دورية أكاديمية

Inhibition of apoptosis by gamma interferon in cells and mice infected with Chlamydia muridarum (the mouse pneumonitis strain of Chlamydia trachomatis)

التفاصيل البيبلوغرافية
العنوان: Inhibition of apoptosis by gamma interferon in cells and mice infected with Chlamydia muridarum (the mouse pneumonitis strain of Chlamydia trachomatis)
المؤلفون: Perfettini, Jean-Luc, Darville, Toni, Dautry-Varsat, Alice, Rank, Roger G., Ojcius, David M.
المصدر: All Dugoni School of Dentistry Faculty Articles
بيانات النشر: Scholarly Commons
سنة النشر: 2002
المجموعة: University of the Pacific, McGeorge School of Law: Scholarly Commons
مصطلحات موضوعية: Biochemistry, Biophysics, and Structural Biology, Immunity, Immunology of Infectious Disease, Life Sciences, Medical Immunology, Medicine and Health Sciences
الوصف: The effect of gamma interferon (IFN-γ) on apoptosis due to infection by Chlamydia muridarum (the mouse pneumonitis strain of Chlamydia trachomatis) was studied in epithelial cells in culture and in the genital tracts of mice. IFN-γ concentrations that induce the formation of aberrant, persistent chlamydiae inhibit apoptosis due to C. muridarum infection. In cells treated with an IFN-γ concentration that leads to the development of a heterogenous population of normal and aberrant Chlamydia vacuoles, apoptosis was inhibited preferentially in cells that contained the aberrant vacuoles. The inhibitory effect of IFN-γ appears to be due in part to expression of host cell indoleamine 2,3-dioxygenase activity, since inhibition of apoptosis could be partially reversed through coincubation with exogenous tryptophan. Apoptotic cells were observed in the genital tracts of wild-type mice infected with C. muridarum, and a significantly larger number of apoptotic cells was detected in infected IFN-γ-deficient mice. These results suggest that IFN-γ may contribute to pathogenesis of persistent Chlamydia infections in vivo by preventing apoptosis of infected cells.
نوع الوثيقة: text
وصف الملف: application/pdf
اللغة: unknown
العلاقة: https://scholarlycommons.pacific.edu/dugoni-facarticles/147Test; https://scholarlycommons.pacific.edu/context/dugoni-facarticles/article/1146/viewcontent/Infect._20Immun._2002_Perfettini_2559_65.pdfTest
DOI: 10.1128/IAI.70.5.2559-2565.2002
الإتاحة: https://doi.org/10.1128/IAI.70.5.2559-2565.2002Test
https://scholarlycommons.pacific.edu/dugoni-facarticles/147Test
https://scholarlycommons.pacific.edu/context/dugoni-facarticles/article/1146/viewcontent/Infect._20Immun._2002_Perfettini_2559_65.pdfTest
رقم الانضمام: edsbas.EF9089F1
قاعدة البيانات: BASE