Research in the Jordt laboratory focuses on the mechanisms that enable humans and animals to sense touch, pain and irritation. These fundamental sensations originate in peripheral sensory neurons which contain signaling pathways that translate environmental physical and chemical stimuli into neural activity. Our aims are to identify the molecular components of these pathways and to understand how sensory neurons become activated and sensitized during injury, inflammation and chronic painful conditions. The lab uses molecular, genetic and physiological techniques with a focus on models that closely mimic human conditions.
Current projects focus on:
- Ion channels and New Targets in Pain: The Jordt lab investigates the role of Transient Receptor Potential (TRP) ion channels, a group of ion channels that activate sensory neurons and pain sensations in response to thermal (hot, cold) and chemical stimuli. TRP channels were identified through their interactions with natural products such as capsaicin (in chili peppers), mustard oil (in mustard and wasabi) and menthol (in peppermint), and were shown to be involved in many painful conditions, including arthritis, diabetes and infections. The Jordt lab is studying the actions of TRP channel inhibitors in pain models and investigates mechanisms through which natural products elicit or inhibit acute and inflammatory pain.
- Allergies, Asthma and Itch: Sensory neurons mediate the sensations of itch, irritation and respiratory discomfort in allergic conditions. Research in the Jordt laboratory has revealed that blocking sensory nerves by targeting their receptors alleviates asthmatic conditions and also diminishes itch and inflammation in allergic contact dermatitis. We developed a unique model of poison ivy contact dermatitis we study to identify novel treatments to suppress itch in conditions unresponsive to antihistamines.
- Chemical Exposure Injuries and Tear Gas Agents: Supported by the National Institute of Environmental Health Sciences (NIEHS) and the NIH Countermeasures Against Chemical Threats (CounterACT) program since 2006, the Jordt laboratory has made key contributions to research understanding the injury mechanisms following toxic chemical exposures. We identified TRPA1 as a target of chlorine gas and many other toxic exposures eliciting incapacitating pain, inflammation and organ injury. The Jordt laboratory is actively working with federal agencies and industry partners to identify additional targets and develop countermeasures that improve health outcomes following chemical exposures. Other studies focus on tear gas agents (CS, CN) and their potentially toxic effects, a topic Dr. Jordt has been interviewed on frequently by the public press.
- Tobacco Regulatory Science: Menthol cigarettes are increasingly popular, especially with adolescent beginning smokers. Applying our expertise in chemical sensory biology the Jordt lab demonstrated that menthol reduces the irritation sensed when inhaling smoke and increases markers of nicotine uptake. These effects are mediated by TRPM8, the cold/menthol receptor in sensory neurons innervating the respiratory system. This work is supported by programs from the FDA and NIDA through a Tobacco Center of Regulatory Science (TCORS), also supporting studies on flavor additives in electronic cigarettes and smokeless tobacco.
November 8, 2016
Jordt Lab Study On Poison Ivy Mechanism Featured on CBS News Page.
August 28, 2014
Jordt Lab Science Featured on Duke Today
August 24, 2014
New York Magazine: Dr. Jordt on Tear Gas Effects
August 21, 2014
Dr. Jordt Interviewed on MSNBC on Health Effects of Tear Gas
August 19, 2014
Dr. Jordt Describes Action of Tear Gas in USA Today
- Balakrishna S, Song W, Achanta S, Doran SF, Liu B, Kaelberer MM, Yu Z, Sui A, Cheung M, Leishman E, Eidam HS, Ye G, Willette RN, Thorneloe KS, Bradshaw HB, Matalon S, Jordt SE. TRPV4 inhibition counteracts edema and inflammation and improves pulmonary function and oxygen saturation in chemically induced acute lung injury. Am J Physiol Lung Cell Mol Physiol. 2014 Jul 15;307(2):L158-72. Epub 2014 May 16.
- Gui J, Liu B, Cao G, Lipchik AM, Perez M, Dekan Z, Mobli M, Daly NL, Alewood PF, Parker LL, King GF, Zhou Y, Jordt SE, Nitabach MN. A tarantula-venom peptide antagonizes the TRPA1 nociceptor ion channel by binding to the S1-S4 gating domain. Curr Biol. 2014 Mar 3;24(5):473-83. Epub 2014 Feb 13.
- Liu B, Fan L, Balakrishna S, Sui A, Morris JB, Jordt SE. TRPM8 is the principal mediator of menthol-induced analgesia of acute and inflammatory pain. Pain. 2013 Oct;154(10):2169-77. Epub 2013 Jun 29.
- Liu B, Escalera J, Balakrishna S, Fan L, Caceres AI, Robinson E, Sui A, McKay MC, McAlexander MA, Herrick CA, Jordt SE. TRPA1 controls inflammation and pruritogen responses in allergic contact dermatitis. FASEB J. 2013 Sep;27(9):3549-63. Epub 2013 May 30.
- Willis DN, Liu B, Ha MA, Jordt SE, Morris JB. Menthol attenuates respiratory irritation responses to multiple cigarette smoke irritants. FASEB J. 2011 Dec;25(12):4434-44. Epub 2011 Sep 8.
- Schulze C, McGowan M, Jordt SE, Ehrlich BE. Prolonged oxaliplatin exposure alters intracellular calcium signaling: a new mechanism to explain oxaliplatin-associated peripheral neuropathy. Clin Colorectal Cancer. 2011 Jun;10(2):126-33. Epub 2011 Apr 22.
- Jordt SE. Trigeminal TRPs and the scent of pain. Pain. 2011 Jan;152(1):4-5. Epub 2010 Nov 30.
- Bessac BF, Jordt SE. Sensory detection and responses to toxic gases: mechanisms, health effects, and countermeasures. Proc Am Thorac Soc. 2010 Jul;7(4):269-77.
- Lanosa MJ, Willis DN, Jordt S, Morris JB. Role of metabolic activation and the TRPA1 receptor in the sensory irritation response to styrene and naphthalene. Toxicol Sci. 2010 Jun;115(2):589-95. Epub 2010 Feb 22.
- Caceres AI, Brackmann M, Elia MD, Bessac BF, del Camino D, D’Amours M, Witek JS, Fanger CM, Chong JA, Hayward NJ, Homer RJ, Cohn L, Huang X, Moran MM, Jordt SE. A sensory neuronal ion channel essential for airway inflammation and hyperreactivity in asthma. Proc Natl Acad Sci U S A. 2009 Jun 2;106(22):9099-104. Epub 2009 May 19.