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Richard Friedman, PhD

Professor
Primary Affiliation: 

Department of Immunobiology

Member: BIO5 Institute

Biography: 

Richard Friedman received both his Master’s and Ph.D. degrees at Michigan State University, in 1976 and 1979, respectively.  There he did research on the interactions of the pathogen Salmonella enterica serotype Typhimurium with liver Kupffer cells and the role serum components played in killing the microbe. He then did postdoctoral training in the Department of Microbiology at the Oregon Health Sciences University, Portland, OR in the laboratory of Dr. Barbara Iglewski. Work involved studies on the pathogenesis of two human pathogens, Pseudomonas aeruginosa and Legionella pneumophila. After three years of training he took a position as a Research Scientist to develop vaccines against Bordetella pertussis, at the Swiss Serum and Vaccine Institute in Bern, Switzerland.  He left the Vaccine Institute in 1984 when he was offered an Assistant Professor position in the Department of Microbiology and Immunology, College of Medicine, University of Arizona. Dr. Friedman continued research on B. pertussis for many years. Taking the unique opportunity to do a one year sabbatical oversees, with the support of a Fogarty International Fellowship Award; he began studies on the mechanism of Mycobacterium tuberculosis (Mtb) pathogenesis in the human host. Training to safely work with Mtb and to begin research with this challenging pathogen took place in the laboratory of Douglas Young, Department of Medical Microbiology, St. Mary’s Hospital Medical School, Imperial College, London, England.  Presently, the focuses of investigations in Dr. Friedman’s laboratory are various mechanisms of pathogenesis in Mtb and Campylobacter jejuni.  This microbe is the leading cause of food poisoning in the USA.  The C. jejuni work is being done in active collaboration with Lynn Joens, Ph.D. Department of Veterinary Science and Microbiology, College of Agriculture.

Research Overview: 

Studies that were initiated by Dr. Friedman, while on sabbatical, identified a unique Mtb protein that enhances intracellular survival (Eis) of M. smegmatis in macrophages. This secreted protein was named Eis.  Studies observed that Mtb-infected macrophage would produce Eis in phagosomes which was released into the macrophage cytoplasm and then secreted from the infected macrophage. Bioinformatic analysis found that Eis is an N-acetyltransferase which appears to play an important role in its biological activities. In further collaborative studies Eis was found to suppress macrophage authophagy, inflammation, and cell death via the inhibition of reactive oxygen species. Studies show that these Eis functions are dependent on its N-acetyltransferase domain.  Thus, Mtb Eis suppresses a variety of macrophage immune responses, improving mycobacterial survival within these critical phagocytic cells.

 

Other investigations in the lab involve studies on adherence factors of Mtb.  Many other laboratories have reported the presence of various adhesions on the surface of Mtb which may play a role in binding to various types of host cells. This would then lead to initial attachment, colonization of the host, and the development of infection.  Many pathogenic microbes (Gram-positive and Gram-negative) produce a common adhesive organelle called pili.  Until recently, it was a common view that mycobacteria do produce pili.  Interesting studies done in the Friedman lab discovered that Mtb and other mycobacterial species do indeed produce pili (MTP in Mtb) by various criteria.  Thus it is very compelling to suggest that MTP may play an important role in the colonization of the human host.

Selected Publications

Dong-Min Shin, Bo-Young Jeon, Hye-Mi Lee, Hyo Sun Jin, Jae-Min Yuk, Chang- Hwa Song, Sang-Hee Lee, Zee-Won Lee, Sang-Nae Cho, Jin-Man Kim, Richard L. Friedman, and Eun-Kyeong Jo.  M. tuberculosis Eis regulates autophagic cell death and inflammation through redox-dependent signaling. PLoS Pathogens, 6:e1001230, 2010.

21187903

Alteri, C. J., J. Xicohentencatl-Cortes, S. Hess, G. Caballero-Olin, J. A. Giron, and R. L. Friedman. Mycobacterium tuberculosis produces pili during human infection.  PNAS. 104:5145-5150. 2007.

17360408

Samuel, L. P., C. H. Song, J. Wei, E. A. Roberts, E. K.. Jo, and R. L. Friedman. 2007. Expression, production and release of the Eis protein by Mycobacterium tuberculosis during infection of macrophages and its effect on cytokine secretion. Microbiology 153: 529-540.

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Michigan State University, 1979

Mailing

1656 E. Mabel Street

P.O. Box 245221

Tucson, AZ 85724-5221

 

Physical

Arizona Health Sciences Center Suite 6112A

(520) 626-7807