Bryan P. Hurley, PhD

Hurley Lab--Bryan P. Hurley, PhD

The Hurley Laboratory investigates infectious and inflammatory diseases that disrupt mucosal surfaces of the lung and digestive tract.

Overview

Our overall research objective is to gain a better understanding of how injury, infection, and/or genetics drive mucosal inflammation and damage, manifesting as disease. More specifically, our team explores how bacterial pathogens and other noxious agents impact barrier integrity at the respiratory and digestive surface and elicit inflammatory processes. We are actively exploring cellular and molecular mechanisms involved in orchestrating neutrophil and eosinophil trans-epithelial migration.

We have discovered an inducible, tightly regulated process involving the release of lipid mediators, known as eicosanoids that function as neutrophil chemo-attractants, directing neutrophils to breach intact epithelial barriers.

A more thorough understanding of the mucosal barrier, its vulnerabilities, and how inflammation can disrupt its integrity will greatly inform therapeutic development towards managing excessive inflammation in the face of a diverse array of external and endogenous threats.

Meet our Team

Hurley Lab

PRINCIPAL INVESTIGATOR

Bryan P. Hurley, PhD
Assistant Professor of Pediatrics, Harvard Medical School


RESEARCH TEAM

Michael A. Pazos, PhD
Instructor

Lael M. Yonker, MD
Instructor
Find a Doctor Profile

Bernard B. Lanter, PhD
Postdoctoral Fellow

Kevin S. Gipson, MD
Postdoctoral Fellow

Alex D. Eaton
Research Technician II

Rhianna M. Hibbler
Research Technician II

Research Projects

Our overall research objective is to gain a better understanding of how injury, infection, and/or genetics drive mucosal inflammation and damage, manifesting as disease. More specifically, our team explores how bacterial pathogens and other noxious agents impact barrier integrity at the respiratory and digestive surface and elicit inflammatory processes. We are actively exploring cellular and molecular mechanisms involved in orchestrating neutrophil and eosinophil trans-epithelial migration.

We have discovered an inducible, tightly regulated process involving the release of lipid mediators, known as eicosanoids that function as neutrophil chemo-attractants, directing neutrophils to breach intact epithelial barriers.

A more thorough understanding of the mucosal barrier, its vulnerabilities, and how inflammation can disrupt its integrity will greatly inform therapeutic development towards managing excessive inflammation in the face of a diverse array of external and endogenous threats.

Publications

Hurley, B.P., Goodman, A.L., Murphy, P., Lory, S., McCormick, B.A..  The Two-Component Sensor Response Regulator RoxR / RoxS Plays a Role in Pseudomonas aeruginosa Interactions with Airway Epithelial Cells.  Microbes & Infection.  2010; 12(3):190-8.
PMC2826603 http://www.ncbi.nlm.nih.gov/pubmed/19961952


Hurley, B.P., Pirzai, W., Mumy, K.L., Gronert, K., McCormick B.A..  Selective Eicosanoid Generating Capacity of Cytoplasmic Phospholipase A2 in Pseudomonas aeruginosa Infected Epithelial Cells.  Am J Physiol Lung Cell Mol Physiol.  2011; 300(2):L286-94.
PMC3043809 http://www.ncbi.nlm.nih.gov/pubmed/21097525


Tamang D.L., Pirzai W., Priebe G..P, Traficante D.C., Pier G.B., Falck J.R., Morisseau C., Hammock B.D., McCormick B.A., Gronert K., Hurley B.P..  Hepoxilin A3 Facilitates Neutrophilic Breach of Lipoxygenase-Expressing Airway Epithelial Barriers.  J Immunol. 2012; 189(10):4960-9. 
PMC3490410 http://www.ncbi.nlm.nih.gov/pubmed/23045615


Trebicka E., Jacob S., Pirzai W., Hurley B.P., Cherayil B.J..  Role of anti-lipopolysaccharide antibodies in serum bactericidal activity against Salmonella enterica serovar Typhimurium in healthy adults and children in the United States.  Clin Vaccine Immunol. 2013 Oct;20(10):1491-8.
PMC3807195 http://www.ncbi.nlm.nih.gov/pubmed/23803904


Bhowmick R., Tin Maung N.H., Hurley B.P., Ghanem E.B., Gronert K., McCormick B.A., Leong J.M.. Systemic disease during Streptococcus pneumoniae acute lung infection requires 12-lipoxygenase-dependent inflammation. J Immunol. 2013 Nov 15;191(10):5115-23.PMC3836588 http://www.ncbi.nlm.nih.gov/pubmed/24089193


Kusek, M.E., Pazos, M.A., Pirzai W., Hurley, B.P.In Vitro Co-Culture Assay to Assess Pathogen Induced Neutrophil Trans-Epithelial Migration.  J. Vis. Exp. 2014; jan 6;(83):e50823. PMC4063550 http://www.ncbi.nlm.nih.gov/pubmed/24430378


Kubala S.A., Patil S.U., Shreffler W.G., Hurley B.P.. Pathogen induced chemo-attractant hepoxilin A3 drives neutrophils, but not eosinophils across epithelial barriers.  Prostaglandins Other Lipid Mediat. 2014 Jan; 108:1-8. PMC4004677 http://www.ncbi.nlm.nih.gov/pubmed/24315875


Hurley BP (2014) Phospholipases in Health and Disease.  Tappia PS, Dhalla NS, editors.  New York, NY: Springer. Chapter 8, Phospholipase A2 Activity Exhibited by a Bacterial Virulence Protein that Enters and Operates within a Variety of Host Cells; p.135-146. 410p


Pazos M.A., Pirzai W., Yonker L.M., Morisseau C., Gronert K., Hurley B.P.. Distinct cellular sources of hepoxilin A3 and leukotriene B4 are used to coordinate bacterial-induced neutrophil transepithelial migration. J Immunol. 2015 Feb 1; 194(3):1304-15. PMC4297725 http://www.ncbi.nlm.nih.gov/pubmed/25548217


Yonker LM, Cigana C, Hurley BP, Bragonzi A (2015) Host-pathogen interplay in the respiratory environment of cystic fibrosis.  J Cyst Fibros.  14(4):431-9. PMC4485938 http://www.ncbi.nlm.nih.gov/pubmed/25800687


Hurley B.P., Pirzai W., Eaton A.D., Harper M., Roper J., Zimmermann C., Ladics G.S., Layton R.J., Delaney B.. An experimental platform using human intestinal epithelial cell lines to differentiate between hazardous and non-hazardous proteins.  Food Chem Toxicol. 2016 Jun;92:75-87.  http://www.ncbi.nlm.nih.gov/pubmed/27060235


Johnston N, Ondrey F, Rosen R, Hurley BP, Gould J, Allen J, DelGaudio J, Altman KW. (2016) Airway reflux. Ann N Y Acad Sci. [Epub ahead of print] http://www.ncbi.nlm.nih.gov/pubmed/27310222


Chen K., Shanmugam N.K., Pazos M.A., Hurley B.P., Cherayil B.J.. Commensal Bacteria-Induced Inflammasome Activation in Mouse and Human Macrophages Is Dependent on Potassium Efflux but Does Not Require Phagocytosis or Bacterial Viability.  PLoS One. 2016 Aug 9;11(8):e0160937. http://www.ncbi.nlm.nih.gov/pubmed/27505062

Back to Top