Dr Celli conducts a research program studying the mechanisms of intracellular survival and proliferation of Brucella abortus, the causative agent of the world-wide zoonotic disease brucellosis. Dr. Celli developed an interest in studying molecular aspects of brucellosis twelve years ago and has been recognized for his work on how Brucella subverts host cell functions to generate an intracellular replicative niche.
Dr. Celli’s primary research is in understanding:
- the functions of Type IV secretion effector proteins in Brucella abortus intracellular pathogenesis.
- the role of the host autophagy pathway in Brucella dissemination.
Brucella delivers into host cells an array of effector proteins via its VirB Type IV secretion system that modulates host functions to promote bacterial survival, proliferation, persistence and disease. Deciphering the functions of these effectors is key to a molecular understanding of Brucella pathogenesis. Additional research includes how Brucella subverts autophagy, a normally bactericidal host defense mechanism, to promote its dissemination during infection.
Dr Celli’s current work towards characterizing bacterial and host factors contributing to Brucella-host cell interactions can be used to define targets for the development of new treatments against the disease.
Dr. Celli is an associate professor in the Paul G. Allen School for Global Animal Health.
Figure 1: Human HeLa cell infected with Brucella abortus (red) for 72h showing extensive bacterial replicationa dn formation of autophagic bacterial vacuoles (green) that promote bacterial release.