Doug Johnston, PhD

Research Assistant Professor of Microbiology

1901 Perdido St.
Box P6-1
Microbiology, Immunology & Parasitology
New Orleans, LA 70112
Phone: (504) 568-4071; Fax: (504) 568-2918
djoh13@lsuhsc.edu

BS, Microbiology
Cal State University Long Beach

MS, Microbiology
Cal State University Long Beach

PhD, Biological Sciences
University of California Irvine

Dr. Johnston began his research career as a Master's student in the Division of Infectious Diseases at Harbor-UCLA Medical Center in Torrance, CA. Upon graduation, he was invited to continue his work there as a Research Associate, under the tutelage of Dr. Scott Filler. Research in the Filler lab was focused on two medically important fungi, the human pathogens Candida and Aspergillus. Utilizing techniques from biochemistry, molecular biology, and immunology, Dr. Johnston helped to identify and characterize many novel aspects of pathogenesis and drug resistance in these two genera. After several years at Harbor-UCLA, Dr. Johnston switched gears and began his PhD studies in the lab of Dr. Chris Hughes at UC Irvine where the focus was vascular biology, particularly the mechanisms involved in inflammation, wound healing & angiogenesis. 

Dr. Johnston's research helped to identify numerous components of the signaling pathways that are differentially regulated upon endothelial cell exposure to inflammatory cytokines, including TNF-a, that are important for maintaining vascular integrity and controlling outgrowth. 

Dr. Johnston joined the Department of Microbiology, Immunology and Parasitology in 2008 when, for his postdoctoral work, he joined the lab of Dr. Joy Sturtevant- coming full circle back to the field of fungal pathogenesis. In 2010, after helping to characterize many aspects of mutant Candida biology, Dr. Johnston accepted an appointment as Assistant Professor-Research where he is now working to characterize the molecular interactions between pathogenic fungi and the endothelium.

Research in the Johnston lab is focused on defining mechanisms of fungal pathogenesis, particularly the human host response to bloodstream infection. Many species of the Genus Candida are commonly found as part of the normal flora of the skin, gut, and genitourinary tract of healthy individuals, yet changes to host immune status, flora composition, or mucosal integrity allow opportunistic Candida to become pathogenic. The severity of candidiasis ranges from relatively benign superficial infections to systemic disease that is often fatal. In fact, C. albicans is the most commonly isolated fungal pathogen among severely immunocompromised patients and is the fourth most common cause of nosocomial infections. Under these conditions, Candida penetrates the natural barriers to infection, such as the skin or mucosa, where it gains access to the bloodstream, allowing the organism to spread throughout the body. Once bloodborne, Candida is capable of escaping the vasculature and invading nearly every tissue. Mortality attributed to disseminated candidiasis is often greater than 50%, even with aggressive antifungal treatment. Importantly, for Candida to exit the bloodstream, it requires significant interaction between the fungus and both the endothelial cells lining the vascular wall and the underlying extracellular matrix (ECM). 

We use molecular, genetic, biochemical, immunochemical, and cell-based approaches to define the human endothelial cell response to adherence, invasion, and damage by C. albicans. Our most recent results suggest that invasion by C. albicans results in widespread endothelial apoptosis and the suppression of components of the normal wound healing response, including migration, proliferation, and differentiation. Vascular dysfunction in this setting might provide Candida a greater window of opportunity for the establishment of infection. The ability to manipulate the endothelial response to Candida may strengthen its barrier function and provide for enhanced immune function. Our goal is to define the key mechanisms involved in the host endothelial response to Candida and to identify novel potential targets for the development of new antifungal therapies.

Johnston DA, Eberle KE, Sturtevant JE, Palmer GE. 2009. A role for endosomal and vacuolar  GTPases in Candida albicans pathogenesis. Infection & Immunity. 7, 6:1458-08. 

Kelly MN, Johnston DA, Peel B, Palmer GE, Sturtevant JE. 2009. Bmh1p (14-3-3) mediates pathways associated with virulence in Candida albicans. Microbiology. 155:1536-1546.  

Johnston DA, Dong B, Hughes CC. 2009. TNF induction of jagged-1 expression in endothelial cells is NFkB-dependent. Gene. 435:36-44. 

Sainson RA, Johnston DA, Chu HC, Holderfield MT, Nakatsu MN, Crampton SP, Davis J, Conn E, Hughes CC. 2008. TNF induces Jagged-1 expression in endothelial cells and promotes development of an angiogenic phenotype. Blood. 111(10):4997-5007. 

Sanchez AA, Johnston DA, Myers C, Edwards JE Jr, Mitchell AP, Filler SG. 2004. Relationship between Candida albicans virulence during experimental hematogenously disseminated infection and endothelial cell damage in vitro. Infect Immun. 72(1):598-601. 

Spellberg B, Johnston D, Phan QT, Edwards JE Jr, French SW, Ibrahim AS, Filler SG. 2003. Parenchymal organ, and not splenic, immunity correlates with host survival during disseminated candidiasis. Infect Immun. 71(10):5756-64. 

Fukuoka T, Johnston DA, Winslow CA, de Groot MJ, Burt C, Hitchcock CA, Filler SG. 2003. Genetic basis for differential activities of fluconazole and voriconazole against Candida krusei. Antimicrob Agents Chemother. 47(4):1213-9. 

Belanger PH, Johnston DA, Fratti RA, Zhang M, Filler SG. 2002. Endocytosis of Candida albicans by vascular endothelial cells is associated with tyrosine phosphorylation of specific host cell proteins. Cell Microbiol. 4(12):805-12. 

Cannom RR, French SW, Johnston D, Edwards Jr JE, Filler SG. 2002. Candida albicans stimulates local expression of leukocyte adhesion molecules and cytokines in vivo. J Infect Dis. 186(3):389-96.