Discipline: Biological Sciences
David Martin - Alabama State University
Co-Author(s): Saurabh Dixit, Skyla Duncan, Shree R. Singh, and Vida A. Dennis, Center for NanoBiotechnology and Life Sciences Research, Alabama State University, AL
Chlamydia trachomatis (CT) is a Gram-negative, obligate intracellular pathogen and the most reported bacterial sexually transmitted pathogen globally. A hallmark of CT infection is its capacity to mount a massive inflammatory response such as pelvic inflammatory disease (PID) in the female genital tract. Suppressor of cytokine signaling (SOCS) proteins are negative regulators for various cytokines, and SOCS1 is known to negatively regulate IFN-Y signaling. We have observed that CT induced the up-regulation of SOCS1 in mouse J774 macrophages, which suggest that SOCS1 may act as a direct modulator of IFN-Y cytokine signaling in macrophages to control its own inflammation. The objective of this research project is to investigate the functional role of induced SOCS1 by CT on IFN-Y signaling in mouse J774 macrophages. Our hypothesis is that SOCS1 protein, induced by stimulation of macrophages with CT, inhibits the expression of IFN-Y and therefore prevents macrophage activation. Mouse macrophages were exposed to various concentrations of IFN-Y (12.5 to 50 ng/mL) and LPS (1 µg/mL) and TaqMan qRT-PCR was performed to assess expressions of SOCS1 mRNA gene transcripts, with SOCS3 serving as a control. We also performed western blot to assess SOCS protein expression. Our results showed that all concentrations of IFN-Y induced marked upregulation of SOCS1 in macrophages as compared to SOCS3 over a 24 hr time-period. Western blotting further confirmed the raised level of the corresponding SOCS1 protein. We have shown that CT has the capacity to regulate its own inflammation by inducing SOCS proteins. The ability of CT to also induce SOCS3 suggest that it may regulate other cytokines, like IL-6, in addition to IFN-Y. These results will uncover a potential mechanism of how CT controls its induced inflammation early after infection of the host. Studies are ongoing to determine the capacity of CT-induced SOCS1 to negatively regulate the expression of STAT1 (signal transducer and activator of transcription 1) in mouse macrophages.
Funder Acknowledgement(s): MSEIP (Minority Science and Engineering Improvement Program)
Faculty Advisor: Vida A. Dennis, firstname.lastname@example.org
Role: I performed all of the experiments within my research under minimal or no supervision.