Discipline: Biological Sciences
Room: Exhibit Hall A
Etinosa Iyayi - Tuskegee University
Co-Author(s): Ramesh Kumar, Indiana University, Indianapolis, Indiana ;Nicole Ramos-Solis, Indiana University, Indianapolis, Indiana; Wilbert A. Derbigny, Indiana University,Indianapolis, Indiana.
Chlamydia is the most widespread bacterial sexually transmitted disease and is commonly transmitted through vaginal, oral, and anal sex with an infected person. This sexually transmitted disease, caused by Chlamydia trachomatis, could result in damage of the female reproductive system, ovarian scaring, and ectopic pregnancy in humans. The main purpose of our study is to determine the role of the Interferon-β in the immune response to this Chlamydia infection. We previously reported that a disruption in TLR3 function leads to a reduction in several cytokines and chemokines including interferon-β (IFN-β) synthesis. Our data showed that disruption in IFN-β function causes an increase in Chlamydia inclusion and genital tract fibrosis, as well as a dysregulation in the gene expression and protein activation of multiple inflammatory mediators. To determine the mechanism of how IFN-β function affects the outcome of genital tract Chlamydia infection, we investigated the role of IFN-β by comparing outcomes of infection between the IFN-β knockout mice and wild type mice C57BL/6 as a control. Quantitative real-time polymerase chain reaction (qPCR) was used to analyze the genes linked with various cell- signaling components associated with the immune response to Chlamydia infection in IFN-β knockout mice and wild type mice. Our qPCR data showed IFN-β knockout mice had an increase in Chlamydia replication and a significant decrease in IL-6 synthesis. From the data, we hypothesize that the interferon-β knockout mice will suffer increased Chlamydia-caused genital tract pathology when compared to wild type mice.
Funder Acknowledgement(s): IUPUI; IU School of Medicine; This work is supported by Grant: National Institutes of Health (NIH) Grant R01AI104944
Faculty Advisor: Wilbert A. Derbigny, firstname.lastname@example.org
Role: I took part in optimizing the qPCR database used in the lab for better understanding of mutations made in the Toll like receptor (TLR3). Also, I play a role as a collaborator under transactional study from mice to human.