Course of Brugia malayi infection in C57BL/6J NOS2 +/+ and -/- mice

Previous results from our laboratory using pharmacological approaches suggested a role for nitric oxide (NO) in the host defense against the human filarial parasite, Brugia malayi. We sought to determine whether a complementary genetic approach, using mice homozygous for a targeted mutation in the gene encoding inducible nitric oxide-synthase (NOS2), would confirm our observation. We hypothesized that such mice would exhibit some deficit in their ability to clear B. malayi. Our data show that the course of infection in NOS2-/- mice is the same as in wild-type mice. Thus, peritoneal cellular responses to infection are similar in NOS2-/- and wild-type mice, with the exception that T cells form a higher percentage of total peritoneal cells in the former. We find virtually no serum IgE in NOS2-/- mice, suggesting a less robust Th2 response. In contrast, NOS2-/- mice demonstrate an early rise in IgG2a titers compared to B6 +/+ mice. Our data suggest that NO is not an obligate requirement for the elimination of B. malayi from the peritoneal cavities of mice.