat4^-/-, and wild type mice following N. brasiliensis infection inhibited the development of T_H2-associated peripheral eosinophilia. Mortality of coinfected Stat6-deficient mice was higher than that of Stat4 and wild type mice. Splenocytes of Stat6 ^-/- mice produced lower levels of interferon-gamma during concurrent infection with E. falciformis than Stat6-deficient mice infected with N. brasiliensis alone; suggesting alternative mechanisms of cytokine production. These results demonstrate that a concurrent infection with the protozoan, E. falciformis strongly modulates multiple aspects of an established T_H2 immunity to N. brasiliensis and consequently impairs the development of protective immunity to this intestinal helminth infection.