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

Previous results from our laboratory using pharmacological approaches sugge sted a role for nitric oxide (NO) in the host defense against the human fil arial parasite, Brugia malayi. We sought to determine whether a complementa ry genetic approach, using mice homozygous for a targeted mutation in the g ene encoding inducible nitric oxide-synthase (NOS2), would confirm our obse rvation. 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 re sponses to infection are similar in NOS2-/- and wild-type mice, with the ex ception 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 le ss 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 a n obligate requirement for the elimination of B. malayi from the peritoneal cavities of mice. (C) 2001 Academic Press.