VMP Adjunct Faculty
- WSU Paul G. Allen School for Global Health (primary appointment)
- School of Molecular Biosciences, WSU (affiliate faculty)
- Department of Veterinary Microbiology and Pathology, WSU (affiliate faculty)
- American Society of Microbiology (ASM)
- American Association for the Advancement of Science (AAAS)
Dr. Celli obtained his PhD from the Université Pierre & Marie Curie, Paris 6, France in 1997. His thesis focused on genetic mobile elements that transfer antibiotic resistance among pathogenic bacteria. He moved in 1998 to Vancouver, Canada, for a postdoctoral position in bacterial pathogenesis in the laboratory of Dr. B. Brett Finlay at the University of British Columbia, where he studied how Enteropathogenic Escherichia coli (EPEC) prevents its uptake by immune phagocytes. In 2001, he obtained an INSERM Research scientist position and joined the group of Dr. Jean-Pierre Gorvel at the Centre d’Immunologie de Marseille-Luminy, France, where he started studying the intracellular cycle of the zoonotic bacterial pathogen Brucella abortus. In 2004, he obtained an NIH investigator position at the Rocky Mountain Laboratories, NIAID in Montana, where he continued his studies of bacterial pathogen interactions with phagocytes, focusing on Brucella abortus and Francisella tularensis. Dr. Celli was recruited to the WSU Paul G. Allen School for Global Animal Health as an Associate Professor in July 2013, to further pursue his research on the pathogenesis of zoonotic bacteria.
I grew up in the suburbs of Paris, wandering through some rebel teenage years, when my high school biology teacher managed to trigger my interest for the scientific method in biology, and ultimately convinced me to take the path I am still walking today. My fascination for the bacterial world came from summer internships in some dark basements of the Pasteur Institute as an undergraduate student, and subsequent brighter training experiences in bacterial genetics during my PhD. Drawn into the field of bacterial pathogenesis, I moved to Canada for some postdoctoral training in the laboratory of Dr. B. Brett Finlay in Vancouver, which cemented my admiration and curiosity for pathogenic microbes and how they exploit host cell functions to cause disease. After a couple of transatlantic moves and additional training that further focused my interests, I finally settled in the US to develop a research career on the pathogenesis of zoonotic intracellular bacteria.
Although I grew up in an urban environment, my travels and most recent workplaces have opened me to the wonders of the outdoors. When not at work, I often escape mountain biking and hiking in some wilder places.
Education and Training
- BSc - Université Paris 11
- PhD - Université Pierre & Marie Curie, Paris 6
- Postdoctoral training at the University of British Columbia
General Research / Expertise
Our lab studies the mechanisms used by intracellular bacterial pathogens to survive and proliferate within host phagocytes, counteracting innate immune defenses. We use a combination of genetic, cell biological and biochemical approaches to tease apart how Brucella abortus, the bacterial causative agent of the worldwide disease brucellosis, modulates macrophage functions to ensure its intracellular survival, persistence and proliferation, as part of its ability to cause disease. We currently focus on the following specific areas of research:
- Role of the VirB Type IV secretion system and its effectors in the Brucella intracellular cycle
- Contribution of host autophagy in the Brucella intracellular cycle
- Brucella modulation of host secretory functions
Most pathogenic microbes, from viruses to bacteria to protozoan parasites, undergo an intracellular lifecycle in their host for survival, persistence or proliferation purposes, exploiting cellular functions to their advantage. These strategies cause pathogenic manifestations and disease and need to be understood to design effective therapeutics. Additionally, these microbes can serve as tools to tease apart the cellular processes they modulate, teaching us a great deal about basic biological principles. Using Brucella abortus as a model pathogen, our research aims to tackle these questions, therefore contributing knowledge that can ultimately used to the design of countermeasures against infectious diseases.
The Celli lab is focused on understanding the molecular mechanisms used by intracellular vacuolar bacteria to exploit host cell functions and generate niches of survival and proliferation. We use Brucella abortus as a model vacuolar pathogen that modulates host secretory and autophagic functions to generate a replicative vacuole derived from the endoplasmic reticulum (ER). Using a multidisciplinary combination of genetic, cell biology and biochemistry approaches, we aim to decipher at the cellular and molecular levels how specific bacterial effectors delivered into host cells via Type IV secretion alter various pathways associated with ER functions, Golgi-associated vesicular traffic and autophagic machineries, to promote biogenesis of the Brucella replicative vacuole and bacterial intracellular growth.
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.
- Miller CN, Smith EP, Cundiff JA, Knodler LA, Bailey Blackburn J, Lupashin V, Celli J. (2017) A Brucella Type IV Effector Targets the COG Tethering Complex to Remodel Host Secretory Traffic and Promote Intracellular Replication. Cell Host Microbe 22(3):317-329.e7. doi: 10.1016/j.chom.2017.07.017. Epub 2017 Aug 24. PMID: 28844886 PMCID: PMC5599354
- Smith EP, Miller CN, Child R, Cundiff JA, Celli J. (2016) Postreplication Roles of the Brucella VirB Type IV Secretion System Uncovered via Conditional Expression of the VirB11 ATPase. mBio. 7(6). pii: e01730-16. doi: 10.1128 PMID: 27899503 PMCID: PMC5137499
- Case ED, Chong A, Wehrly TD, Hansen B, Child R, Hwang S, Virgin HW, Celli J. (2014) The Francisella O-antigen mediates survival in the macrophage cytosol via autophagy avoidance. Cell Microbiol. 16(6):862-77 PMID: 24286610 PMCID: PMC4028363
- Starr T, Child R, Wehrly TD, Hansen B, Hwang S, López-Otin C, Virgin HW, Celli J. (2012) Selective subversion of autophagy complexes facilitates completion of the Brucella intracellular cycle. Cell Host Microbe. 11(1):33-45 PMID: 22264511 PMCID: PMC3266535
- Celli J, de Chastellier C, Franchini DM, Pizarro-Cerda J, Moreno E, Gorvel JP. (2003) Brucella evades macrophage killing via VirB-dependent sustained interactions with the endoplasmic reticulum. J Exp Med. 198(4):545-56. PMID: 12925673 PMCID: PMC2194179
- Fighting a sly, crippling disease
- Brucellosis microbe infects, performs like giant
- Tenure and promotions for 2018 announced
- New Brucella abortus findings will support more opportunities for mitigation of Brucellosis
- Identification of Brucella protein could lead to infection treatment
- Removal of Brucellosis protein combats bacterial infection