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School of Medicine
Lintao Qu, M.D., Ph.D.
Assistant Professor of Neurosurgery
Research Interests: Cellular and molecular mechanisms of arthritis pain
Dr. Qu is an assistant professor in the Department of Neurosurgery. His research interest mainly focuses on the peripheral neural mechanisms of chronic pain and itch in the context of nerve injury and inflammation using a combination of approaches, including immunohistochemistry, whole-cell recordings, calcium imaging, molecular biology, in vivo calcium imaging and electrophysiological recordings on the intact DRG, and pain related behavioral assessments.
Dr. Qu earned his Ph.D. degree from University of Western Ontario, Canada in 2009. After completion of his degree, He joined Dr. Robert LaMotte’s laboratory as a postdoc associate in the Department of Anesthesiology at Yale University. Dr. Qu joined the Johns Hopkins faculty in 2014.
- Assistant Professor of Neurosurgery
Departments / Divisions
Centers & Institutes
- M.D., North China University of Science and Technology School of Medicine (China) (1999)
- Ph.D., University of Western Ontario (Canada) (2009)
Research & Publications
Treatment for joint pain in rheumatoid arthritis (RA) continues to be a challenge and represents a large unmet medical need. Although RA pain is often thought to result from inflammation, it often persists even after optimal control of inflammation with currently available therapies, indicating the involvements of other non-inflammatory mechanisms. Our lab is exploring the potential inflammation-independent mechanisms of RA pain using mouse genetics and behavioral/physiological approaches. Moreover, to visualize and analyze the alterations of the activity of joint sensory neurons, we recently developed two powerful approaches, including in vivo dorsal root ganglion (DRG) neuron imaging and in vivo electrophysiological recordings on the intact DRG. The long-term goal of my research is to illuminate a novel peripheral neural mechanism underlying RA pain independent of joint inflammation and define a promising therapeutic target for RA pain that is resistant to current anti-inflammatory treatments or occurs in patients for whom such treatments are infeasible or poorly tolerated.
Our lab is interested in studying the peripheral immune and neural mechanisms of arthritis pain using a combination of approaches including immunostaining, mouse behavior, in vivo and in vitro DRG electrophysiology and calcium imaging, molecular biology and transgenic mice.
Technology Expertise Keywordsarthritis pain, miRNAs, TRP channels, In Vivo and in vitro electrophysiology, In vivo DRG imaging
Selected PublicationsView all on Pubmed
Qu L. and Caterina MJ. (2016).Enhanced excitability and suppression of A-type K+ currents in joint sensory neurons in a murine model of antigen-induced arthritis. Scientific Reports. 6:28899. * Corresponding author
Qu L, Fu K, Yang J, Shimada S, and LaMotte RH. (2015). CXCR3 chemokine receptor signaling mediates itch in experimental allergic contact dermatitis. Pain. Sep;156(9):1737-1746. Featured as Editor’s Choice.
Qu L, Fan N, Ma C, Wang T, Han L, Fu K, Wang Y, Shimada S, Dong X and LaMotte RH. (2014) Enhanced excitability of MrgprA3+ and MrgprD+ nociceptors in a model of inflammatory itch and pain. Brain 137(Pt 4):1039-1050.
Han L, Ma C, Liu Q, McNeil B, Wend HJ, Cui Y, Tang Z, Kim. Y, Nie H, Qu L, Patel K, Li Z, Xiao B, LaMotte RH and Dong X. (2013). A subpopulation of nociceptors specifically linked to itch. Nat: Neurosci.16(2):174-182.
Qu L,Li Y, Pan XH, Zhang P, LaMotte RH and Ma C. (2012) TRPC3 is required for IgG-immune complex-induced depolarization of DRG neurons. J Neurosci. 32(28):9554-9562. Highlighted in ‘This Week In The Journal’.
Academic Affiliations & Courses
Graduate Program Affiliation
Cellular and Molecular Medicine Graduate Program
Activities & Honors
- Society For Neuroscience (2005-current)
- International Association for the Study of Pain (IASP) (2010-current)
- American Pain Society (2017-current)
- The Association of Rheumatology Health Professionals (2018-current)