Host resistance of mice to Naegleria fowleri infections.
Naegleria fowleri is an etiological agent of primary amoebic meningoencephalitis in humans and laboratory animals. The determinative factors in host resistance of mice to N. fowleri infections have not been fully characterized. Male or female B6C3F1 mice stimulated by intraperitoneal administration of 10(6) amoebae of N. fowleri nN68 per mouse produced agglutinating activity and markedly elevated levels of serum and immunoglobulins M and G. Despite a marked humoral response, protective immunity was increased only marginally by active immunization. Host resistance was not impaired by prior treatment with 350 rads of 60Co radiation or 200 mg of cyclophosphamide per kg or by concurrent daily treatment with 30 mg of cyclophosphamide per kg for 14 days. Moreover, host resistance was not impaired by daily treatment with 4 mg of diethylstilbestrol per kg for 14 days, with challenge on day 2 of drug exposure or 24 h after the last drug treatment. Mice depleted of hemolytic complement by cobra venom factor were more susceptible to N. fowleri infection than were untreated mice.
D000372:Agglutination Tests; D000562:Amebiasis / Q000276:immunology*; D000656:Amoeba / Q000187:drug effects / Q000472:pathogenicity / Q000528:radiation effects; D000818:Animals; D003165:Complement System Proteins / Q000502:physiology; D003520:Cyclophosphamide / Q000494:pharmacology; D004054:Diethylstilbestrol / Q000494:pharmacology; D005260:Female; D007113:Immunity, Innate; D007136:Immunoglobulins / Q000032:analysis; D008214:Lymphocytes / Q000276:immunology; D008297:Male; D051379:Mice; D008815:Mice, Inbred Strains
D007136:Immunoglobulins; D004054:Diethylstilbestrol; D003520:Cyclophosphamide; D003165:Complement System Proteins