#  Darren E. Higgins 

Professor of Microbiology

 

 

 



   ![higgins_darren.jpg](/sites/g/files/omnuum3501/files/styles/hwp_4_5__480x600/public/dms/files/higgins_darren.jpg?itok=OaQQVEYv) 

 



 

 location\_on Harvard Medical School New Research Building, Room 854 77 Ave. Louis Pasteur Boston, MA 02115 

 smartphone [617-432-4156](tel:617-432-4156) 

 email <dhiggins@hms.harvard.edu> 

 laptop\_windows [Lab Website](https://higginslab.med.harvard.edu/) 

 laptop\_windows [Publications](https://pubmed.ncbi.nlm.nih.gov/?dispmax=20&pmfilter_EDatLimit=added+to+PubMed+in+the+last+5+years&cmd_current=Limits&orig_db=PubMed&cmd=Search&term=Higgins+DE&doptcmdl=DocSum) 

 

 



 

 Bacterial pathogens that grow within human cells are responsible for multiple diseases and millions of deaths worldwide. The primary goal of our research is to elucidate both the pathogen and host cell-specific mechanisms involved in the growth, spread, and virulence of intracellular bacterial pathogens. We take a multidisciplinary approach in our investigations employing molecular genetics, cell biology, immunology, high-resolution microscopy, structural biology, tissue culture and mouse infection models.

 Because of its rich history as a model intracellular pathogen for immunological and cell biological research, we primarily utilize the bacterium Listeria monocytogenes for our studies. L. monocytogenes is a foodborne pathogen capable of causing severe life-threatening infections in humans, including meningitis and encephalitis. Current research areas include: determining the mechanisms of host cell invasion, cell-to-cell spread, and colonization of distal sites within the host, such as the brain. Furthermore, we are using organoid infection models to determine the molecular mechanisms of host defense and bacterial virulence strategies, studying the coordinate regulation of bacterial gene expression required for pathogenesis, and characterizing pathogen-specific antigenic targets and host cell mediators that lead to protective T cell-mediated immunity.



 

 

 





 

 

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