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Michael Reed

Associate Professor

Michael Reed

Molecular Pathogenesis of Tuberculosis

Medicine, Infectious Diseases
Montreal General Hospital
1625 Pine Avenue West
Montreal, QC H3G 1A4
Tel: (514) 934-1934 x.43543
Fax: (514) 934-8261
michael [dot] reed [at] mcgill [dot] ca (Email)

 

 

Research Orientations

The research of my laboratory focuses on molecular aspects of the pathogenesis of Mycobacterium tuberculosis, the bacterial agent responsible for the infectious disease, tuberculosis (TB).  Despite the existence of effective antibacterial drugs and a partially effective vaccine for more than half a century, TB still remains the cause of 2 million deaths worldwide each year - the most due to any single infectious agent.  This situation reflects very poorly on the current level of understanding of the pathogenic processes associated with this important pathogen.

Although early studies considered TB strains to be restricted in terms of their genetic and antigenic variability, more recent evidence indicates that M. tuberculosis has evolved into several genetically diverse lineages of strains that are likely to possess unique attributes related to the transmission and development of disease.  My laboratory utilizes a combination of microbial genetics, biochemistry and whole animal (mouse) in vivo infection studies to investigate the array of metabolic and virulence strategies available to this phenotypically diverse pathogen.  Increasing our knowledge and understanding of this diversity will greatly enhance future efforts aimed at developing new strategies to successfully diagnose and treat TB disease.

 Selected Recent Publications:

 Follow on PubMed 

  1. Albanna AS, Reed MB, Kotar KV, Fallow A, McIntosh FA, Behr MA & Menzies D (2011).  Reduced transmissibility of East African Indian strains of Mycobacterium tuberculosis.  PLoS ONE 6: e25075.
  2. Domenech P, Kolly GS, Leon-Solis L, Fallow A & Reed MB (2010).  Massive gene duplication event among clinical isolates of the Mycobacterium tuberculosis W/Beijing family. Journal of Bacteriology 192: 4562-4570.
  3. Fallow A, Domenech P & Reed MB (2010).  Strains of the East Asian (W/Beijing) lineage of Mycobacterium tuberculosis are DosS/DosT-DosR two-component regulatory system natural mutants. Journal of Bacteriology 192: 2228-2238.
  4. Domenech P & Reed MB (2009).  Rapid and spontaneous loss of phthiocerol dimycocerosate (PDIM) from Mycobacterium tuberculosis grown in vitro: implications for virulence studies.  Microbiology 155: 3532-3543.
  5. Coulombe F, Divangahi M, Veyrier F, Gleason J, Yang Y, Kelliher MA, Pandey AK, Sassetti CM, Reed MB & Behr MA (2009).  Increased NOD2-mediated recognition of N-glycolyl muramyl dipeptide.  The Journal of Experimental Medicine 206: 1709-1716.
  6. Reed MB, Pichler VK, McIntosh F, Mattia A, Fallow A, Masala S, Domenech P, Zwerling A, Thibert L, Menzies D, Schwartzman K & Behr MA (2009).  Major Mycobacterium tuberculosis lineages associate with patient country of origin.  Journal of Clinical Microbiology 47: 1119-1128.
  7. Reed MB, Gagneux S, Deriemer K, Small PM & Barry, CE 3rd. (2007) The W-Beijing lineage of Mycobacterium tuberculosis overproduces triglycerides and has the DosR dormancy regulon constitutively upregulated.  Journal of Bacteriology 189: 2583-2589.

 

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