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РЖ ВИНИТИ 34 (BI39) 97.02-04К1.156

Igietseme, J. U.
The molecular mechanism of T-cell control of Chlamydia in mice: Role of nitic oxide [Text] / J. U. Igietseme // Immunology. - 1996. - Vol. 87, N 1. - P1-8 . - ISSN 0019-2805
Перевод заглавия: Молекулярный механизм T-клеточного контроля хламидий у мышей. Роль оксида азота
Аннотация: T-cell mediated immunity (CMI) is crucial for protection against genital chlamydial infection in mice. Several T-cell clones generated against the Chlamydia trachomatis agent of mouse pneumonitis (MoPn) were analysed in an in vitro model of the mucosal epithelium, the polarized epithelial-lymphocyte co-culture (PELC) system, for immunobiological functions that correlated with chlamydial inhibition. The results revealed a direct relationship between the ability of a clone to protect in vivo and to inhibit the multiplication of MoPn in vitro. The protective ability of a clone correlated with its capacity to elaborate relatively high levels of interferon-'гамма' (IFN-'гамма') and to induce nitric oxide (NO) production. Neutralizing anti-IFN-'гамма' antibodies used alone at 50 'мю'g/ml or in combination with anti-tumour necrosis-factor (TNF-'альфа'), and the L-arginine analogue and NO synthase inhibitor. N{G}-monomethyl-L-arginine monoacetate (MLA), could significantly suppress the ability of protective clones to inhibit MoPh in epithelial cells. The results suggested that the IFN-'гамма'-inducible NO synthease pathway is important for chlamydial control in mice. IFN-'гамма' could stimulate infected murine epithelial cells (line TM3) to secrete NO, resulting in inhibition of MoPn growth. The degree of MoPn inhibition obtained with IFN-'гамма' alone was less than that observed when T cells were co-cultured with infected epithelial cells. T-cell-derived NO could partly explain the enhanced chlamydial inhibition when T cells were co-cultured with infected epithelial cells. These results are consistent with the hypothesis that, besides T-cell-derived IFN-'гамма', other factors associated with lymphoepithelial interactions are likely to contribute an important role in chlamydial control by T cells in mice. США, Dep. Microbiol. and Immunol., Univ. Arkansas Med. Sci., Little Rock, AR 72205. Библ. 36

ГРНТИ	34.43.29

ВИНИТИ 341.43.29.11
Рубрики: ЛИМФОЦИТЫ T
АНТИБАКТЕРИАЛЬНЫЙ ЭФФЕКТ
МЕХАНИЗМЫ
ПОДАВЛЕНИЕ ХЛАМИДИАЛЬНОЙ ИНФЕКЦИИ
МЫШИ

РЖ ВИНИТИ 34 (BI14) 97.03-04Б4.222

Igietseme, J. U.
The molecular mechanism of T-cell control of Chlamydia in mice: Role of nitic oxide [Text] / J. U. Igietseme // Immunology. - 1996. - Vol. 87, N 1. - P1-8 . - ISSN 0019-2805
Перевод заглавия: Молекулярный механизм T-клеточного контроля хламидий у мышей. Роль оксида азота
Аннотация: T-cell mediated immunity (CMI) is crucial for protection against genital chlamydial infection in mice. Several T-cell clones generated against the Chlamydia trachomatis agent of mouse pneumonitis (MoPn) were analysed in an in vitro model of the mucosal epithelium, the polarized epithelial-lymphocyte co-culture (PELC) system, for immunobiological functions that correlated with chlamydial inhibition. The results revealed a direct relationship between the ability of a clone to protect in vivo and to inhibit the multiplication of MoPn in vitro. The protective ability of a clone correlated with its capacity to elaborate relatively high levels of interferon-'гамма' (IFN-'гамма') and to induce nitric oxide (NO) production. Neutralizing anti-IFN-'гамма' antibodies used alone at 50 'мю'g/ml or in combination with anti-tumour necrosis-factor (TNF-'альфа'), and the L-arginine analogue and NO synthase inhibitor. N{G}-monomethyl-L-arginine monoacetate (MLA), could significantly suppress the ability of protective clones to inhibit MoPh in epithelial cells. The results suggested that the IFN-'гамма'-inducible NO synthease pathway is important for chlamydial control in mice. IFN-'гамма' could stimulate infected murine epithelial cells (line TM3) to secrete NO, resulting in inhibition of MoPn growth. The degree of MoPn inhibition obtained with IFN-'гамма' alone was less than that observed when T cells were co-cultured with infected epithelial cells. T-cell-derived NO could partly explain the enhanced chlamydial inhibition when T cells were co-cultured with infected epithelial cells. These results are consistent with the hypothesis that, besides T-cell-derived IFN-'гамма', other factors associated with lymphoepithelial interactions are likely to contribute an important role in chlamydial control by T cells in mice. США, Dep. Microbiol. and Immunol., Univ. Arkansas Med. Sci., Little Rock, AR 72205. Библ. 36

ГРНТИ	34.27.29

ВИНИТИ 341.27.29.21.09
Рубрики: ЛИМФОЦИТЫ T
АНТИБАКТЕРИАЛЬНЫЙ ЭФФЕКТ
МЕХАНИЗМЫ
ПОДАВЛЕНИЕ ХЛАМИДИАЛЬНОЙ ИНФЕКЦИИ
МЫШИ

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