4 research outputs found

    Indomethacin treatment slows disease progression and enhances a Th1 response in susceptible BALB/c mice infected with Leishmania major.

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    Submitted by Ana Maria Fiscina Sampaio ([email protected]) on 2014-07-10T12:30:06Z No. of bitstreams: 1 Freitas LA Indomethacin treatment slows....pdf: 120581 bytes, checksum: c18d299d9b2068ca5c74e80986fe775a (MD5)Made available in DSpace on 2014-07-10T12:30:06Z (GMT). No. of bitstreams: 1 Freitas LA Indomethacin treatment slows....pdf: 120581 bytes, checksum: c18d299d9b2068ca5c74e80986fe775a (MD5) Previous issue date: 1999Fundação Oswaldo Cruz. Centro de Pesquisa Gonçalo Moniz. Laboratório de Patologia e Biologia Celular. Salvador, BA, BrasilColorado State University. Department of Pathology. College of Veterinary Medicine and Biomedical Sciences. Fort Collins, USAColorado State University. Department of Pathology. College of Veterinary Medicine and Biomedical Sciences. Fort Collins, USAColorado State University. Department of Pathology. College of Veterinary Medicine and Biomedical Sciences. Fort Collins, USAColorado State University. Department of Pathology. College of Veterinary Medicine and Biomedical Sciences. Fort Collins, USAProstaglandins of the E series inhibit the development of Th1 responses. When infected with Leishmania major, BALB/c mice fail to develop a Th1 response, but instead mount a Th2 response and die of the disease. Therefore, we treated L. major-infected BALB/c mice with indomethacin, which inhibits prostaglandin production. Indomethacin lessened disease severity (parasite burden and pathology), and promoted a Th1 response, but the mice still succumbed to infection. The explanation for these observations may be two-fold: (1) the beneficial effects of indomethacin were predominantly observed later in infection (beyond two weeks), a time at which indomethacin was unable to sufficiently block the development of a Th2 response; (2) indomethacin was unable to induce a Th1 response in BALB/c mice that was of the same magnitude as the Th1 response observed in C57BL/6 mice infected with L. major
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