Inhibition of Chlamydia trachomatis growth by recombinant tumor necrosis factor

Shemer‐Avni, Yonat; Wallach, David; Sarov, Israel

doi:10.1128/iai.56.9.2503-2506.1988

Cited by 101 publications

(57 citation statements)

References 26 publications

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“…In our study, C. trachomatis infection also up-regulated the cervical production of TNF-a which plays an important role in the initiation of inflammatory response. It is reported that TNF-a displays antichlamydial properties [34] and infertility associated with endometriosis is related to the production of TNF-a in the mouse genital tract [35]. Marginal increase in IL-1 was observed in the cervix in this study.…”

Section: Discussionsupporting

confidence: 58%

Cytokine expression pattern in the genital tract ofChlamydia trachomatispositive infertile women – implication for T-cell responses

Reddy

Rastogi

Das

et al. 2004

Clinical and Experimental Immunology

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SUMMARYHuman genital infection caused by C hlamydia trachomatis is thought to be immunologically mediated, resulting in local recruitment of lymphocyte subsets and inducing the production of cytokines. Little information is available about the role of lymphocyte recruitment and the regulation of cytokine production in the genital tract of C. trachomatis positive infertile women. We have evaluated the recruitment of lymphocyte subsets in the genital tract and production of Th1/Th2 cytokines in cervical secretions and laparoscopic specimens from the fallopian tubes of C. trachomatis positive infertile women ( n = 17) and compared them with controls, viz. C. trachomatis negative infertile women ( n = 20) using ELISA and flow cytometry. None of these patients were found to be infected either with Candida sps., bacterial vaginosis, Trichomonas vaginalis , Neisseria gonorrhoeae, Mycoplasma hominis or Ureaplasma urealyticum in the cervix. Flow cytometric analysis of cervical secretions in Chlamydia positive women revealed recruitment of both CD4 and CD8 lymphocytes to the genital tract was up-regulated and a variation in the production rates of different cytokines in cervical secretions and fallopian tube was observed. We found that the immune responses in cervical secretions were of Th0 type, since all the analysed cytokines, viz. IFN-g , TNF-a , IL-10 and IL-12 were up-regulated. As, both CD4 and CD8 cells contribute to the production of IFN-g and IL-10, these results suggest that along with CD4 cells, CD8 lymphocytes also may be important for local regulation of Th1/Th2 responses in the genital tract during C. trachomatis infection.

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Section: Discussionsupporting

confidence: 58%

Cytokine expression pattern in the genital tract ofChlamydia trachomatispositive infertile women – implication for T-cell responses

Reddy

Rastogi

Das

et al. 2004

Clinical and Experimental Immunology

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“…As with many anti-inflammatory agents, these therapies cause immunosuppression; hence, their use has also been linked to serious adverse events, most notably to an increased risk of infection (Bongartz et al, 2006;Curtis et al, 2007;Salliot et al, 2007). In vitro inhibition of TNF-a has been associated with enhanced fungal growth in human monocytes and alveolar macrophages and enhanced growth of Chlamydia trachomatis in human epithelial cell lines (Shemer-Avni et al, 1988;Wood et al, 2003).…”

Section: Introductionmentioning

confidence: 99%

In vitroneutralization of tumor necrosis factor-Î± duringChlamydia pneumoniaeinfection impairs dendritic cells maturation/function and increases chlamydial progeny

Njau

Wittkop

Rohde

et al. 2009

FEMS Immunology &Amp; Medical Microbiology

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Dendritic cells (DCs) produce tumor necrosis factor (TNF)-alpha upon infection and contribute in various ways to defense against pathogenic agents. Several biological agents have been designed to inhibit TNF-alpha activity. However, the use of these inhibitors has been associated with an increased rate of certain opportunistic infections. To study the effect of TNF-alpha inhibition, human monocyte-derived DCs were infected with Chlamydia pneumoniae. TNF-alpha was neutralized by adalimumab, a human anti-TNF-alpha monoclonal antibody. Chlamydiae induced the maturation of DC as determined by flow cytometry and quantitative real-time PCR. However, DC maturation was impaired in the presence of adalimumab. Moreover, neutralization of TNF-alpha resulted in a significant increase of infectious progeny, 16S rRNA gene copy number and development of larger inclusions consisting of different stages of chlamydial development. Additionally, chlamydial infection induced secretion of cytokines/chemokines, which were downregulated by adalimumab treatment. Our data reveal an indirect effect on maturation of DC by C. pneumoniae and that maturation is crucial for the restriction of chlamydial development. The results also demonstrate an increase in infectious progeny after TNF-alpha inhibition, suggesting a contribution of TNF-alpha produced by DCs to chlamydial growth arrest. These data suggest a possible mechanism by which TNF-alpha inhibition enhances the risk of intracellular infections.

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“…Draining lymph node cells from both BALB/c and C3H mice yielded predominantly IFN-␥ and TNF-␣ with a little IL-10. Although IFN-␥ and TNF-␣ have protective effects (8,12,27,38) and have also been implicated in pathology (1,6,36), production by BALB/c and C3H lymph node cells was similar. Darville et al have recently reported more severe genital tract disease in C3H mice than in C57 mice despite a dominant Th1 response in both strains (9).…”

Section: Discussionmentioning

confidence: 90%

Protection against Ascending Infection of the Genital Tract byChlamydia trachomatisIs Associated with Recruitment of Major Histocompatibility Complex Class II Antigen-Presenting Cells into Uterine Tissue

et al. 1998

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A mouse model of ascending infection following intravaginal inoculation with a strain of Chlamydia trachomatis isolated from humans has been used to identify immune mechanisms associated with protection against genital infection. BALB/c and C3H mice differed in their susceptibilities to infection and inflammatory disease. In both mouse strains, ascension of the organism and recruitment of bone marrow-derived mononuclear leukocytes were evident in uterine tissue 1 week postinfection. By 3 weeks the organism had been cleared and inflammation had been resolved in the BALB/c mice, but both persisted in the C3H animals. In athymic nude BALB/c mice both the organism and inflammation persisted, indicating the influence of the hosts' immune response on the outcome of infection. Both BALB/c and C3H mice had a Th1 response in draining lymph nodes, with predominant production of gamma interferon and tumor necrosis factor alpha, low levels of interleukin-10, and no detectable levels of interleukin-4. However, the composition of the early uterine infiltrate differed in these two mouse strains. Cell surface labeling and analysis of light scatter properties by flow cytometry identified a population of large, CD45 ؉ major histocompatibility complex class II mononuclear cells, which were a prominent feature of the infiltrates in BALB/c mice but were present in significantly lower numbers in C3H mice. These cells expressed the costimulatory molecules CD86 and CD40 and stimulated allogeneic T cells, suggesting that these mononuclear cells are a population of antigen-presenting cells and that they may play a role in clearing antigen and protecting against inflammatory disease in BALB/c mice. An additional level of immunological control may thus exist in genital chlamydial infection.

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Inhibition of Chlamydia trachomatis growth by recombinant tumor necrosis factor

Cited by 101 publications

References 26 publications

Cytokine expression pattern in the genital tract ofChlamydia trachomatispositive infertile women – implication for T-cell responses

Cytokine expression pattern in the genital tract ofChlamydia trachomatispositive infertile women – implication for T-cell responses

In vitroneutralization of tumor necrosis factor-Î± duringChlamydia pneumoniaeinfection impairs dendritic cells maturation/function and increases chlamydial progeny

Protection against Ascending Infection of the Genital Tract byChlamydia trachomatisIs Associated with Recruitment of Major Histocompatibility Complex Class II Antigen-Presenting Cells into Uterine Tissue

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