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DOI 10.1016/j.molimm.2018.12.007

Медицинская библиотека · Molecular immunology · 2018

Chlamydia trachomatis ct143 stimulates secretion of proinflammatory cytokines via activating the p38/MAPK signal pathway in THP-1 cells.

Jia Lina, Sun Feng, Wang Jie, Gong Ding, Yang Lina

СтатьяПоддержка исследования: вне правительства СШАПеревод в очереди

Аннотация

Chlamydia trachomatis (Ct) infections can cause bacterial sexually-transmitted and preventable blindness. The Ct infections induced excessive cytokines generation which attributed to pathologic changes in host cells. However, the precise mechanisms of Ct-induced cytokines production are still unclear.CT143 protein was identified as a novel Ct specific protein with high immunogenicity. In the present study. The CT143 fusion protein was recombined and purified. The mice immune serum was prepared by immunizing BALB/c mice with the purified fusion protein. The specificity of the antibody was confirmed using Immunoblotting. Indirect immunoflurescence assay (IFA) and Immunoblotting assays were performed to detect the temporal and spatial characteristics of CT143 in Ct infected cells. ELISA was performed to analyze the secretion of proinflammatory cytokines IL-1β, IL-8 and TNF-α by human macrophages under the stimulation of CT143 protein. Finally, the involvement of p38 signaling in CT143-induced cytokine secretion was validated. CT143 protein was located in the inclusion body and represented an Elementary body (EB)-related protein, which may be encoded by the mid- and late-stage expressing genes. CT143 protein could stimulate the secretion of inflammatory cytokines in macrophages which differentiated from THP-1 This induction may be mediated by the activation of p38 signaling. In summary, CT143 protein is involved in inflammatory processes during Ct infection.

Для цитирования: Jia Lina, Sun Feng, Wang Jie, Gong Ding, Yang Lina. Chlamydia trachomatis ct143 stimulates secretion of proinflammatory cytokines via activating the p38/MAPK signal pathway in THP-1 cells.. Molecular immunology. 2018. DOI: 10.1016/j.molimm.2018.12.007.

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