1. Regulation of Chlamydia Development and Stress Responses
Chlamydia undergoes a developmental cycle that alternates between the infectious elementary body (EB) and the proliferative reticulate body (RB). EBs enter host cells and differentiate into RBs within cytoplasmic vacuoles known as inclusions. Following several rounds of replication, RBs differentiate back into EBs, which exit host cells through either host cell rupture or inclusion extrusion.
This biphasic development can be disrupted by various stressors, leading to the formation of abnormally large RBs termed aberrant bodies (ABs), which cannot differentiate into EBs. This suspension of normal RB replication and EB formation is called chlamydial persistence. Persistence is a major factor in chlamydial pathogenesis, as it can be triggered by host defense mechanisms or antibiotic treatment. When the stress subsides, ABs revert to RBs, resuming the productive developmental cycle. Persistence contributes significantly to treatment failure and chronic infections, leading to complications such as infertility.
We study the regulation of the chlamydial developmental cycle and stress responses. Our investigations have revealed transcriptomic signatures linked to different developmental stages and identified regulators essential for progeny formation. Additionally, we have discovered regulators critical for stress responses. Our ongoing work aims to uncover the mechanisms underlying these two classes of regulators and their roles in shaping chlamydial biology.
2. Development of Novel Chlamydia Vaccines
Despite decades of research, no licensed Chlamydia vaccine is currently available. Our lab is pioneering novel approaches to vaccinology, focusing on developing live attenuated Chlamydia vaccines to prevent chlamydial diseases.