Joseph E. Qualls, PhD

Assistant Professor, UC Department of Pediatrics

Phone 513-636-9102

Email joseph.qualls@cchmc.org

Immunology; innate immunity; macrophage biology; amino acid metabolism; intracellular pathogenesis 

Dr. Qualls completed his undergraduate work in 2002, receiving his BA summa cum laude in Biology from Thomas More College in Crestview Hills, KY. He then joined the laboratory of Don Cohen, PhD, in the Department of Microbiology, Immunology, and Molecular Genetics at the University of Kentucky, where he studied the role of macrophages and dendritic cells during the development of inflammatory bowel disease. After defending his thesis and receiving his PhD in 2007, Dr. Qualls began his postdoctoral training with Peter Murray, PhD, in the Department of Infectious Diseases and Immunology at St. Jude Children’s Research Hospital in Memphis, TN, where his research helped to define the functional plasticity of macrophages in response to infection and cancer. During his postdoctoral training, Dr. Qualls received a Ruth L. Kirschstein National Research Service Award and actively participated as Vice Chair of Mentoring Activities within the Postdoctoral Association Council and as a member of the Education Programs Committee.

Dr. Qualls’ long-term goals are to understand the interplay between nutrition, metabolism, and immune regulation during anti-pathogen defense. He has focused on how macrophages use the amino acid, L-arginine, to combat intracellular pathogens. As a starting point to appreciate broader principles of immunity and metabolism he established a map of L-arginine metabolism at the transcriptomic and metabolomic levels. His laboratory now uses this map to dissect how L-arginine generates anti-microbial effectors, how this pathway is regulated, and how microbes can hijack the pathway. His current research has two complementary tracks that retain initial focus on L-arginine metabolism in macrophages, but will eventually broaden into larger issues concerning metabolism in immunity.

Current research: Many groups have shown that T cell function is inhibited via byproducts of L-arginine metabolism or when extracellular L-arginine becomes limiting. In one project, the laboratory is focused on characterizing the in vivo function of L-arginine utilization by macrophages during mycobacterial infection, and how this affects anti-pathogen T cell function. In parallel, the laboratory is addressing the provocative role of L-arginine biosynthesis from L-citrulline during intracellular infection, and how this mechanism is regulated at the cellular level. While greatly unexplored, this pathway of amino acid recycling is vital as mice deficient in L-arginine biosynthesis, compared to normal mice, lack efficient control of both M. bovis BCG and M. tuberculosis infection.

BA: Thomas More College, Crestview Hills, KY, 2002.

PhD: University of Kentucky, Lexington, KY, 2007.

Postdoctoral Fellowship: St. Jude Children’s Research Hospital, Memphis, TN, 2012.

View PubMed Publications

Haverkamp JM, Smith AM, Weinlich R, Dillon CP, Qualls JE, Neale G, Koss B, Kim Y, Bronte V, Herold MJ, Green DR, Opferman JT, Murray PJ. Myeloid-derived suppressor activity is mediated by monocytic lineages maintained by continuous inhibition of extrinsic and intrinsic death pathways. Immunity. 2014 Dec 18;41(6):947-59.

Duque-Correa MA, Kuhl A, Rodriquez PC, Zedler U, Schommer-Leitner S, Rao M, Weiner J, Hurwitz R, Qualls JE, Kosmiadi GA, Murray PJ, Kaufmann SHE, Reece ST. Macrophage arginase-1 controls bacterial growth and pathology in hypoxic tuberculosis granulomas. Proceedings of the National Academy of Sciences – USA. 2014 Sep 23;111(38):E4024-32.

Barron L, Smith AM, El Kasmi KC, Qualls JE, Huang X, Cheever A, Borthwick LA, Wilson MS, Murray PJ, Wynn TA. Role of arginase 1 from myeloid cells in Th2-dominated lung inflammation. PLOS One. 2013 Apr 24;8(4):e61961.

Qualls JE, Subramanian C, Smith AM, Balouzian L, DeFreitas AA, Shirey KA, Reutterer B, Kernbauer E, Stockinger S, Decker T, Miyairi I, Vogel SN, Rock CO, Murray PJ. Sustained generation of nitric oxide and control of mycobacterial infection requires argininosuccinate synthase 1. Cell Host & Microbe. 2012 Sep 13;12(3):313-23.

Smith AM, Qualls JE, O’Brien K, Balouzian L, Johnson PF, Schultz-Cherry S, Smale ST, Murray PJ. A Distal Enhancer in Il12b is the Target of Transcriptional Repression by the Stat3 Pathway and Requires the B-Zip Protein NFIL-3. Journal of Biological Chemistry. 2011 Jul 1; 286(26):23582-90.

Qualls JE, Murray PJ. Tumor Macrophages: Protective and Pathogenic Roles in Cancer Development. Current Topics in Developmental Biology. 2011; 94: 309-28.

Qualls JE, Neale G, Smith AM, Koo MS, DeFreitas AA, Zhang H, Kaplan G, Watowich SS, Murray PJ. Arginine usage in mycobacteria-infected macrophages depends on autocrine-paracrine cytokine signaling. Science Signaling. 2010 Aug 17;3(135):ra62.

Qualls JE and Murray PJ. A double agent in cancer: stopping macrophages wounds tumors. Nature Medicine. 2010 Aug;16(8):863-4.

El Kasmi KC, Qualls JE (co-primary author), Pesce JT, Smith AM, Thompson RW, Henao-Tamayo M, Basaraba RJ, König T, Schleicher U, Koo M, Kaplan G, Fitzgerald KA, Tuomanen EI, Orne IM, Kanneganti T, Bogdan C, Wynn TA, Murray PJ. TLR-induced Arginase 1 thwarts effective immunity against intracellular pathogens. Nature Immunology. 2008 Dec;9(12):1399-406.

Qualls JE, Kaplan AM, van Rooijen N, Cohen DA. Suppression of Experimental Colitis by Intestinal Mononuclear Phagocytes. Journal of Leukocyte Biology. 2006 Oct; 80(4):802-15.

L-citrulline and host defenses to mycobacteria. Principle Investigator. American Heart Association. Jan 2015–Dec 2017.