Tritrichomonas foetus: pathogenesis of acute infection in normal, estradiol-treated, and stressed mice.

Tritrichomonas foetus: pathogenesis of acute infection in normal, estradiol-treated, and stressed mice. Research Abstract Details 

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Tritrichomonas foetus: pathogenesis of acute infection in normal, estradiol-treated, and stressed mice. Abstract Text:

Melanie R Rutkowski,Allen G Harmsen,

Environmental stress and endocrine control can affect pathogenesis of sexually transmitted diseases such as trichomoniasis. Acute Tritrichomonas foetus infection was compared in female BALB/c mice to infections in mice treated with high doses of estradiol or housed in constant bright illumination (stressed). In untreated mice, T. foetus readily colonized the reproductive tract, causing minimal epithelial damage and inflammation. Several fold increases of IFN-gamma, TNF-alpha, MCP-1, and IL-6 cytokines were detected after estradiol-treatment of mice, resulting in greatly enhanced inflammation and tissue damage throughout the reproductive tract. Interestingly, estradiol-treatment of mice resulted in reduced T. foetus colonization compared to untreated mice. Infection in stressed mice resulted in increased tissue damage, inflammation, and inflammatory cytokine expression, although parasite colonization within the reproductive tract was similar to that in untreated mice. These results indicate that either estradiol-treatment or stress result in pathogenesis often observed during severe disease. Alternatively, infection in non-treated mice results in chronic colonization, with little inflammation or pathology.

Tritrichomonas foetus: pathogenesis of acute infection in normal, estradiol-treated, and stressed mice. Publishing Authors By Initials

MR Rutkowski,AG Harmsen,

For similar animals: invertebrates: protozoa: sarcomastigophora: mastigophora: zoomastigophora: trichomonadida: tritrichomonas: tritrichomonas foetus research abstracts see: animals: invertebrates: protozoa: sarcomastigophora: mastigophora: zoomastigophora: trichomonadida: tritrichomonas: tritrichomonas foetus research

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Tritrichomonas foetus: pathogenesis of acute infection in normal, estradiol-treated, and stressed mice. Journal Published:

PUBLICATION TYPE: Research Support, N.I.H., Extr

Journal: Experimental parasitology

VOLUME: 115

Page Numbers: 143-59

Journal Abbreviation: Exp. Parasitol.

ISSN: 0014-4894

DAY: 2

MONTH: 10

YEAR: 2006

Tritrichomonas foetus: pathogenesis of acute infection in normal, estradiol-treated, and stressed mice. Information

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LANGUAGE: eng

NlmUniqueID: 370713

Tritrichomonas foetus: pathogenesis of acute infection in normal, estradiol-treated, and stressed mice. Keywords Mesh Terms:

KEYWORDS: Tritrichomonas foetus

MESH TERMS: pathogenicity

Chemical & Substance for Abstract: Tritrichomonas foetus: pathogenesis of acute infection in normal, estradiol-treated, and stressed mice. Information

Substance Name: Estradiol

Registry Number: 50-28-2

Grant and Affiliation Information for Tritrichomonas foetus: pathogenesis of acute infection in normal, estradiol-treated, and stressed mice.

AFFILIATION: Department of Veterinary Molecular Biology, Montana State University, Molecular Biosciences Building, 960 Technology Blvd., Bozeman, MT 59718, USA. mellyrae@earthlink.net

Country: United States

AGENCY: United States NCRR

GRANT: 1P20RR020185

ACRONYM: RR

MEDLINETA: Exp Parasitol

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