Complement activation in SCID and nude mice is related to severity of tissue inflammation in the Candida mastitis model

Abstract A small animal model of localised candidiasis is needed for the evaluation of new antifungal compounds. Mammary glands of immunocompetent (BALB/cJ) and immunodeficient (SCID and athymic nude) mice were infected with a wild-type of Candida albicans. Some of the animals were treated with amph...

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Published inFEMS microbiology letters Vol. 192; no. 1; pp. 27 - 31
Main Authors Guhad, Faisal A., Jensen, Henrik E., Hau, Jann
Format Journal Article
LanguageEnglish
Published Oxford, UK Blackwell Publishing Ltd 01.11.2000
Blackwell
Oxford University Press
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Summary:Abstract A small animal model of localised candidiasis is needed for the evaluation of new antifungal compounds. Mammary glands of immunocompetent (BALB/cJ) and immunodeficient (SCID and athymic nude) mice were infected with a wild-type of Candida albicans. Some of the animals were treated with amphotericin B (AmB) while others were treated with saline and acted as controls. The histologic changes of infected mammary gland tissues and a number of other organs were evaluated. Complement (C) activation was analysed by immunoelectrophoretic quantification of molecules with C3c epitopes (C3, C3b, iC3b, and C3c) in serum. In all animals the organisms were confined to the mammary glands. Serum C3c levels were significantly higher (P<0.05) in infected untreated BALB/cJ and SCID mice, which also had severe mammary gland tissue inflammation, compared with control mice treated with AmB (4 mg kg−1 i.p. once daily for 4 days). Both treated and control nude mice showed less tissue inflammation compared to BALB/cJ and SCID mice, and revealed insignificant activation of the complement system. It is concluded that innate immune response is important in the control of candidiasis and that the murine mastitis model is useful for immunopathological studies as well as evaluation of potential antifungal compounds.
Bibliography:1
Department of Veterinary Sciences, University of Texas, MD Anderson Cancer Center, Science Park, Route 2, P.O. Box 151‐B1, Bastrop, TX 78602, USA.
ObjectType-Article-1
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ISSN:0378-1097
1574-6968
DOI:10.1111/j.1574-6968.2000.tb09354.x