Complement-Mediated Regulation of Trichomonas vaginalis Infection in Mice

P. Caterina; D. Lynch; R.B. Ashman; A. Warton; John Papadimitriou

doi:10.1159/000019101

Complement-Mediated Regulation of Trichomonas vaginalis Infection in Mice

P. Caterina, D. Lynch, R.B. Ashman, A. Warton, John Papadimitriou

Graduate Research School

Research output: Contribution to journal › Article › peer-review

3 Citations (Scopus)

Abstract

Trichomonas vaginalis is a flagellated protozoan which causes trichomoniasis, a sexually transmitted disease of the human genitourinary tract, The importance of the alternative complement pathway in host defence against T. vaginalis was investigated in vitro. Kinetic studies utilising immunofixation following electrophoresis showed that both a strongly and weakly virulent strain of T, vaginalis activated murine serum C3. In vivo studies with congenic-resistant, C5-deficient, B10.D2/OSn- and C5-sufficient, B10.D2/nSn mice showed that the presence of C5 is a significant factor in the innate host resistance to primary infection with a strongly virulent, but not a weakly virulent trichomonad strain.

Original language	English
Pages (from-to)	107-116
Journal	Experimental and Clinical Immunogenetics
Volume	16
Issue number	N/A
DOIs	https://doi.org/10.1159/000019101
Publication status	Published - 1999

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title = "Complement-Mediated Regulation of Trichomonas vaginalis Infection in Mice",

abstract = "Trichomonas vaginalis is a flagellated protozoan which causes trichomoniasis, a sexually transmitted disease of the human genitourinary tract, The importance of the alternative complement pathway in host defence against T. vaginalis was investigated in vitro. Kinetic studies utilising immunofixation following electrophoresis showed that both a strongly and weakly virulent strain of T, vaginalis activated murine serum C3. In vivo studies with congenic-resistant, C5-deficient, B10.D2/OSn- and C5-sufficient, B10.D2/nSn mice showed that the presence of C5 is a significant factor in the innate host resistance to primary infection with a strongly virulent, but not a weakly virulent trichomonad strain.",

author = "P. Caterina and D. Lynch and R.B. Ashman and A. Warton and John Papadimitriou",

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doi = "10.1159/000019101",

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T1 - Complement-Mediated Regulation of Trichomonas vaginalis Infection in Mice

AU - Caterina, P.

AU - Lynch, D.

AU - Ashman, R.B.

AU - Warton, A.

AU - Papadimitriou, John

PY - 1999

Y1 - 1999

N2 - Trichomonas vaginalis is a flagellated protozoan which causes trichomoniasis, a sexually transmitted disease of the human genitourinary tract, The importance of the alternative complement pathway in host defence against T. vaginalis was investigated in vitro. Kinetic studies utilising immunofixation following electrophoresis showed that both a strongly and weakly virulent strain of T, vaginalis activated murine serum C3. In vivo studies with congenic-resistant, C5-deficient, B10.D2/OSn- and C5-sufficient, B10.D2/nSn mice showed that the presence of C5 is a significant factor in the innate host resistance to primary infection with a strongly virulent, but not a weakly virulent trichomonad strain.

AB - Trichomonas vaginalis is a flagellated protozoan which causes trichomoniasis, a sexually transmitted disease of the human genitourinary tract, The importance of the alternative complement pathway in host defence against T. vaginalis was investigated in vitro. Kinetic studies utilising immunofixation following electrophoresis showed that both a strongly and weakly virulent strain of T, vaginalis activated murine serum C3. In vivo studies with congenic-resistant, C5-deficient, B10.D2/OSn- and C5-sufficient, B10.D2/nSn mice showed that the presence of C5 is a significant factor in the innate host resistance to primary infection with a strongly virulent, but not a weakly virulent trichomonad strain.

U2 - 10.1159/000019101

DO - 10.1159/000019101

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VL - 16

SP - 107

EP - 116

JO - Experimental and Clinical Immunogenetics

JF - Experimental and Clinical Immunogenetics

IS - N/A

ER -

Complement-Mediated Regulation of Trichomonas vaginalis Infection in Mice

Abstract

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