In vivo prenatal chlordane exposure induces development of endogenous inflammatory macrophages.

Macrophages (m phi s), important cells in host resistance, undergo a series of biochemical changes during their progression from the resident to the fully activated stage. Both resident and inflammatory m phi s are characterized by some unique properties. In the present study, female BALB/c mice were prenatally treated with 8 mg/kg body weight of chlordane, a cyclodiene poly-chlorinated hydrocarbon that appears to reduce immunocompetence by selectively impairing m phi function. Therefore, we examined functions in m phi s from chlordane-treated mice that had been stimulated with thioglycollate. The 5'-nucleotidase activity, present in high levels in resident m phi s but low levels in inflammatory m phi s was elevated in resident m phi s from vehicle-exposed animals. Conversely, inflammatory m phi s from these animals showed significantly diminished levels of this function. Moreover, chlordane-exposed m phi s, regardless of whether they were resident or inflammatory, exhibited decreased 5'-nucleotidase responses. When a second function, transferrin receptor binding, was analyzed, vehicle-treated inflammatory m phi s displayed high levels of activity whereas the resident m phi s showed very little transferrin binding. However, both resident and inflammatory m phi s from the chlordane-exposed group demonstrated transferrin binding activity similar in magnitude to that of the vehicle-treated inflammatory m phi s. Finally, two-dimensional polyacrylamide gel electrophoresis analysis of m phi s from chlordane-exposed mice have characteristics of normal m phi s that have advanced to the inflammatory stage.