Sean P. Riley, Assistant Professor
2014 - 2019: Research Assistant Professor, Louisiana State University School of Veterinary Medicine, Baton Rouge, LA
2009 - 2013: Postdoctoral Scholar, University of Chicago, Chicago, IL
2008: Ph.D., Microbiology, University of Kentucky, Lexington, KY
2002: B.S., Microbiology, University of Illinois-Urbana/Champaign, Urbana, IL
2019 - present: Assistant Professor, Virginia-Maryland School of Veterinary Medicine, University of Maryland, College Park, MD
Sean’s research focuses on molecular and cellular interactions between intracellular bacteria and mammalian cells. In specific, he studies tick-transmitted pathogens of the genus Rickettsia, which causes life-threatening diseases like Rocky Mountain spotted fever. Through millennia of evolution, these bacteria have lost many genes for survival outside of a host cell. Instead, these bacteria manipulate the host to provide a nutrient-rich and hospitable environment for growth. The problem occurs when Rickettsia is injected into the bloodstream by an infected tick and parasitize the blood vessels of mammals. The blood vessel cells, called endothelial cells, are so overwhelmed by the bacteria and the immune system that the endothelial cells can no longer form a barrier to contain blood. Needless to say, it is not good when your blood vessels start leaking blood into the rest of your body. This is where the “spotted fever” disease name comes from. The blood vessels of the infected mammal are actually becoming leaky in a process we call vascular discontinuity. This leads to the most severe manifestations of the infection.
Despite the severity of these infections, we can logically deduce that Rickettsia has an inherent weakness in their lifecycle. The weakness is that the bacteria are completely and utterly reliant on the host cell for survival. By identifying the molecular interactions between the host cell and the bacteria through research, we are actually identifying very clear targets for therapeutic development. And since the bacteria wholly rely on these host-pathogen interactions to cause disease, we can introduce compounds that prevent the bacteria from manipulating the host. This is the goal of the host-pathogens interaction laboratory… to identify the molecular interactions between the host cell and the bacteria that allow Rickettsia to parasitize the host cell. With this knowledge, we can develop new and improved therapeutic interventions.
Riley SP, Fish AI, Del Piero F, Martinez JJ. Immunity against the Obligate Intracellular Bacterial Pathogen Rickettsia australis Requires a Functional Complement System. Infect Immun. 2018 Jun;86(6). doi:10.1128/IAI.00139-18. Print 2018 Jun. PubMed PMID: 29581196; PubMed Central PMCID: PMC5964522.
Riley SP, Pruneau L, Martinez JJ. Evaluation of changes to the Rickettsia rickettsii transcriptome during mammalian infection. PLoS One. 2017;12(8):e0182290. doi: 10.1371/journal.pone.0182290. eCollection 2017. PubMed PMID: 28832688; PubMed Central PMCID: PMC5568294
Riley SP, Fish AI, Garza DA, Banajee KH, Harris EK, del Piero F, Martinez JJ. Nonselective Persistence of a Rickettsia conorii Extrachromosomal Plasmid during Mammalian Infection. Infect Immun. 2016 Jan 11;84(3):790-7. doi: 10.1128/IAI.01205-15. PubMed PMID: 26755154; PubMed Central PMCID: PMC4771360
Riley SP, Cardwell MM, Chan YG, Pruneau L, Del Piero F, Martinez JJ. Failure of a heterologous recombinant Sca5/OmpB protein-based vaccine to elicit effective protective immunity against Rickettsia rickettsii infections in C3H/HeN mice. Pathog Dis. 2015 Dec;73(9):ftv101. doi:10.1093/femspd/ftv101. Epub 2015 Oct 29. PubMed PMID: 26519448; PubMed Central PMCID: PMC4732028
Riley SP, Macaluso KR, Martinez JJ. Electrotransformation and Clonal Isolation of Rickettsia Species. Curr Protoc Microbiol. 2015 Nov 3;39:3A.6.1-20. doi:10.1002/9780471729259.mc03a06s39. PubMed PMID: 26528784; PubMed Central PMCID: PMC4664152.
Czyż DM, Potluri LP, Jain-Gupta N, Riley SP, Martinez JJ, Steck TL, Crosson S, Shuman HA, Gabay JE. Host-directed antimicrobial drugs with broad-spectrum efficacy against intracellular bacterial pathogens. MBio. 2014 Jul 29;5(4):e01534-14. doi: 10.1128/mBio.01534-14. PubMed PMID: 25073644; PubMed Central PMCID: PMC4128363.
Riley SP, Patterson JL, Nava S, Martinez JJ. Pathogenic Rickettsia species acquire vitronectin from human serum to promote resistance to complement-mediated killing. Cell Microbiol. 2014 Jun;16(6):84961. doi: 10.1111/cmi.12243. Epub 2013 Dec 13. PubMed PMID: 24286496; PubMed Central PMCID: PMC4028375.
Riley SP, Patterson JL, Martinez JJ. The rickettsial OmpB β-peptide of Rickettsia conorii is sufficient to facilitate factor H-mediated serum resistance. Infect Immun. 2012 Aug;80(8):2735-43. doi:10.1128/IAI.00349-12. Epub 2012 May 21. PubMed PMID: 22615250; PubMed Central PMCID: PMC343
Riley SP, Goh KC, Hermanas TM, Cardwell MM, Chan YG, Martinez JJ. The Rickettsia conorii autotransporter protein Sca1 promotes adherence to nonphagocytic mammalian cells. Infect Immun. 2010 May;78(5):1895-904. doi: 10.1128/IAI.01165-09. Epub 2010 Feb 22. PubMed PMID: 20176791; PubMed Central PMCID: PMC2863548.
Riley SP, Bykowski T, Cooley AE, Burns LH, Babb K, Brissette CA, Bowman A, Rotondi M, Miller MC, DeMoll E, Lim K, Fried MG, Stevenson B. Borrelia burgdorferi EbfC defines a newly-identified, widespread family of bacterial DNA-binding proteins. Nucleic Acids Res. 2009 Apr;37(6):1973-83. doi:10.1093/nar/gkp027. Epub 2009 Feb 10. PubMed PMID: 19208644; PubMed Central PMCID: PMC2665219.